diff --git a/.DS_Store b/.DS_Store new file mode 100644 index 0000000000000000000000000000000000000000..4545ef51b5f6c710f146177c5591d8150b2c0aaa Binary files /dev/null and b/.DS_Store differ diff --git a/008252c8-5656-408f-9f9f-d1664f73a7e1.json b/008252c8-5656-408f-9f9f-d1664f73a7e1.json new file mode 100644 index 0000000000000000000000000000000000000000..80bf083808b8c1cff0498d662f4153b3f27581e7 --- /dev/null +++ b/008252c8-5656-408f-9f9f-d1664f73a7e1.json @@ -0,0 +1,50 @@ +{ + "id": "008252c8-5656-408f-9f9f-d1664f73a7e1", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "12351479", + "text": "OBJECTIVE:\nTo determine whether components of the metabolic syndrome precede the 5-year incidence of cardiovascular disease and diabetes.\n\nRESEARCH DESIGN AND METHODS:\nA population of individuals aged 43-84 years was evaluated from 1988 to 1990 and again 5 years later. Medical history, blood pressure, and laboratory measures were obtained at both examinations following the same protocols. Subjects without diabetes were classified according to level of glycemia, high blood pressure, high-risk lipid levels, high uric acid levels, and proteinuria at baseline. History of incident myocardial infarction, angina, stroke, and diabetes was obtained at follow-up.\n\nRESULTS:\nOf the 4,423 subjects without diabetes, 6.9% had elevated levels of glycemia, 18.4% had high blood pressure, 82.7% had high-risk lipid levels (either high serum total cholesterol or low HDL cholesterol or high ratio of these two levels), 27% had elevated uric acid levels, 33.2% had high BMI, and 3.3% had proteinuria (\u003e or =30 mg/dl). The risk of incident cardiovascular disease 5 years later increased with the number of the components present; 2.5% of those with one component developed cardiovascular disease, whereas 14.9% of those with four or more components developed cardiovascular disease. Of those with one component, diabetes developed in 1.1% 5 years later, whereas diabetes developed in 17.9% of those with four or more components.\n\nCONCLUSIONS:\nComponents of the metabolic syndrome are common and are associated with incident cardiovascular disease and diabetes after 5 years. Interventions to alter BMI, lipid levels, and blood pressure may decrease incident diabetes and cardiovascular disease." + }, + "questions": [ + { + "id": "ad9f6434-15af-436c-8e80-5d31b010ac51", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1432, + "text": "Components of the metabolic syndrome" + }, + { + "answer_start": 721, + "text": "elevated levels of glycemia" + }, + { + "answer_start": 760, + "text": "high blood pressure" + }, + { + "answer_start": 791, + "text": "high-risk lipid levels (either high serum total cholesterol or low HDL cholesterol or high ratio of these two levels)" + }, + { + "answer_start": 955, + "text": "high BMI" + } + ] + } + ] +} \ No newline at end of file diff --git a/02551e49-54f9-4d1a-a797-476104decd03.json b/02551e49-54f9-4d1a-a797-476104decd03.json new file mode 100644 index 0000000000000000000000000000000000000000..5e900ba9cc88e00df1d74842a3af3d51a7f3c14c --- /dev/null +++ b/02551e49-54f9-4d1a-a797-476104decd03.json @@ -0,0 +1,43 @@ +{ + "id": "02551e49-54f9-4d1a-a797-476104decd03", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "17050892", + "text": "BACKGROUND:\nReduced lung function in early infancy has been associated with later obstructive airway diseases. We assessed whether reduced lung function shortly after birth predicts asthma 10 years later.\n\nMETHODS:\nWe conducted a prospective birth cohort study of healthy infants in which we measured lung function shortly after birth with the use of tidal breathing flow-volume loops (the fraction of expiratory time to peak tidal expiratory flow to total expiratory time [t(PTEF)/t(E)]) in 802 infants and passive respiratory mechanics, including respiratory-system compliance, in 664 infants. At 10 years of age, 616 children (77%) were reassessed by measuring lung function, exercise-induced bronchoconstriction, and bronchial hyperresponsiveness (by means of a methacholine challenge) and by conducting a structured interview to determine whether there was a history of asthma or current asthma.\n\nRESULTS:\nAs compared with children whose t(PTEF)/t(E) shortly after birth was above the median, children whose t(PTEF)/t(E) was at or below the median were more likely at 10 years of age to have a history of asthma (24.3% vs. 16.2%, P=0.01), to have current asthma (14.6% vs. 7.5%, P=0.005), and to have severe bronchial hyperresponsiveness, defined as a methacholine dose of less than 1.0 micromol causing a 20% fall in the forced expiratory volume in 1 second (FEV1) (9.1% vs. 4.9%, P=0.05). As compared with children whose respiratory-system compliance was above the median, children with respiratory compliance at or below the median more often had a history of asthma (27.4% vs. 14.8%; P=0.001) and current asthma (15.0% vs. 7.7%, P=0.009), although this measure was not associated with later measurements of lung function. At 10 years of age, t(PTEF)/t(E) at birth correlated weakly with the maximal midexpiratory flow rate (r=0.10, P=0.01) but not with FEV1 or forced vital capacity.\n\nCONCLUSIONS:\nReduced lung function at birth is associated with an increased risk of asthma by 10 years of age." + }, + "questions": [ + { + "id": "a8b372a0-70f9-446c-b705-b229e08cb70e", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1907, + "text": "Reduced lung function at birth" + }, + { + "answer_start": 998, + "text": "children whose t(PTEF)/t(E) was at or below the median" + }, + { + "answer_start": 1480, + "text": "children with respiratory compliance at or below the median" + } + ] + } + ] +} \ No newline at end of file diff --git a/03063f69-25c7-4f99-af64-34e0c16638db.json b/03063f69-25c7-4f99-af64-34e0c16638db.json new file mode 100644 index 0000000000000000000000000000000000000000..47f69ccc0eb75c0581c570367dda0eccba16875f --- /dev/null +++ b/03063f69-25c7-4f99-af64-34e0c16638db.json @@ -0,0 +1,38 @@ +{ + "id": "03063f69-25c7-4f99-af64-34e0c16638db", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "7888928", + "text": "OBJECTIVE:\nTo examine the association between smoking, alcohol consumption, and the incidence of non-insulin dependent diabetes mellitus in men of middle years and older.\n\nDESIGN:\nCohort questionnaire study of men followed up for six years from 1986.\n\nSETTING:\nThe health professionals' follow up study being conducted across the United States.\n\nSUBJECTS:\n41,810 male health professionals aged 40-75 years and free of diabetes, cardiovascular disease, and cancer in 1986 and followed up for six years.\n\nMAIN OUTCOME MEASURE:\nIncidence of non-insulin dependent diabetes mellitus diagnosed in the six years.\n\nRESULTS:\nDuring 230,769 person years of follow up 509 men were newly diagnosed with diabetes. After controlling for known risk factors men who smoked 25 or more cigarettes daily had a relative risk of diabetes of 1.94 (95% confidence interval 1.25 to 3.03) compared with non-smokers. Men who consumed higher amounts of alcohol had a reduced risk of diabetes (P for trend \u003c 0.001). Compared with abstainers men who drank 30.0-49.9 g of alcohol daily had a relative risk of diabetes of 0.61 (95% confidence interval 0.44 to 0.91).\n\nCONCLUSIONS:\nCigarette smoking may be an independent, modifiable risk factor for non-insulin dependent diabetes mellitus. Moderate alcohol consumption among healthy people may be associated with increased insulin sensitivity and a reduced risk of diabetes." + }, + "questions": [ + { + "id": "2c3fd709-0411-444f-8d0e-293a10e37339", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 742, + "text": "men who smoked 25 or more cigarettes daily" + }, + { + "answer_start": 1150, + "text": "Cigarette smoking" + } + ] + } + ] +} \ No newline at end of file diff --git a/030e07f4-3960-4b5d-b42b-1baa0c4cb5bd.json b/030e07f4-3960-4b5d-b42b-1baa0c4cb5bd.json new file mode 100644 index 0000000000000000000000000000000000000000..44037f0bfdaaca54742f26e7f9f84a571354d1a6 --- /dev/null +++ b/030e07f4-3960-4b5d-b42b-1baa0c4cb5bd.json @@ -0,0 +1,38 @@ +{ + "id": "030e07f4-3960-4b5d-b42b-1baa0c4cb5bd", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "11889155", + "text": "Insulin resistance is common in adults with polycystic ovary syndrome (PCOS). Although recent data demonstrate that insulin resistance is present in the early stages of PCOS, the prevalence of insulin resistance in adolescents with PCOS has not been determined. Likewise, the prevalence of impaired glucose tolerance (IGT) or type 2 diabetes mellitus (DM) in adolescent cohorts has not been established. In this study we sought to obtain preliminary data regarding the prevalence of IGT and DM in adolescents with PCOS and to assess the ability of screening tests to predict these abnormalities within this population. Twenty-seven adolescents with PCOS underwent oral glucose tolerance tests. Plasma glucose and insulin levels were obtained at baseline, and glucose was measured 2 h after a 75-g glucose challenge. The 2-h plasma glucose level was used to categorize subjects as having IGT or the provisional diagnosis of DM. Eight of our 27 subjects had IGT, and 1 had previously undiagnosed DM. These abnormalities were seen among lean and obese subjects. Fasting plasma glucose levels and simple measures of insulin resistance were suboptimal predictors of IGT and DM within our cohort. As in adults, our results indicate that adolescents with PCOS are at increased risk for IGT and DM and that the 2-h plasma glucose level after an oral glucose challenge appears to be the most reliable screening test for these abnormalities. Our results need to be corroborated by future studies that determine the prevalence of abnormalities in glucose tolerance among large populations of adolescents, both with and without PCOS. However, as DM may be preventable by lifestyle modifications, we would recommend that adolescents with PCOS undergo periodic screening for abnormal glucose tolerance using 2-h postchallenge plasma glucose levels." + }, + "questions": [ + { + "id": "265016af-0f85-4011-9891-5c1f9a6dc332", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1231, + "text": "adolescents with PCOS" + }, + { + "answer_start": 44, + "text": "polycystic ovary syndrome (PCOS)" + } + ] + } + ] +} \ No newline at end of file diff --git a/039ecaa9-9b14-4d71-8373-19bc54f60418.json b/039ecaa9-9b14-4d71-8373-19bc54f60418.json new file mode 100644 index 0000000000000000000000000000000000000000..79f0cae2cdd39ab3f75d9521b0c0b1f002d29b4b --- /dev/null +++ b/039ecaa9-9b14-4d71-8373-19bc54f60418.json @@ -0,0 +1,38 @@ +{ + "id": "039ecaa9-9b14-4d71-8373-19bc54f60418", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "12610050", + "text": "OBJECTIVE:\nInsulin resistance (IR) and the metabolic syndrome (MS) are associated with type 2 diabetes and adverse cardiovascular disease (CVD) risk factor profiles. Whether IR and MS predict CVD independently of diabetes and other CVD risk factors is not known. This study examines whether IR and/or presence of MS are independently associated with CVD in nondiabetic American Indians (AI).\n\nRESEARCH DESIGN AND METHODS:\nWe examined 2283 nondiabetic AI who were free of CVD at the baseline examination of the Strong Heart Study (SHS). CVD risk factors were measured, IR was quantified using the homeostasis model assessment (HOMA), and MS as defined by the National Cholesterol Education Program Adult Treatment Panel (ATP III) was assessed for each participant. Incident CVD and diabetes were ascertained during follow-up.\n\nRESULTS:\nMS was present in 798 individuals (35%), and 181 participants (7.9%) developed CVD over 7.6 +/- 1.8 years of follow-up. Age, BMI, waist circumference, and triglyceride levels increased and HDL cholesterol decreased across tertiles of HOMA-IR. Risk of diabetes increased as a function of baseline HOMA-IR (6.3, 14.6, and 30.1%; P \u003c 0.001) and MS (12.8 vs. 24.5%). In Cox models adjusted for CVD risk factors, risk of CVD did not increase either as a function of baseline HOMA-IR or MS, but individual CVD risk factors predicted subsequent CVD.\n\nCONCLUSIONS:\nAmong nondiabetic AI in the SHS, HOMA-IR and MS both predict diabetes, but neither predicts CVD independently of other established CVD risk factors." + }, + "questions": [ + { + "id": "b78ca6d5-3d16-4b44-be9d-e0d2bd8fb1bd", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 11, + "text": "Insulin resistance (IR)" + }, + { + "answer_start": 43, + "text": "metabolic syndrome (MS) " + } + ] + } + ] +} \ No newline at end of file diff --git a/03b94b86-3d51-4507-8fa2-fe337d186e02.json b/03b94b86-3d51-4507-8fa2-fe337d186e02.json new file mode 100644 index 0000000000000000000000000000000000000000..c5424dae9047a0cf623740fc3e67fa2bbfcee9e5 --- /dev/null +++ b/03b94b86-3d51-4507-8fa2-fe337d186e02.json @@ -0,0 +1,43 @@ +{ + "id": "03b94b86-3d51-4507-8fa2-fe337d186e02", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "24876226", + "text": "BACKGROUND:\nFew prospective studies have examined the relationship between sun exposure, other potential risk factors, and risk of different skin cancers [including basal cell carcinoma (BCC), squamous cell carcinoma (SCC), and melanoma] simultaneously.\n\nMETHODS:\nWe evaluated the association between a number of potential risk factors and skin cancer risk in a cohort of 108,916 US women, the Nurses' Health Study II (1989-2009).\n\nRESULTS:\nDuring 2.05 million years of follow-up, we identified 6,955, 880, and 779 diagnoses of BCC, SCC, and melanoma, respectively. Compared with participants in the lowest quintile of cumulative ultraviolet flux in adulthood, participants in the highest quintile had multivariable-adjusted relative risks (RR) of 2.35 (Ptrend \u003c 0.0001) for BCC, 2.53 (Ptrend = 0.009) for SCC, and 0.68 (Ptrend = 0.38) for melanoma. In contrast, the RRs were 1.68 (95% CI, 1.55-1.82) for BCC, 1.68 (95% CI, 1.34-2.11) for SCC, and 1.80 (95% CI, 1.42-2.28) for melanoma for participants with ≥5 blistering sunburns when compared with participants without sunburn between ages 15 and 20 years. We found significant interactions between family history of melanoma, number of blistering sunburns between ages 15 and 20 years and BCC risk, and between sunburn reaction as a child/adolescent and SCC risk (all Pinteraction \u003c 0.05).\n\nCONCLUSION:\nIn a cohort of U.S. women, we found that sun exposures in both early life and adulthood were predictive of BCC and SCC risks, whereas melanoma risk was predominantly associated with sun exposure in early life.\n\nIMPACT:\nOur results may have potential implications for the prevention of skin cancers. Cancer Epidemiol Biomarkers Prev; 23(6); 1080-9. ©2014 AACR." + }, + "questions": [ + { + "id": "f66e889f-0816-4ea9-a296-fef0b984d9d2", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 1008, + "text": "≥5 blistering sunburns" + }, + { + "answer_start": 1151, + "text": "family history of melanoma" + }, + { + "answer_start": 1179, + "text": "number of blistering sunburns between ages 15 and 20 years" + } + ] + } + ] +} \ No newline at end of file diff --git a/03c10014-aab4-422f-9401-5df2267318ec.json b/03c10014-aab4-422f-9401-5df2267318ec.json new file mode 100644 index 0000000000000000000000000000000000000000..543b77aef561bfedbd089731e5dfb2c7327f8678 --- /dev/null +++ b/03c10014-aab4-422f-9401-5df2267318ec.json @@ -0,0 +1,39 @@ +{ + "id": "03c10014-aab4-422f-9401-5df2267318ec", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "26103029", + "text": "IMPORTANCE:\nThe target for the oral erectile dysfunction drugs, phosphodiesterase type 5 (PDE5) inhibitors, is part of a pathway implicated in the development of malignant melanoma. An increased risk of melanoma in sildenafil users was recently reported.\n\nOBJECTIVE:\nTo examine the association between use of PDE5 inhibitors and melanoma risk, including data on specific PDE5 inhibitors, number of prescriptions, and melanoma stage.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nNationwide, population-based, nested case-control study in the Swedish Prescribed Drug Register, the Swedish Melanoma Register, and other health care registers and demographic databases in Sweden, including 4065 melanoma cases diagnosed from 2006 through 2012 and 5 randomly selected controls per case with matching year of birth.\n\nEXPOSURES:\nNumber of filled prescriptions for the PDE5 inhibitors sildenafil and vardenafil or tadalafil.\n\nMAIN OUTCOMES AND MEASURES:\nRisk of melanoma; overall and by stage and risk of basal cell carcinoma in multivariable logistic regression analyses.\n\nRESULTS:\nOf 4065 melanoma cases, 435 men (11%) had filled prescriptions for PDE5 inhibitors, as did 1713 men of 20,325 controls (8%). In multivariable analysis, there was an increased risk of melanoma in men taking PDE5 inhibitors (OR, 1.21 [95% CI, 1.08-1.36]). The most pronounced increase in risk was observed in men who had filled a single prescription (OR, 1.32 [95% CI, 1.10-1.59]; exposure rate, 4% for cases vs 3% for controls), but was not significant among men with multiple filled prescriptions (for 2-5 prescriptions: OR, 1.14 [95% CI, 0.95-1.37], 4% for cases and 3% for controls; for ≥6 prescriptions: OR, 1.17 [95% CI, 0.95-1.44], 3% for cases vs 2% for controls). PDE5 inhibitors were significantly associated with melanoma stage 0 (OR, 1.49 [95% CI, 1.22-1.83], 13% for cases vs 8% for controls) and stage I (OR, 1.21 [95% CI, 1.02-1.43], 12% for cases vs 10% for controls), but not stage II through IV (OR, 0.83 [95% CI, 0.63-1.09], 6% for cases vs 7% for controls). The risk estimates were similar for sildenafil and vardenafil or tadalafil. PDE5 inhibitor use was also associated with an increased risk of basal cell carcinoma (OR, 1.19 [95% CI, 1.14-1.25], 9% for cases vs 8% for controls). Men taking PDE5 inhibitors had a higher educational level and annual income, factors that were also significantly associated with melanoma risk.\n\nCONCLUSIONS AND RELEVANCE:\nIn a Swedish cohort of men, the use of PDE5 inhibitors was associated with a modest but statistically significant increased risk of malignant melanoma. However, the pattern of association (eg, the lack of association with multiple filled prescriptions) raises questions about whether this association is causal." + }, + "questions": [ + { + "id": "fb0f9948-9bca-457c-b987-fcc734259374", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 2473, + "text": "use of PDE5 inhibitors" + }, + { + "answer_start": 1260, + "text": "men taking PDE5 inhibitors" + } + ] + } + ] +} \ No newline at end of file diff --git a/03e788ac-cd54-4c16-98a9-fbcd7b0ac5d3.json b/03e788ac-cd54-4c16-98a9-fbcd7b0ac5d3.json new file mode 100644 index 0000000000000000000000000000000000000000..ec5e9053c9235e33ac33504e7652d305130ca62c --- /dev/null +++ b/03e788ac-cd54-4c16-98a9-fbcd7b0ac5d3.json @@ -0,0 +1,46 @@ +{ + "id": "03e788ac-cd54-4c16-98a9-fbcd7b0ac5d3", + "disease": { + "id": "H00408", + "names": [ + "Type 1 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E10" + ], + "mesh": [ + "D003922" + ] + }, + "category": "Metabolic disease; Immune system disease; Endocrine disease" + }, + "article": { + "id": "9165223", + "text": "The relationship between the incidence of childhood-onset insulin-dependent diabetes mellitus and levels of nitrate in drinking water in the former Yorkshire Regional Health Authority was investigated by means of an ecological analysis. A population-based register contributed 1797 0-16-year-olds diagnosed with diabetes between 1978 and 1994. Nitrate data were based on 9330 samples of drinking water tested between 1990 and 1995 in 148 water supply zones, for which 1991 census small area statistics were taken on population density, ethnicity and socio-economic status. Diabetes incidence was positively associated with raised mean nitrate levels with a standardised incidence ratio of 115 in zones with greater than 14.85 mg.1-1 (chi2 = 26.81, 1 df, p \u003c 0.001). Significant negative trends were found between standardised incidence ratios and proportion of non-whites in the population (chi2 = 33.57, 1 df, p \u003c 0.001), childhood population density (chi2 = 30.81, 1 df, p \u003c 0.001) and the Townsend deprivation score (chi2 = 33.89, 1 df, p \u003c 0.001). Poisson regression modelling, adjusting for the other factors, showed a significant increase in relative incidence rate ratio from a baseline of 1 at nitrate levels below 3.22 mg.1-1 to 1.27 (95% confidence interval 1.09, 1.48) for mean nitrate levels above 14.85 mg.1-1. An association between higher nitrate levels in domestic drinking water and incidence of childhood diabetes has been demonstrated. This was not explained by the ethnic composition of the population, population density or socioeconomic status. Nitrate in drinking water may be a precursor of chemicals which are toxic to the pancreas." + }, + "questions": [ + { + "id": "7027e957-4d75-47cb-926d-e84f8dbebe31", + "text": "What are the risk factors of Type 1 diabetes mellitus?", + "answers": [ + { + "answer_start": 847, + "text": "proportion of non-whites in the population" + }, + { + "answer_start": 992, + "text": "Townsend deprivation score" + }, + { + "answer_start": 1347, + "text": "higher nitrate levels in domestic drinking water" + }, + { + "answer_start": 1567, + "text": "Nitrate in drinking water" + } + ] + } + ] +} \ No newline at end of file diff --git a/041e9e0a-7de7-4121-a69d-17677c5fb5e1.json b/041e9e0a-7de7-4121-a69d-17677c5fb5e1.json new file mode 100644 index 0000000000000000000000000000000000000000..e3e968c1e0a53aa5fcfcb1489ca9b9c9f4fc2e8e --- /dev/null +++ b/041e9e0a-7de7-4121-a69d-17677c5fb5e1.json @@ -0,0 +1,46 @@ +{ + "id": "041e9e0a-7de7-4121-a69d-17677c5fb5e1", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "18666209", + "text": "BACKGROUND:\nThe Gail model has been commonly used to estimate a woman's risk of breast cancer within a certain time period. High bone mineral density (BMD) is also a significant risk factor for breast cancer, but it appears to play no role in the Gail model. The objective of the current study was to investigate whether hip BMD predicts postmenopausal breast cancer risk independently of the Gail score.\n\nMETHODS:\nIn this prospective study, 9941 postmenopausal women who had a baseline hip BMD and Gail score from the Women's Health Initiative were included in the analysis. Their average age was 63.0 +/- 7.4 years at baseline.\n\nRESULTS:\nAfter an average of 8.43 years of follow-up, 327 incident breast cancer cases were reported and adjudicated. In a multivariate Cox proportional hazards model, the hazards ratios (95% confidence interval [95% CI]) for incident breast cancer were 1.35 (95% CI, 1.05-1.73) for high Gail score (\u003eor=1.67%) and 1.25 (95% CI, 1.11-1.40) for each unit of increase in the total hip BMD T-score. Restricting the analysis to women with both BMD and a Gail score above the median, a sharp increase in incident breast cancer for women with the highest BMD and Gail scores was found (P \u003c .05).\n\nCONCLUSIONS:\nThe contribution of BMD to the prediction of incident postmenopausal breast cancer across the entire population was found to be independent of the Gail score. However, among women with both high BMD and a high Gail score, there appears to be an interaction between these 2 factors. These findings suggest that BMD and Gail score may be used together to better quantify the risk of breast cancer." + }, + "questions": [ + { + "id": "48e36c34-b11a-41f1-849f-63789c476ac5", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 914, + "text": "high Gail score (\u003eor=1.67%)" + }, + { + "answer_start": 975, + "text": "each unit of increase in the total hip BMD T-score" + }, + { + "answer_start": 1172, + "text": "highest BMD and Gail scores" + }, + { + "answer_start": 124, + "text": "High bone mineral density (BMD)" + } + ] + } + ] +} \ No newline at end of file diff --git a/04a49704-1bf6-45ce-b36d-87003e0402fb.json b/04a49704-1bf6-45ce-b36d-87003e0402fb.json new file mode 100644 index 0000000000000000000000000000000000000000..b9d199c3f326b9f0d8bf47ea92ce82472c971540 --- /dev/null +++ b/04a49704-1bf6-45ce-b36d-87003e0402fb.json @@ -0,0 +1,34 @@ +{ + "id": "04a49704-1bf6-45ce-b36d-87003e0402fb", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "33626252", + "text": "BACKGROUND:\nMost data regarding the association between the glycemic index and cardiovascular disease come from high-income Western populations, with little information from non-Western countries with low or middle incomes. To fill this gap, data are needed from a large, geographically diverse population.\n\nMETHODS:\nThis analysis includes 137,851 participants between the ages of 35 and 70 years living on five continents, with a median follow-up of 9.5 years. We used country-specific food-frequency questionnaires to determine dietary intake and estimated the glycemic index and glycemic load on the basis of the consumption of seven categories of carbohydrate foods. We calculated hazard ratios using multivariable Cox frailty models. The primary outcome was a composite of a major cardiovascular event (cardiovascular death, nonfatal myocardial infarction, stroke, and heart failure) or death from any cause.\n\nRESULTS:\nIn the study population, 8780 deaths and 8252 major cardiovascular events occurred during the follow-up period. After performing extensive adjustments comparing the lowest and highest glycemic-index quintiles, we found that a diet with a high glycemic index was associated with an increased risk of a major cardiovascular event or death, both among participants with preexisting cardiovascular disease (hazard ratio, 1.51; 95% confidence interval [CI], 1.25 to 1.82) and among those without such disease (hazard ratio, 1.21; 95% CI, 1.11 to 1.34). Among the components of the primary outcome, a high glycemic index was also associated with an increased risk of death from cardiovascular causes. The results with respect to glycemic load were similar to the findings regarding the glycemic index among the participants with cardiovascular disease at baseline, but the association was not significant among those without preexisting cardiovascular disease.\n\nCONCLUSIONS:\nIn this study, a diet with a high glycemic index was associated with an increased risk of cardiovascular disease and death. (Funded by the Population Health Research Institute and others.)." + }, + "questions": [ + { + "id": "c6c65161-d4d8-4390-982f-1e1ad65f2aa7", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1910, + "text": "diet with a high glycemic index" + } + ] + } + ] +} \ No newline at end of file diff --git a/04b50bc5-9c21-4313-9f41-e6f9e7ddd036.json b/04b50bc5-9c21-4313-9f41-e6f9e7ddd036.json new file mode 100644 index 0000000000000000000000000000000000000000..52a4c8b45c685ae12c0765aea00ea39e911bd801 --- /dev/null +++ b/04b50bc5-9c21-4313-9f41-e6f9e7ddd036.json @@ -0,0 +1,43 @@ +{ + "id": "04b50bc5-9c21-4313-9f41-e6f9e7ddd036", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "22952297", + "text": "RATIONALE:\nAlthough epidemiological studies suggest that exposure to maternal smoking during fetal and early life increases the risk of childhood wheezing and asthma, previous studies were not able to differentiate the effects of prenatal from postnatal exposure.\n\nOBJECTIVES:\nTo assess the effect of exposure to maternal smoking only during pregnancy on wheeze and asthma among preschool-age children.\n\nMETHODS:\nA pooled analysis was performed based on individual participant data from eight European birth cohorts. Cohort-specific effects of maternal smoking during pregnancy, but not during the first year, on wheeze and asthma at 4 to 6 years of age were estimated using logistic regression and then combined using a random effects model. Adjustments were made for sex, parental education, parental asthma, birth weight, and siblings.\n\nMEASUREMENTS AND MAIN RESULTS:\nAmong the 21,600 children included in the analysis, 735 children (3.4%) were exposed to maternal smoking exclusively during pregnancy but not in the first year after birth. In the pooled analysis, maternal smoking only during pregnancy was associated with wheeze and asthma at 4 to 6 years of age, with adjusted odds ratios of 1.39 (95% confidence interval, 1.08-1.77) and 1.65 (95% confidence interval, 1.18-2.31), respectively. The likelihood to develop wheeze and asthma increased statistically significantly in a linear dose-dependent manner in relation to maternal daily cigarette consumption during the first trimester of pregnancy.\n\nCONCLUSIONS:\nMaternal smoking during pregnancy appears to increase the risk of wheeze and asthma among children who are not exposed to maternal smoking after birth." + }, + "questions": [ + { + "id": "3f68731e-9e28-4e20-9f7c-784fbb742b2e", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1068, + "text": "maternal smoking only during pregnancy" + }, + { + "answer_start": 1432, + "text": "maternal daily cigarette consumption during the first trimester of pregnancy" + }, + { + "answer_start": 1524, + "text": "Maternal smoking during pregnancy" + } + ] + } + ] +} \ No newline at end of file diff --git a/0532f382-af42-4e7d-b059-cc5831307410.json b/0532f382-af42-4e7d-b059-cc5831307410.json new file mode 100644 index 0000000000000000000000000000000000000000..919cbf2a3d708a08d009d5f3223f59319c1c6251 --- /dev/null +++ b/0532f382-af42-4e7d-b059-cc5831307410.json @@ -0,0 +1,41 @@ +{ + "id": "0532f382-af42-4e7d-b059-cc5831307410", + "disease": { + "id": "M2023_04_26_16_38_52", + "names": [ + "Migraine" + ], + "dbLinks": { + "icd10": [ + "G43" + ], + "icd11": [ + "8A80" + ], + "mesh": [ + "C10.228.140.546.399.750" + ] + }, + "description": "Migraine is a chronic neurological disorder characterized by recurrent episodes of unilateral, pulsatile headaches associated with autonomic symptoms such as nausea, vomiting, photophobia, and phonophobia. The pathophysiology of migraine is multifactorial and involves complex interactions between genetic, environmental, and neurochemical factors that modulate cerebral vascular tone and nociception. Migraine attacks can be triggered by a variety of factors, including stress, hormonal changes, sleep disturbances, and certain foods or medications. Treatment options for migraine include pharmacotherapy for acute attacks, preventive medications for frequent or severe headaches, and lifestyle modifications to avoid triggers. In refractory cases, interventional therapies such as nerve blocks or neuromodulation techniques may be considered." + }, + "article": { + "id": "23636092", + "text": "Migraine is a common disabling disorder with a significant genetic component, characterized by severe headache and often accompanied by nausea, vomiting, and light sensitivity. We identified two families, each with a distinct missense mutation in the gene encoding casein kinase Iδ (CKIδ), in which the mutation cosegregated with both the presence of migraine and advanced sleep phase. The resulting alterations (T44A and H46R) occurred in the conserved catalytic domain of CKIδ, where they caused reduced enzyme activity. Mice engineered to carry the CKIδ-T44A allele were more sensitive to pain after treatment with the migraine trigger nitroglycerin. CKIδ-T44A mice also exhibited a reduced threshold for cortical spreading depression (believed to be the physiological analog of migraine aura) and greater arterial dilation during cortical spreading depression. Astrocytes from CKIδ-T44A mice showed increased spontaneous and evoked calcium signaling. These genetic, cellular, physiological, and behavioral analyses suggest that decreases in CKIδ activity can contribute to the pathogenesis of migraine." + }, + "questions": [ + { + "id": "ae99a30d-5e0f-4158-8efe-2d523a3f4f02", + "text": "what are the risk factors of Migraine?", + "answers": [ + { + "answer_start": 1032, + "text": "decreases in CKIδ activity" + }, + { + "answer_start": 265, + "text": "casein kinase Iδ (CKIδ)" + } + ] + } + ] +} \ No newline at end of file diff --git a/05d967dc-437a-463c-9d91-34696585b7a9.json b/05d967dc-437a-463c-9d91-34696585b7a9.json new file mode 100644 index 0000000000000000000000000000000000000000..44d2f8266dcf9f15c49c5887591d1c5b106aaca6 --- /dev/null +++ b/05d967dc-437a-463c-9d91-34696585b7a9.json @@ -0,0 +1,39 @@ +{ + "id": "05d967dc-437a-463c-9d91-34696585b7a9", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "16141442", + "text": "BACKGROUND:\nAlthough research has shown that early life exposure to household endotoxin protects against development of allergies, studies are less clear on the relationship between household endotoxin exposure and prevalence of wheezing and asthma. We assayed 2,552 house dust samples in a representative nationwide sam- ple to explore relationships between endotoxin exposures and risk factors for asthma, asthma symptoms, and medication use.\n\nMETHODS:\nHouse dust was vacuum-sampled from five locations within homes and assayed for endotoxin. Health, demographic, and housing information was assessed through questionnaire and on-site evaluation of 2,456 residents of 831 homes selected to represent the demographics of the United States.\n\nRESULTS:\nEndotoxin concentration (EU/mg) and load (EU/m(2)) were highly correlated (r = 0.73-0.79). Geometric mean endotoxin concentrations were as follows (in EU/mg): bedroom floors, 35.3 (5th-95th percentile, 5.0-260); bedding, 18.7 (2.0-142); family room floors, 63.9 (11.5-331); sofas, 44.8 (6.4-240); and kitchen floors, 80.5 (9.8-512). Multivariate analysis demonstrated significant relationships between increasing endotoxin levels and diagnosed asthma, asthma symptoms in the past year, current use of asthma medications, and wheezing among residents of the homes. These relationships were strongest for bedroom floor and bedding dust and were observed in adults only. Modeling the joint effect of bedding and bedroom floor endotoxin on recent asthma symptoms yielded an adjusted odds ratio of 2.83 (95% confidence interval, 1.01-7.87). When stratified by allergy status, allergic subjects with higher endotoxin exposure were no more likely to have diagnosed asthma or asthma symptoms than nonallergic subjects.\n\nCONCLUSION:\nThis study demonstrates that household endotoxin exposure is a significant risk factor for increased asthma prevalence." + }, + "questions": [ + { + "id": "c80ed6a6-6cc7-4559-96f5-4df4be5eb15d", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1804, + "text": "household endotoxin exposure" + }, + { + "answer_start": 1153, + "text": "increasing endotoxin levels" + } + ] + } + ] +} \ No newline at end of file diff --git a/05db10b1-2fd8-435a-a5be-1363f8684bd1.json b/05db10b1-2fd8-435a-a5be-1363f8684bd1.json new file mode 100644 index 0000000000000000000000000000000000000000..f0c6949b975933ac24eb16392d0c1a1f0e228a44 --- /dev/null +++ b/05db10b1-2fd8-435a-a5be-1363f8684bd1.json @@ -0,0 +1,42 @@ +{ + "id": "05db10b1-2fd8-435a-a5be-1363f8684bd1", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "11545456", + "text": "BACKGROUND:\nUsing a combined analysis of 11 case-control studies from Europe, we have investigated the relationship between cigarette smoking and bladder cancer in women.\n\nMETHODS:\nAvailable smoking information on 685 female bladder cancer cases and 2416 female controls included duration of smoking habit, number of cigarettes smoked per day, and time since cessation of smoking habit for ex-smokers.\n\nRESULTS:\nThere was an increasing risk of bladder cancer with increasing duration of smoking, ranging from approximately a two-fold increased risk for a duration of less than 10 years (odds ratio (OR) = 1.9, 95% confidence interval (CI) 1.1-3.1) to over a four-fold increased risk for a duration of greater than 40 years (OR = 4.1, 95% CI 3.0-5.5). A dose-response relationship was observed between number of cigarettes smoked per day and bladder cancer up to a threshold limit of 15-20 cigarettes per day, OR = 3.8 (95% CI 2.7-5.4), after which no increased risk was observed. An immediate decrease in risk of bladder cancer was observed for those who gave up smoking. This decrease was over 30% in the immediate 1-4 years after cessation, OR = 0.68 (95% CI 0.38-1.2). However, even after 25 years the decrease in risk did not reach the level of the never-smokers, OR = 0.27 (95% CI 0.21-0.35).\n\nCONCLUSION:\nThe proportion of bladder cancer cases among women attributable to ever smoking was 0.30, (0.25-0.35) and to current smoking was 0.18 (0.14-0.22). These attributable proportions are less than those observed among men, although they are likely to increase in the future as the smoking-related disease epidemic among women matures." + }, + "questions": [ + { + "id": "3135a5e9-427a-4716-947d-430f9066c6af", + "text": "What are the risk factors of Bladder Cancer?", + "answers": [ + { + "answer_start": 464, + "text": "increasing duration of smoking" + }, + { + "answer_start": 1378, + "text": "ever smoking" + }, + { + "answer_start": 1420, + "text": "current smoking" + } + ] + } + ] +} \ No newline at end of file diff --git a/061d870f-1d33-45e1-9a4c-f7f888e336b0.json b/061d870f-1d33-45e1-9a4c-f7f888e336b0.json new file mode 100644 index 0000000000000000000000000000000000000000..3c9ed97238574a8a4224f8e19392503b1a423483 --- /dev/null +++ b/061d870f-1d33-45e1-9a4c-f7f888e336b0.json @@ -0,0 +1,46 @@ +{ + "id": "061d870f-1d33-45e1-9a4c-f7f888e336b0", + "disease": { + "id": "H00408", + "names": [ + "Type 1 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E10" + ], + "mesh": [ + "D003922" + ] + }, + "category": "Metabolic disease; Immune system disease; Endocrine disease" + }, + "article": { + "id": "14519705", + "text": "CONTEXT:\nDietary exposures in infancy have been implicated, albeit inconsistently, in the etiology of type 1 diabetes mellitus (DM).\n\nOBJECTIVE:\nTo examine the association between cereal exposures in the infant diet and appearance of islet autoimmunity (IA).\n\nDESIGN:\nBirth cohort study conducted from 1994 to 2002 with a mean follow-up of 4 years.\n\nSETTING:\nNewborn screening for HLA was done at St Joseph's Hospital in Denver, Colo. First-degree relatives of type 1 DM individuals were recruited from the Denver metropolitan area.\n\nPARTICIPANTS:\nWe enrolled 1183 children at increased type 1 DM risk, defined as either HLA genotype or having a first-degree relative with type 1 DM, at birth and followed them prospectively. We obtained exposure and outcome measures for 76% of enrolled children. Participants had variable lengths of follow-up (9 months to 9 years).\n\nMAIN OUTCOME MEASURES:\nBlood draws for the detection of insulin autoantibody, glutamic acid decarboxylase autoantibody, or IA-2 autoantibody were performed at 9, 15, and 24 months and annually thereafter. Children with IA (n = 34) were defined as those testing positive for at least 1 of the autoantibodies on 2 or more consecutive visits and who tested positive or had diabetes on their most recent visit.\n\nRESULTS:\nChildren initially exposed to cereals between ages 0 and 3 months (hazard ratio [HR], 4.32; 95% confidence interval [CI], 2.0-9.35) and those who were exposed at 7 months or older (HR, 5.36; 95% CI, 2.08-13.8) had increased hazard of IA compared with those who were exposed during the fourth through sixth month, after adjustment for HLA genotype, family history of type 1 DM, ethnicity, and maternal age. In children who were positive for the HLA-DRB1*03/04,DQB8 genotype, adjusted HRs were 5.55 (95% CI, 1.92-16.03) and 12.53 (95% CI, 3.19-49.23) for initial cereal exposure between ages 0 to 3 months and at 7 months or older, respectively.\n\nCONCLUSION:\nThere may be a window of exposure to cereals in infancy outside which initial exposure increases IA risk in susceptible children." + }, + "questions": [ + { + "id": "c54996c9-73e7-4025-b6b1-dde8c060d4d1", + "text": "What are the risk factors of Type 1 diabetes mellitus?", + "answers": [ + { + "answer_start": 1286, + "text": "Children initially exposed to cereals between ages 0 and 3 months" + }, + { + "answer_start": 1422, + "text": "those who were exposed at 7 months or older" + }, + { + "answer_start": 1695, + "text": "children who were positive for the HLA-DRB1*03/04,DQB8 genotype" + }, + { + "answer_start": 1968, + "text": "exposure to cereals in infancy" + } + ] + } + ] +} \ No newline at end of file diff --git a/074019cb-a9f4-47ef-80c0-80367a653174.json b/074019cb-a9f4-47ef-80c0-80367a653174.json new file mode 100644 index 0000000000000000000000000000000000000000..a909232d4ea467761e4ab166a7cd0e61262790d0 --- /dev/null +++ b/074019cb-a9f4-47ef-80c0-80367a653174.json @@ -0,0 +1,49 @@ +{ + "id": "074019cb-a9f4-47ef-80c0-80367a653174", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "24037561", + "text": "BACKGROUND:\nIncreasing evidence suggests that diabetes mellitus (DM) is associated with increased cancer incidence and mortality. Several mechanisms involved in diabetes, such as promotion of cell proliferation and decreased apoptosis, may foster carcinogenesis. This study investigated the association between DM and cancer incidence and cancer-specific mortality in patients with breast and colorectal carcinoma.\n\nMETHODS:\nA meta-analysis of controlled trials, prospective cohort studies and pooled cohort studies published after 2007 was conducted. Embase, PubMed and the Cochrane Library were searched. Summary hazard ratios (HRs) were calculated using a random-effects model. Sensitivity and subgroup analyses were performed to adjust for confounders, mode of DM assessment and follow-up time.\n\nRESULTS:\nTwenty studies were included to investigate the association between DM and breast and colorectal cancer incidence and cancer-specific mortality. The studies predominantly comprised patients with type II DM. The overall HR for breast cancer incidence was 1·23 (95 per cent confidence interval 1·12 to 1·34) and that for colorectal cancer was 1·26 (1·14 to 1·40) in patients with DM compared with those without diabetes. The overall HR was 1·38 (1·20 to 1·58) for breast cancer- and 1·30 (1·15 to 1·47) for colorectal cancer-specific mortality in patients with DM compared with those without diabetes.\n\nCONCLUSION:\nThis meta-analysis indicated that DM is a risk factor for breast and colorectal cancer, and for cancer-specific mortality." + }, + "questions": [ + { + "id": "821c8fe4-809d-4e4a-9a81-0533ec758d0f", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 990, + "text": "patients with type II DM" + }, + { + "answer_start": 1173, + "text": "patients with DM" + }, + { + "answer_start": 1456, + "text": "DM" + }, + { + "answer_start": 46, + "text": "diabetes mellitus (DM)" + } + ] + } + ] +} \ No newline at end of file diff --git a/07d8bf30-1ff4-463c-b4e7-09241fdfe69e.json b/07d8bf30-1ff4-463c-b4e7-09241fdfe69e.json new file mode 100644 index 0000000000000000000000000000000000000000..b647da9442fdf27036e5d3e912457d8fab4614bd --- /dev/null +++ b/07d8bf30-1ff4-463c-b4e7-09241fdfe69e.json @@ -0,0 +1,35 @@ +{ + "id": "07d8bf30-1ff4-463c-b4e7-09241fdfe69e", + "disease": { + "id": "H00056", + "names": [ + "Alzheimer disease", + "Dementia due to Alzheimer disease" + ], + "dbLinks": { + "icd10": [ + "G30" + ], + "mesh": [ + "D000544" + ] + }, + "category": "Neurodegenerative disease" + }, + "article": { + "id": "8113792", + "text": "Almost all patients \u003e 40 years of age with Down's syndrome (DS) develop the pathology characteristic of Alzheimer's disease: abundant beta-amyloid plaques and neurofibrillary tangles. We have investigated the gene expression of beta-amyloid protein precursor (APP) and tau in DS and age-matched control brains and found that levels of both mRNAs were significantly elevated in DS. Such up-regulation was not observed in two other neuronal proteins. A correlation between total APP and tau mRNA levels was also found in DS brain but distinct from the pattern observed in normal brain. Although a proportionality existed between APP-695 mRNA and three-repeat tau mRNA in DS, the proportionality between APP-751 mRNA and four-repeat tau mRNA, which is normally present, was not observed. Thus, DS brains are primarily characterized by the up-regulation of tau mRNA as well as APP mRNA and disruption of the coordinate expression between APP-751 and four-repeat tau." + }, + "questions": [ + { + "id": "5e05a017-96ba-4e63-8c92-85faa233dc56", + "text": "What are the risk factors of Alzheimer disease?", + "answers": [ + { + "answer_start": 11, + "text": "patients \u003e 40 years of age with Down's syndrome (DS)" + } + ] + } + ] +} \ No newline at end of file diff --git a/07f11fd4-babc-46d7-bf8d-4394fa354e74.json b/07f11fd4-babc-46d7-bf8d-4394fa354e74.json new file mode 100644 index 0000000000000000000000000000000000000000..3f345067f746a8714af9dbd4b18e8a7f2daca0ae --- /dev/null +++ b/07f11fd4-babc-46d7-bf8d-4394fa354e74.json @@ -0,0 +1,34 @@ +{ + "id": "07f11fd4-babc-46d7-bf8d-4394fa354e74", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "11416288", + "text": "In a follow up of elderly Framingham men and women, and after multivariate adjustment, the total/high-density lipoprotein-cholesterol ratio remained highly associated with the incidence of coronary heart disease in both sexes, whereas total cholesterol level was associated with coronary heart disease only in women. Whereas total cholesterol values decline in the very elderly, and the association of coronary heart disease with total cholesterol level alone is weaker in the elderly than among those of middle age, the total/high-density lipoprotein-cholesterol ratio remains a strong predictor of coronary heart disease. In assessing the elderly for coronary risk, lipid measurements should include high-density lipoprotein-cholesterol and cholesterol determinations." + }, + "questions": [ + { + "id": "d4d51f7a-2b33-4a5a-bb6e-6fb8650ef4d4", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 521, + "text": "total/high-density lipoprotein-cholesterol ratio " + } + ] + } + ] +} \ No newline at end of file diff --git a/085f5b41-4786-4417-8b47-73bb742cf2f1.json b/085f5b41-4786-4417-8b47-73bb742cf2f1.json new file mode 100644 index 0000000000000000000000000000000000000000..78009c674523233ae403c3b2df4fb7e726f605dd --- /dev/null +++ b/085f5b41-4786-4417-8b47-73bb742cf2f1.json @@ -0,0 +1,34 @@ +{ + "id": "085f5b41-4786-4417-8b47-73bb742cf2f1", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "17679132", + "text": "BACKGROUND:\nHemoglobin A1c (HbA1c) is a marker of cumulative glycemic exposure over the preceding 2- to 3-month period. Whether mild elevations of this biomarker provide prognostic information for development of clinically evident type 2 diabetes and cardiovascular disease among individuals at usual risk for these disorders is uncertain.\n\nMETHODS:\nWe examined baseline HbA1c levels as a predictor of incident clinical diabetes and cardiovascular disease (nonfatal myocardial infarction, coronary revascularization procedure, ischemic stroke, or death from cardiovascular causes) in a prospective cohort study beginning in 1992 of 26,563 US female health professionals aged 45 years or more without diagnosed diabetes or vascular disease (median follow-up 10.1 years).\n\nRESULTS:\nDuring follow-up, 1238 cases of diabetes and 684 cardiovascular events occurred. In age-adjusted analyses using quintiles of HbA1c, a risk gradient was observed for both incident diabetes and cardiovascular disease. After multivariable adjustment, HbA1c remained a strong predictor of diabetes but was no longer significantly associated with incident cardiovascular disease. In analyses of threshold effects, adjusted relative risks for incident diabetes in HbA1c categories of less than 5.0%, 5.0% to 5.4%, 5.5% to 5.9%, 6.0% to 6.4%, 6.5% to 6.9%, and 7.0% or more were 1.0, 2.9, 12.1, 29.3, 28.2, and 81.2, respectively. Risk associations persisted after additional adjustment for C-reactive protein and after excluding individuals developing diabetes within 2 and 5 years of follow-up.\n\nCONCLUSIONS:\nThese prospective findings suggest that HbA1c levels are elevated well in advance of the clinical development of type 2 diabetes, supporting recent recommendations for lowering of diagnostic thresholds for glucose metabolic disorders. In contrast, the association of HbA1c with incident cardiovascular events is modest and largely attributable to coexistent traditional risk factors." + }, + "questions": [ + { + "id": "6f0c3d34-9e6b-41a7-a9cd-c983e4fe6af7", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1028, + "text": "HbA1c" + } + ] + } + ] +} \ No newline at end of file diff --git a/097cbfac-e787-4450-a4f7-f169b5350ee3.json b/097cbfac-e787-4450-a4f7-f169b5350ee3.json new file mode 100644 index 0000000000000000000000000000000000000000..c651726d007605ba09844e92676972ade6af6a4f --- /dev/null +++ b/097cbfac-e787-4450-a4f7-f169b5350ee3.json @@ -0,0 +1,38 @@ +{ + "id": "097cbfac-e787-4450-a4f7-f169b5350ee3", + "disease": { + "id": "H00408", + "names": [ + "Type 1 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E10" + ], + "mesh": [ + "D003922" + ] + }, + "category": "Metabolic disease; Immune system disease; Endocrine disease" + }, + "article": { + "id": "7589885", + "text": "The risk of developing diabetes is higher in offspring of fathers than of mothers with insulin-dependent diabetes mellitus (IDDM). The reasons for this sex differential are unclear, as early studies were often selected and relatively small. We conducted a prospective study on the risk of IDDM in a cohort of 9,453 offspring from 5,255 Finnish parents with diabetes diagnosed before age 30 years. Age of first admission to the hospital was considered to be the age of diagnosis of IDDM in the offspring; IDDM occurred in 248 offspring. The risk of IDDM tended to be lower in the offspring of the same gender as the diabetic parent (adjusted risk ratio (RR) 0.78; p = 0.50). When offspring were of same gender as the diabetic parent, male offspring had a higher risk of IDDM than female offspring (RR 2.28; 95% confidence interval 1.53-3.38), whereas if the gender of the diabetic parent and the offspring were different, the risk in male offspring was lower (RR 0.43; 95% confidence interval 0.31-0.62). For the offspring of diabetic fathers, the cumulative risk by the age of 20 was higher (7.6%) than for those with diabetic mothers (3.5%) (p \u003c 0.0001). In a multivariate analysis statistically significant predictors of IDDM in the offspring were the sex of the parent, the year of birth and the birth order of the offspring. The risk of IDDM in the offspring increased by 9% per year of birth cohort. By age 20, the cumulative risk of developing IDDM in the offspring of diabetic parents was 5.3%, 10 times higher than in the background population. It is likely that genetic factors seem to have played a major role in the continuous increase of IDDM incidence in Finnish children." + }, + "questions": [ + { + "id": "901f48c7-6a7a-4abc-a811-2ed7a654299a", + "text": "What are the risk factors of Type 1 diabetes mellitus?", + "answers": [ + { + "answer_start": 1353, + "text": "offspring" + }, + { + "answer_start": 1462, + "text": "offspring of diabetic parents" + } + ] + } + ] +} \ No newline at end of file diff --git a/0a4d6add-0662-43be-b84a-5cd360f338af.json b/0a4d6add-0662-43be-b84a-5cd360f338af.json new file mode 100644 index 0000000000000000000000000000000000000000..0406012deb4c33712018e7f1776869d08aeff0ab --- /dev/null +++ b/0a4d6add-0662-43be-b84a-5cd360f338af.json @@ -0,0 +1,36 @@ +{ + "id": "0a4d6add-0662-43be-b84a-5cd360f338af", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "26541532", + "text": "Recent studies suggest that males with chronic obstructive pulmonary disease (COPD) have more emphysema than females. It is not known if these differences persist across degrees of COPD severity. Our aim was to identify sex-specific differences in quantitative emphysema within COPD subgroups based on COPD severity.We included non-Hispanic white and African-American subjects from the COPDGene study with at least 10 pack-years of smoking and COPD Global Initiative for Chronic Obstructive Lung Disease (GOLD) spirometry grade II or greater. We examined sex-specific differences in log-transformed emphysema (log per cent low-attenuation area (%LAA)) by GOLD spirometry grade among subjects with early-onset COPD (\u003c55 years old) and advanced emphysema (\u003e25% emphysema).Compared with females, males had higher log %LAA: overall (1.97±1.4 versus 1.69±1.6, β=0.32 (0.04), p=1.34×10(-14)), and among non-Hispanic white (p=8.37×10(-14)) and African-American subjects (p=0.002). Females with early-onset COPD, severe emphysema and GOLD grade IV COPD had similar emphysema as males, but markedly fewer pack-years smoking (early-onset, p=0.01; severe emphysema and GOLD grade IV, p\u003c0.001).This study identifies subsets of female smokers with COPD who are particularly susceptible to parenchymal destruction." + }, + "questions": [ + { + "id": "53dcb947-f557-44e7-aa13-95a647b58d50", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 1215, + "text": "female smokers" + } + ] + } + ] +} \ No newline at end of file diff --git a/0ae2dfe1-b4f1-4098-8f4a-3b23038c29f9.json b/0ae2dfe1-b4f1-4098-8f4a-3b23038c29f9.json new file mode 100644 index 0000000000000000000000000000000000000000..d362f081d8a5593e2531dfa492e700744e6e4c47 --- /dev/null +++ b/0ae2dfe1-b4f1-4098-8f4a-3b23038c29f9.json @@ -0,0 +1,50 @@ +{ + "id": "0ae2dfe1-b4f1-4098-8f4a-3b23038c29f9", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "10080459", + "text": "OBJECTIVE:\nTo assess the relationship between dysglycemia and myocardial infarction in nondiabetic individuals.\n\nBACKGROUND:\nNondiabetic hyperglycemia may be an important cardiac risk factor. The relationship between myocardial infarction and glucose, insulin, abdominal obesity, lipids and hypertension was therefore studied in South Asians-a group at high risk for coronary heart disease and diabetes.\n\nMETHODS:\nDemographics, waist/hip ratio, fasting blood glucose (FBG), insulin, lipids and glucose tolerance were measured in 300 consecutive patients with a first myocardial infarction and 300 matched controls.\n\nRESULTS:\nCases were more likely to have diabetes (OR 5.49; 95% CI 3.34, 9.01), impaired glucose tolerance (OR 4.08; 95% CI 2.31, 7.20) or impaired fasting glucose (OR 3.22; 95% CI 1.51, 6.85) than controls. Cases were 3.4 (95% CI 1.9, 5.8) and 6.0 (95% CI 3.3, 10.9) times more likely to have an FBG in the third and fourth quartile (5.2-6.3 and \u003e6.3 mmol/1); after removing subjects with diabetes, impaired glucose tolerance and impaired fasting glucose, cases were 2.7 times (95% CI 1.5-4.8) more likely to have an FBG \u003e5.2 mmol/l. A fasting glucose of 4.9 mmol/l best distinguished cases from controls (OR 3.42; 95% CI 2.42, 4.83). Glucose, abdominal obesity, lipids, hypertension and smoking were independent multivariate risk factors for myocardial infarction. In subjects without glucose intolerance, a 1.2 mmol/l (21 mg/dl) increase in postprandial glucose was independently associated with an increase in the odds of a myocardial infarction of 1.58 (95% CI 1.18, 2.12).\n\nCONCLUSIONS:\nA moderately elevated glucose level is a continuous risk factor for MI in nondiabetic South Asians with either normal or impaired glucose tolerance." + }, + "questions": [ + { + "id": "7a353a7a-9da9-43b1-93e4-e4852d0fb260", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1610, + "text": "moderately elevated glucose level" + }, + { + "answer_start": 1260, + "text": "abdominal obesity" + }, + { + "answer_start": 1279, + "text": "lipids" + }, + { + "answer_start": 1287, + "text": "hypertension" + }, + { + "answer_start": 1304, + "text": "smoking" + } + ] + } + ] +} \ No newline at end of file diff --git a/0b840514-c1a2-4e20-bc5b-8162fca8321e.json b/0b840514-c1a2-4e20-bc5b-8162fca8321e.json new file mode 100644 index 0000000000000000000000000000000000000000..9dca4e903acffadd67aaeb15cd0e40027ab10540 --- /dev/null +++ b/0b840514-c1a2-4e20-bc5b-8162fca8321e.json @@ -0,0 +1,42 @@ +{ + "id": "0b840514-c1a2-4e20-bc5b-8162fca8321e", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "26453955", + "text": "BACKGROUND \u0026 AIMS:\nEarly nutrition may affect the risk of celiac disease. We investigated whether amount of gluten in diet until 2 years of age increases risk for celiac disease.\n\nMETHODS:\nWe performed a 1-to-3 nested case-control study of 146 cases, resulting in 436 case-control pairs matched for sex, birth year, and HLA genotype generated from Swedish children at genetic risk for celiac disease. Newborns were annually screened for tissue transglutaminase autoantibodies (tTGA). If tested tTGA positive, time point of seroconversion was determined from frozen serum samples taken every 3 months. Celiac disease was confirmed by intestinal biopsies. Gluten intake was calculated from 3-day food records collected at ages 9, 12, 18 and 24 months. Odds ratios (OR) were calculated through conditional logistic regression.\n\nRESULTS:\nBreastfeeding duration (median, 32 wk) and age at first introduction to gluten (median, 22 wk) did not differ between cases and tTGA-negative controls. At the visit before tTGA seroconversion, cases reported a larger intake of gluten than controls (OR, 1.28; 95% confidence interval [CI], 1.13-1.46; P = .0002). More cases than controls were found in the upper third tertile (ie, \u003e5.0 g/d) before they tested positive for tTGA seroconversion than controls (OR, 2.65; 95% CI, 1.70-4.13; P \u003c .0001). This finding was similar in children homozygous for DR3-DQ2 (OR, 3.19; 95% CI, 1.61-6.30; P = .001), heterozygous for DR3-DQ2 (OR, 2.24; 95% CI, 1.08-4.62; P = .030), and for children not carrying DR3-DQ2 (OR, 2.43; 95% CI, 0.90-6.54; P = .079).\n\nCONCLUSIONS:\nThe amount of gluten consumed until 2 years of age increases the risk of celiac disease at least 2-fold in genetically susceptible children. These findings may be taken into account for future infant feeding recommendations." + }, + "questions": [ + { + "id": "7c4d8c08-fc66-42eb-a53f-3a8cbade06c2", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 1592, + "text": "The amount of gluten consumed until 2 years of age" + }, + { + "answer_start": 1044, + "text": "larger intake of gluten" + }, + { + "answer_start": 1189, + "text": "upper third tertile (ie, \u003e5.0 g/d)" + } + ] + } + ] +} \ No newline at end of file diff --git a/0c99389b-42d3-4255-976b-03bcbf58ea87.json b/0c99389b-42d3-4255-976b-03bcbf58ea87.json new file mode 100644 index 0000000000000000000000000000000000000000..8c6a67bd4c77756f1d2979ba4b515102e4704a0d --- /dev/null +++ b/0c99389b-42d3-4255-976b-03bcbf58ea87.json @@ -0,0 +1,45 @@ +{ + "id": "0c99389b-42d3-4255-976b-03bcbf58ea87", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "15956652", + "text": "BACKGROUND:\nCurrent evidence suggests that high red meat intake is associated with increased colorectal cancer risk. High fish intake may be associated with a decreased risk, but the existing evidence is less convincing.\n\nMETHODS:\nWe prospectively followed 478 040 men and women from 10 European countries who were free of cancer at enrollment between 1992 and 1998. Information on diet and lifestyle was collected at baseline. After a mean follow-up of 4.8 years, 1329 incident colorectal cancers were documented. We examined the relationship between intakes of red and processed meat, poultry, and fish and colorectal cancer risk using a proportional hazards model adjusted for age, sex, energy (nonfat and fat sources), height, weight, work-related physical activity, smoking status, dietary fiber and folate, and alcohol consumption, stratified by center. A calibration substudy based on 36 994 subjects was used to correct hazard ratios (HRs) and 95% confidence intervals (CIs) for diet measurement errors. All statistical tests were two-sided.\n\nRESULTS:\nColorectal cancer risk was positively associated with intake of red and processed meat (highest [\u003e160 g/day] versus lowest [\u003c20 g/day] intake, HR = 1.35, 95% CI = 0.96 to 1.88; Ptrend = .03) and inversely associated with intake of fish (\u003e80 g/day versus \u003c10 g/day, HR = 0.69, 95 % CI = 0.54 to 0.88; Ptrend\u003c.001), but was not related to poultry intake. Correcting for measurement error strengthened the associations between colorectal cancer and red and processed meat intake (per 100-g increase HR = 1.25, 95% CI =1.09 to 1.41, Ptrend = .001 and HR = 1.55, 95% CI = 1.19 to 2.02, Ptrend = .001 before and after calibration, respectively) and for fish (per 100 g increase HR = 0.70, 95% CI = 0.57 to 0.87, Ptrend\u003c.001 and HR = 0.46, 95% CI = 0.27 to 0.77, Ptrend = .003; before and after correction, respectively). In this study population, the absolute risk of development of colorectal cancer within 10 years for a study subject aged 50 years was 1.71% for the highest category of red and processed meat intake and 1.28% for the lowest category of intake and was 1.86% for subjects in the lowest category of fish intake and 1.28% for subjects in the highest category of fish intake.\n\nCONCLUSIONS:\nOur data confirm that colorectal cancer risk is positively associated with high consumption of red and processed meat and support an inverse association with fish intake." + }, + "questions": [ + { + "id": "0c197850-f433-48ce-97d6-32fad36b4bfb", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 2334, + "text": "high consumption of red and processed meat" + }, + { + "answer_start": 1114, + "text": "intake of red and processed meat (highest [\u003e160 g/day]" + }, + { + "answer_start": 1506, + "text": "red and processed meat intake (per 100-g" + } + ] + } + ] +} \ No newline at end of file diff --git a/0d195070-7f03-447f-9a14-ba2273db9665.json b/0d195070-7f03-447f-9a14-ba2273db9665.json new file mode 100644 index 0000000000000000000000000000000000000000..0d40b1b97edd4dea01e6004f7ed1e33ab543232c --- /dev/null +++ b/0d195070-7f03-447f-9a14-ba2273db9665.json @@ -0,0 +1,35 @@ +{ + "id": "0d195070-7f03-447f-9a14-ba2273db9665", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "1728015", + "text": "The relationship between parental smoking and both subsequent development of asthma and subsequent lung function (before age 12) was studied in more than 700 children enrolled before age 5. Children of mothers with 12 or fewer years of education and who smoked 10 or more cigarettes per day were 2.5 times more likely (95% confidence interval 1.42 to 4.59; P = .0018) to develop asthma and had 15.7% lower maximal midexpiratory flow (P less than .001) than children of mothers with the same education level who did not smoke or smoked fewer than 10 cigarettes per day. These relationships were independent of self-reported respiratory symptoms in parents. There was no association between maternal smoking and subsequent incidence of asthma or maximal midexpiratory flow among children of mothers with more than 12 years of education. It is concluded that children of lower socioeconomic status may be at considerable risk of developing asthma if their mothers smoke 10 or more cigarettes per day. It is speculated that recently reported increases in prevalence of childhood asthma may be in part related to the increased prevalence of smoking among less educated women." + }, + "questions": [ + { + "id": "ca7c2279-304b-428f-83df-565adc95c86b", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 190, + "text": "Children of mothers with 12 or fewer years of education and who smoked 10 or more cigarettes per day" + } + ] + } + ] +} \ No newline at end of file diff --git a/0dce1a7d-02ab-45fd-9dd0-742ec2fb9a5a.json b/0dce1a7d-02ab-45fd-9dd0-742ec2fb9a5a.json new file mode 100644 index 0000000000000000000000000000000000000000..138647cac4e45c5524b75efba89d362f607bad59 --- /dev/null +++ b/0dce1a7d-02ab-45fd-9dd0-742ec2fb9a5a.json @@ -0,0 +1,39 @@ +{ + "id": "0dce1a7d-02ab-45fd-9dd0-742ec2fb9a5a", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "19151010", + "text": "BACKGROUND:\nPrevious studies have reported an interaction between ever cigarette smoking and the presence of the human leukocyte antigen (HLA)-DRB1 shared epitope (SE) genotype and rheumatoid arthritis (RA) risk. To address the effect of dosage, a case-control study nested within two prospective cohorts to determine the interaction between heavy smoking and the HLA-SE was conducted.\n\nMETHODS:\nBlood was obtained from 32 826 women in the Nurses' Health Study and 29 611 women in the Nurses' Health Study II. Incident RA diagnoses were validated by chart review. Controls were matched for age, menopausal status and postmenopausal hormone use. High-resolution HLA-DRB1 genotyping was performed for SE alleles. HLA-SE, smoking, HLA-SE* smoking interactions and RA risk, were assessed using conditional logistic regression models, adjusted for age and reproductive factors. Additive and multiplicative interactions were tested.\n\nRESULTS:\nIn all, 439 Caucasian matched pairs were included. Mean age at RA diagnosis was 55.2 years; 62% of cases were seropositive. A modest additive interaction was observed between ever smoking and HLA-SE in seropositive RA risk. A strong additive interaction (attributable proportion due to interaction (AP) = 0.50; p\u003c0.001) and significant multiplicative interaction (p = 0.05) were found between heavy smoking (\u003e10 pack-years) and any HLA-SE in seropositive RA risk. The highest risk was in heavy smokers with double copy HLA-SE (odds ratio (OR) 7.47, 95% CI 2.77 to 20.11).\n\nCONCLUSIONS:\nA strong gene-environment interaction was observed between HLA-SE and smoking when stratifying by pack-years of smoking rather than by ever smoking. Future studies should assess cumulative exposure to cigarette smoke when testing for gene-smoking interactions." + }, + "questions": [ + { + "id": "05bfd05d-f100-431b-aba0-bca6a5fef11b", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 1425, + "text": "heavy smokers with double copy HLA-SE" + }, + { + "answer_start": 1330, + "text": "heavy smoking (\u003e10 pack-years) and any HLA-SE" + } + ] + } + ] +} \ No newline at end of file diff --git a/0dfcd9e7-b11c-44f0-a175-ac24a015ad1d.json b/0dfcd9e7-b11c-44f0-a175-ac24a015ad1d.json new file mode 100644 index 0000000000000000000000000000000000000000..a01f57ec21c3f2572226e9c7516d02fd5f0b86f5 --- /dev/null +++ b/0dfcd9e7-b11c-44f0-a175-ac24a015ad1d.json @@ -0,0 +1,41 @@ +{ + "id": "0dfcd9e7-b11c-44f0-a175-ac24a015ad1d", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "15644546", + "text": "CONTEXT:\nDiabetes is a serious and costly disease that is becoming increasingly common in many countries. The role of diabetes as a cancer risk factor remains unclear.\n\nOBJECTIVE:\nTo examine the relationship between fasting serum glucose and diabetes and risk of all cancers and specific cancers in men and women in Korea.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nTen-year prospective cohort study of 1,298,385 Koreans (829,770 men and 468,615 women) aged 30 to 95 years who received health insurance from the National Health Insurance Corp and had a biennial medical evaluation in 1992-1995 (with follow-up for up to 10 years).\n\nMAIN OUTCOME MEASURES:\nDeath from cancer and registry-documented incident cancer or hospital admission for cancer.\n\nRESULTS:\nDuring the 10 years of follow-up, there were 20,566 cancer deaths in men and 5907 cancer deaths in women. Using Cox proportional hazards models and controlling for smoking and alcohol use, the stratum with the highest fasting serum glucose (\u003e or =140 mg/dL [\u003e or =7.8 mmol/L]) had higher death rates from all cancers combined (hazard ratio [HR], 1.29; 95% confidence interval [CI], 1.22-1.37 in men and HR, 1.23; 95% CI, 1.09-1.39 in women) compared with the stratum with the lowest level (\u003c90 mg/dL [\u003c5.0 mmol/L]). By cancer site, the association was strongest for pancreatic cancer, comparing the highest and lowest strata in men (HR, 1.91; 95% CI, 1.52-2.41) and in women (HR, 2.05; 95% CI, 1.43-2.93). Significant associations were also found for cancers of the esophagus, liver, and colon/rectum in men and of the liver and cervix in women, and there were significant trends with glucose level for cancers of the esophagus, colon/rectum, liver, pancreas, and bile duct in men and of the liver and pancreas in women. Of the 26,473 total cancer deaths in men and women, 848 were estimated as attributable to having a fasting serum glucose level of less than 90 mg/dL. For cancer incidence, the general patterns reflected those found for mortality. For persons with a diagnosis of diabetes or a fasting serum glucose level greater than 125 mg/dL (6.9 mmol/L), risks for cancer incidence and mortality were generally elevated compared with those without diabetes.\n\nCONCLUSION:\nIn Korea, elevated fasting serum glucose levels and a diagnosis of diabetes are independent risk factors for several major cancers, and the risk tends to increase with an increased level of fasting serum glucose." + }, + "questions": [ + { + "id": "900c0189-83b0-4f6c-8355-474572099505", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 2238, + "text": "elevated fasting serum glucose levels" + }, + { + "answer_start": 2282, + "text": "diagnosis of diabetes" + } + ] + } + ] +} \ No newline at end of file diff --git a/0ecb1c40-6106-4355-b746-5ad68883f618.json b/0ecb1c40-6106-4355-b746-5ad68883f618.json new file mode 100644 index 0000000000000000000000000000000000000000..efe0ff970e1f989a67c5c90eca774000b2023902 --- /dev/null +++ b/0ecb1c40-6106-4355-b746-5ad68883f618.json @@ -0,0 +1,38 @@ +{ + "id": "0ecb1c40-6106-4355-b746-5ad68883f618", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "21673031", + "text": "BACKGROUND:\nDespite an increase in the number of molecular epidemiological studies conducted in recent years to evaluate the association between human papillomavirus (HPV) infection and risk of bladder cancer, the studies remain inconclusive.\n\nMETHODS:\nThe prevalence of HPV in bladder cancer was estimated by pooling data from 52 studies, taking into consideration the heterogeneity from major related parameters including study region, histological type, HPV DNA specimen, publication calendar period, and detection method. Moreover, the association of HPV infection with bladder cancer was tested by a meta-analysis with 19 case-control studies.\n\nRESULTS:\nAn HPV prevalence of 16.88% (95% confidence interval [CI], 15.53%-18.31%) among the bladder cancer cases was revealed, most of whom were high-risk HPV types (15.82% [95% CI, 14.37%-17.36%]). The prevalence varied by region, types of HPV DNA specimen, and polymerase chain reaction primers used. A significantly increased risk of bladder cancer was shown for the positivity of overall HPV (odds ratio, 2.84 [95% CI, 1.39-5.80]), which was also infuenced by HPV type, study region, HPV DNA specimen, and detection method.\n\nCONCLUSIONS:\nInfection of high-risk HPV types, especially HPV16, may play a role in bladder carcinogenesis." + }, + "questions": [ + { + "id": "7abdf9e5-9724-4df5-b751-a002ca4f5e3b", + "text": "What are the risk factors of Bladder Cancer?", + "answers": [ + { + "answer_start": 662, + "text": "HPV" + }, + { + "answer_start": 1193, + "text": "Infection of high-risk HPV types, especially HPV16" + } + ] + } + ] +} \ No newline at end of file diff --git a/0f2d9b8c-69e1-4d80-949a-73b137424464.json b/0f2d9b8c-69e1-4d80-949a-73b137424464.json new file mode 100644 index 0000000000000000000000000000000000000000..a022ef6572e98c0e51b88799f86ef7ef227ab456 --- /dev/null +++ b/0f2d9b8c-69e1-4d80-949a-73b137424464.json @@ -0,0 +1,41 @@ +{ + "id": "0f2d9b8c-69e1-4d80-949a-73b137424464", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "23896379", + "text": "BACKGROUND:\nThe p.I1307K adenomatous polyposis coli (APC) gene variant, prevalent among Ashkenazi Jews, may increase the risk for colorectal neoplasia. We studied the clinical importance of screening for this polymorphism in 3305 Israelis undergoing colonoscopy.\n\nPATIENTS AND METHODS:\nClinical data regarding potential risk factors for colorectal cancer (CRC) were collected from individuals undergoing colonoscopic examination at the Tel-Aviv medical center. The APC p.I1307K was detected using real-time PCR (polymerase chain reaction) from DNA extracted from peripheral mononuclear cells.\n\nRESULTS:\nThe overall prevalence of the p.I1307K polymorphism was 8.0% (10.1% among Ashkenazi and 2.7% among Sephardic Jews, p\u003c0.001). The overall adjusted odds ratio (OR) for colorectal neoplasia among carriers was 1.51 (95% confidence intervals (CI), 1.16-1.98). Among average risk Ashkenazi Jews, the adjusted OR was 1.75 (95% CI 1.26-2.45). A multiplicative interaction was identified between Ashkenazi ethnicity and APC p.I1307K carrier status (P(INTERACTION) = 0.055). The histopathological features of adenomas and carcinomas did not differ between carriers and non-carriers.\n\nCONCLUSIONS:\nThe APC p.I1307K gene variant is an important risk factor for colorectal neoplasia in average risk Ashkenazi Jews. Carriers in this group should be considered for screening colonoscopy at the age of 40, to be repeated every 5 years, similar to recommendations in individuals with family history of colorectal cancer." + }, + "questions": [ + { + "id": "37fdb837-2683-431f-a3b1-6a37323088f8", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1194, + "text": "APC p.I1307K gene variant" + }, + { + "answer_start": 633, + "text": "p.I1307K polymorphism" + } + ] + } + ] +} \ No newline at end of file diff --git a/0f315ae2-b4c2-41d2-bcad-9af73252d1f3.json b/0f315ae2-b4c2-41d2-bcad-9af73252d1f3.json new file mode 100644 index 0000000000000000000000000000000000000000..2295b2dfdabb69531bfc45ea80b2f14c8bdb94fb --- /dev/null +++ b/0f315ae2-b4c2-41d2-bcad-9af73252d1f3.json @@ -0,0 +1,39 @@ +{ + "id": "0f315ae2-b4c2-41d2-bcad-9af73252d1f3", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "22736291", + "text": "OBJECTIVE:\nTo examine the relationship of Porphyromonas gingivalis to the presence of autoantibodies in individuals at risk of rheumatoid arthritis (RA).\n\nMETHODS:\nStudy participants included the following: 1) a cohort enriched in subjects with HLA-DR4 and 2) subjects at risk of RA by virtue of having a first-degree relative with RA. None of the study subjects satisfied the American College of Rheumatology 1987 classification criteria for RA. Autoantibodies measured included anti-citrullinated protein antibody (ACPA; by second-generation anti-cyclic citrullinated peptide antibody enzyme-linked immunosorbent assay [ELISA]) and rheumatoid factor (RF; by nephelometry or ELISA for IgA, IgM, or IgG isotype). Individuals were considered autoantibody positive (n = 113) if they had ≥1 RA-related autoantibody; individuals were further categorized as high risk (n = 38) if they had ACPA or positive findings ≥2 assays for RF. Autoantibody-negative individuals (n = 171) served as a comparator group. Antibody to P gingivalis, P intermedia, and F nucleatum were measured. Associations of bacterial antibodies with group status were examined using logistic regression.\n\nRESULTS:\nAnti-P gingivalis concentrations were higher in high-risk (P = 0.011) and autoantibody positive group (P = 0.010) than in the autoantibody negative group. There were no group differences in anti-P intermedia or anti-F nucleatum concentrations. After multivariable adjustment, anti-P gingivalis concentrations (but not anti-P intermedia or anti-F nucleatum) were significantly associated with autoantibody-positive and high-risk status (P \u003c 0.05).\n\nCONCLUSION:\nImmunity to P gingivalis, but not P intermedia or F nucleatum, is significantly associated with the presence of RA-related autoantibodies in individuals at risk of RA. These results support the hypothesis that infection with P gingivalis may play a central role in the early loss of tolerance to self antigens that occurs in the pathogenesis of RA." + }, + "questions": [ + { + "id": "20386f3f-0817-445b-b7a7-6ad83e072bce", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 1179, + "text": "Anti-P gingivalis concentrations" + }, + { + "answer_start": 1849, + "text": "infection with P gingivalis" + } + ] + } + ] +} \ No newline at end of file diff --git a/0f6c198f-8a63-476f-9377-1660e6735e58.json b/0f6c198f-8a63-476f-9377-1660e6735e58.json new file mode 100644 index 0000000000000000000000000000000000000000..7b4e0a9009dc2146ddbaa264c443b04001bf77d6 --- /dev/null +++ b/0f6c198f-8a63-476f-9377-1660e6735e58.json @@ -0,0 +1,43 @@ +{ + "id": "0f6c198f-8a63-476f-9377-1660e6735e58", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "25926142", + "text": "OBJECTIVES:\nTo assess whether HOUSES (HOUsing-based index of socioeconomic status (SES)) is associated with risk of and mortality after rheumatoid arthritis (RA).\n\nDESIGN:\nWe conducted a population-based case-control study which enrolled population-based RA cases and their controls without RA.\n\nSETTING:\nThe study was performed in Olmsted County, Minnesota.\n\nPARTICIPANTS:\nStudy participants were all residents of Olmsted County, Minnesota, with RA identified using the 1987 American College of Rheumatology criteria for RA from 1 January 1988, to 31 December 2007, using the auspices of the Rochester Epidemiology Project. For each patient with RA, one control was randomly selected from Olmsted County residents of similar age and gender without RA.\n\nPRIMARY AND SECONDARY OUTCOME MEASURE:\nThe disease status was RA cases and their matched controls in relation to HOUSES as an exposure. As a secondary aim, post-RA mortality among only RA cases was an outcome event. The associations of SES measured by HOUSES with the study outcomes were assessed using logistic regression and Cox models. HOUSES, as a composite index, was formulated based on a summed z-score for housing value, square footage and number of bedrooms and bathrooms.\n\nRESULTS:\nOf the eligible 604 participants, 418 (69%) were female; the mean age was 56±15.6 years. Lower SES, as measured by HOUSES, was associated with the risk of developing RA (0.5±3.8 for controls vs -0.2±3.1 for RA cases, p=0.003), adjusting for age, gender, calendar year of RA index date, smoking status and BMI. The lowest quartile of HOUSES was significantly associated with increased post-RA mortality compared to higher quartiles of HOUSES (HR 1.74; 95% CI 1.10 to 2.74; p=0.017) in multivariate analysis.\n\nCONCLUSIONS:\nLower SES, as measured by HOUSES, is associated with increased risk of RA and mortality after RA. HOUSES may be a useful tool for health disparities research concerning rheumatological outcomes when conventional SES measures are unavailable." + }, + "questions": [ + { + "id": "33148eba-29a3-402d-807a-674e0c3f01d7", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 1335, + "text": "Lower SES, as measured by HOUSES" + }, + { + "answer_start": 61, + "text": "socioeconomic status (SES))" + }, + { + "answer_start": 1767, + "text": "Lower SES, as measured by HOUSES" + } + ] + } + ] +} \ No newline at end of file diff --git a/0ff7571a-b33e-40b6-8dfa-28fb8d5f8183.json b/0ff7571a-b33e-40b6-8dfa-28fb8d5f8183.json new file mode 100644 index 0000000000000000000000000000000000000000..7d201db19a54d534a59d5d53e5dac410ac8364eb --- /dev/null +++ b/0ff7571a-b33e-40b6-8dfa-28fb8d5f8183.json @@ -0,0 +1,34 @@ +{ + "id": "0ff7571a-b33e-40b6-8dfa-28fb8d5f8183", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "25692500", + "text": "BACKGROUND:\nThe influence of dietary fat upon breast cancer mortality remains largely understudied despite extensive investigation into its influence upon breast cancer risk.\n\nOBJECTIVE:\nTo conduct meta-analyses of studies to clarify the association between dietary fat and breast cancer mortality.\n\nDESIGN:\nMEDLINE and EMBASE were searched for relevant articles published up to March 2012. Risk of all-cause or breast-cancer-specific death was evaluated by combining multivariable adjusted estimates comparing highest versus lowest categories of intake; and per 20 g increase in intake of total and/or saturated fat (g/day) using random-effects meta-analyses.\n\nRESULTS:\nFifteen prospective cohort studies investigating total fat and/or saturated fat intake (g/day) and breast cancer mortality were included. There was no difference in risk of breast-cancer-specific death (n = 6; HR = 1.14; 95% CI: 0.86, 1.52; p = 0.34) or all-cause death (n = 4; HR = 1.73; 95% CI: 0.82, 3.66; p = 0.15) for women in the highest versus lowest category of total fat intake. Breast-cancer-specific death (n = 4; HR = 1.51; 95% CI: 1.09, 2.09; p \u003c 0.01) was higher for women in the highest versus lowest category of saturated fat intake.\n\nCONCLUSIONS:\nThese meta-analyses have shown that saturated fat intake negatively impacts upon breast cancer survival." + }, + "questions": [ + { + "id": "14baabaa-5099-456b-89cd-0fa69564a906", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1271, + "text": "saturated fat intake" + } + ] + } + ] +} \ No newline at end of file diff --git a/1045d2b8-9fed-4874-9117-1e569f05d480.json b/1045d2b8-9fed-4874-9117-1e569f05d480.json new file mode 100644 index 0000000000000000000000000000000000000000..d3eeff25c893f993e0a3350d51d2181a7e80aec8 --- /dev/null +++ b/1045d2b8-9fed-4874-9117-1e569f05d480.json @@ -0,0 +1,47 @@ +{ + "id": "1045d2b8-9fed-4874-9117-1e569f05d480", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "28926373", + "text": "BACKGROUND:\nEarly-life exposure to traffic-related air pollution exacerbates childhood asthma, but it is unclear what role it plays in asthma development.\n\nMETHODS:\nThe association between exposure to primary mobile source pollutants during pregnancy and during infancy and asthma incidence by ages 2 through 6 was examined in the Kaiser Air Pollution and Pediatric Asthma Study, a racially diverse birth cohort of 24,608 children born between 2000 and 2010 and insured by Kaiser Permanente Georgia. We estimated concentrations of mobile source fine particulate matter (PM2.5, µg/m), nitrogen oxides (NOX, ppb), and carbon monoxide (CO, ppm) at the maternal and child residence using a Research LINE source dispersion model for near-surface releases. Asthma was defined using diagnoses and medication dispensings from medical records. We used binomial generalized linear regression to model the impact of exposure continuously and by quintiles on asthma risk.\n\nRESULTS:\nControlling for covariates and modeling log-transformed exposure, a 2.7-fold increase in first year of life PM2.5 was associated with an absolute 4.1% (95% confidence interval, 1.6%, 6.6%) increase in risk of asthma by age 5. Quintile analysis showed an increase in risk from the first to second quintile, but similar risk across quintiles 2-5. Risk differences increased with follow-up age. Results were similar for NOX and CO and for exposure during pregnancy and the first year of life owing to high correlation.\n\nCONCLUSIONS:\nResults provide limited evidence for an association of early-life mobile source air pollution with childhood asthma incidence with a steeper concentration-response relationship observed at lower levels of exposure." + }, + "questions": [ + { + "id": "2054be89-feb5-4631-96dd-c5d471b29889", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1036, + "text": "a 2.7-fold increase in first year of life PM2.5" + }, + { + "answer_start": 1387, + "text": "NOX" + }, + { + "answer_start": 1395, + "text": "CO" + }, + { + "answer_start": 1555, + "text": "early-life mobile source air pollution" + } + ] + } + ] +} \ No newline at end of file diff --git a/1092af1a-3d9b-4ff1-b304-229710e9bf24.json b/1092af1a-3d9b-4ff1-b304-229710e9bf24.json new file mode 100644 index 0000000000000000000000000000000000000000..3edd58c8f0bff14964ba607b88f6877cbacc9f49 --- /dev/null +++ b/1092af1a-3d9b-4ff1-b304-229710e9bf24.json @@ -0,0 +1,44 @@ +{ + "id": "1092af1a-3d9b-4ff1-b304-229710e9bf24", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "20335290", + "text": "BACKGROUND:\nOver half the world is exposed daily to the smoke from combustion of solid fuels. Chronic obstructive pulmonary disease (COPD) is one of the main contributors to the global burden of disease and can be caused by biomass smoke exposure. However, studies of biomass exposure and COPD show a wide range of effect sizes. The aim of this systematic review was to quantify the impact of biomass smoke on the development of COPD and define reasons for differences in the reported effect sizes.\n\nMETHODS:\nA systematic review was conducted of studies with sufficient statistical power to calculate the health risk of COPD from the use of solid fuel, which followed standardised criteria for the diagnosis of COPD and which dealt with confounding factors. The results were pooled by fuel type and country to produce summary estimates using a random effects model. Publication bias was also estimated.\n\nRESULTS:\nThere were positive associations between the use of solid fuels and COPD (OR=2.80, 95% CI 1.85 to 4.0) and chronic bronchitis (OR=2.32, 95% CI 1.92 to 2.80). Pooled estimates for different types of fuel show that exposure to wood smoke while performing domestic work presents a greater risk of development of COPD and chronic bronchitis than other fuels.\n\nCONCLUSION:\nDespite heterogeneity across the selected studies, exposure to solid fuel smoke is consistently associated with COPD and chronic bronchitis. Efforts should be made to reduce exposure to solid fuel by using either cleaner fuel or relatively cleaner technology while performing domestic work." + }, + "questions": [ + { + "id": "c0e4c431-0ec0-46c9-a0e7-628f01f37277", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 965, + "text": "solid fuels" + }, + { + "answer_start": 1126, + "text": "exposure to wood smoke while performing domestic work" + }, + { + "answer_start": 1332, + "text": "exposure to solid fuel smoke" + } + ] + } + ] +} \ No newline at end of file diff --git a/109adb5e-240a-4a5a-9059-021828d9dd30.json b/109adb5e-240a-4a5a-9059-021828d9dd30.json new file mode 100644 index 0000000000000000000000000000000000000000..231c7962ba5258bd15bf6cc036e6353b763d504e --- /dev/null +++ b/109adb5e-240a-4a5a-9059-021828d9dd30.json @@ -0,0 +1,43 @@ +{ + "id": "109adb5e-240a-4a5a-9059-021828d9dd30", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "22833605", + "text": "OBJECTIVE:\nTo estimate the burden of melanoma resulting from sunbed use in western Europe.\n\nDESIGN:\nSystematic review and meta-analysis.\n\nDATA SOURCES:\nPubMed, ISI Web of Science (Science Citation Index Expanded), Embase, Pascal, Cochrane Library, LILACS, and MedCarib, along with published surveys reporting prevalence of sunbed use at national level in Europe.\n\nSTUDY SELECTION:\nObservational studies reporting a measure of risk for skin cancer (cutaneous melanoma, squamous cell carcinoma, basal cell carcinoma) associated with ever use of sunbeds.\n\nRESULTS:\nBased on 27 studies ever use of sunbeds was associated with a summary relative risk of 1.20 (95% confidence interval 1.08 to 1.34). Publication bias was not evident. Restricting the analysis to cohorts and population based studies, the summary relative risk was 1.25 (1.09 to 1.43). Calculations for dose-response showed a 1.8% (95% confidence interval 0% to 3.8%) increase in risk of melanoma for each additional session of sunbed use per year. Based on 13 informative studies, first use of sunbeds before age 35 years was associated with a summary relative risk of 1.87 (1.41 to 2.48), with no indication of heterogeneity between studies. By using prevalence data from surveys and data from GLOBOCAN 2008, in 2008 in the 15 original member countries of the European Community plus three countries that were members of the European Free Trade Association, an estimated 3438 cases of melanoma could be attributable to sunbed use, most (n=2341) occurring among women.\n\nCONCLUSIONS:\nSunbed use is associated with a significant increase in risk of melanoma. This risk increases with number of sunbed sessions and with initial usage at a young age (\u003c35 years). The cancerous damage associated with sunbed use is substantial and could be avoided by strict regulations." + }, + "questions": [ + { + "id": "e2770142-ced4-48a0-911e-21322fd56261", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 1041, + "text": "first use of sunbeds before age 35 years" + }, + { + "answer_start": 1543, + "text": "Sunbed use" + }, + { + "answer_start": 1642, + "text": "number of sunbed sessions and with initial usage at a young age (\u003c35 years)" + } + ] + } + ] +} \ No newline at end of file diff --git a/10cf864e-4503-405d-b363-a14c2f11fcc9.json b/10cf864e-4503-405d-b363-a14c2f11fcc9.json new file mode 100644 index 0000000000000000000000000000000000000000..2840b0eb3f60215ad29ce3501429b816e0ac19c3 --- /dev/null +++ b/10cf864e-4503-405d-b363-a14c2f11fcc9.json @@ -0,0 +1,37 @@ +{ + "id": "10cf864e-4503-405d-b363-a14c2f11fcc9", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "15644544", + "text": "CONTEXT:\nConsumption of red and processed meat has been associated with colorectal cancer in many but not all epidemiological studies; few studies have examined risk in relation to long-term meat intake or the association of meat with rectal cancer.\n\nOBJECTIVE:\nTo examine the relationship between recent and long-term meat consumption and the risk of incident colon and rectal cancer.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nA cohort of 148 610 adults aged 50 to 74 years (median, 63 years), residing in 21 states with population-based cancer registries, who provided information on meat consumption in 1982 and again in 1992/1993 when enrolled in the Cancer Prevention Study II (CPS II) Nutrition Cohort. Follow-up from time of enrollment in 1992/1993 through August 31, 2001, identified 1667 incident colorectal cancers. Participants contributed person-years at risk until death or a diagnosis of colon or rectal cancer.\n\nMAIN OUTCOME MEASURE:\nIncidence rate ratio (RR) of colon and rectal cancer.\n\nRESULTS:\nHigh intake of red and processed meat reported in 1992/1993 was associated with higher risk of colon cancer after adjusting for age and energy intake but not after further adjustment for body mass index, cigarette smoking, and other covariates. When long-term consumption was considered, persons in the highest tertile of consumption in both 1982 and 1992/1993 had higher risk of distal colon cancer associated with processed meat (RR, 1.50; 95% confidence interval [CI], 1.04-2.17), and ratio of red meat to poultry and fish (RR, 1.53; 95% CI, 1.08-2.18) relative to those persons in the lowest tertile at both time points. Long-term consumption of poultry and fish was inversely associated with risk of both proximal and distal colon cancer. High consumption of red meat reported in 1992/1993 was associated with higher risk of rectal cancer (RR, 1.71; 95% CI, 1.15-2.52; P = .007 for trend), as was high consumption reported in both 1982 and 1992/1993 (RR, 1.43; 95% CI, 1.00-2.05).\n\nCONCLUSIONS:\nOur results demonstrate the potential value of examining long-term meat consumption in assessing cancer risk and strengthen the evidence that prolonged high consumption of red and processed meat may increase the risk of cancer in the distal portion of the large intestine." + }, + "questions": [ + { + "id": "45083494-68db-4520-9939-4ff62dc01286", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1007, + "text": "High intake of red and processed meat" + } + ] + } + ] +} \ No newline at end of file diff --git a/1104a25e-028a-4579-ba25-cd5430faaa75.json b/1104a25e-028a-4579-ba25-cd5430faaa75.json new file mode 100644 index 0000000000000000000000000000000000000000..412e71d770a1a1344c2d1194ec75b84580b1df54 --- /dev/null +++ b/1104a25e-028a-4579-ba25-cd5430faaa75.json @@ -0,0 +1,35 @@ +{ + "id": "1104a25e-028a-4579-ba25-cd5430faaa75", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "24299467", + "text": "BACKGROUND:\nAntibiotic use in infancy disrupts gut microflora during a critical period for immune system development. It is hypothesized that this could predispose to the development of allergic diseases. We investigated the associations of antibiotic use in the first 2 yr of life with the development of asthma, eczema or hay fever by age 7.5 yr in a longitudinal birth cohort.\n\nMETHODS:\nSubjects were 4952 children from the Avon Longitudinal Study of Parents and Children (ALSPAC). Child antibiotic use and asthma, eczema and hay fever symptoms were maternally reported. Atopy was assessed by skin prick tests at age 7.5 yr. The total number of antibiotic courses was considered as the main exposure. Data were analysed using multivariate logistic regression.\n\nRESULTS:\nChildren reported to have taken antibiotics during infancy (0-2 yr) were more likely to have asthma at 7.5 yr (OR 1.75, 95% CI 1.40-2.17), and the odds (OR, [95% CI]) increased with greater numbers of courses: once 1.11 [0.84-1.48]; twice 1.50 [1.14-1.98]; three times 1.79 [1.34-2.40]; four times or more 2.82 [2.19-3.63]. Increased antibiotic use was also associated with higher odds of eczema and hay fever but not atopy. The effect appeared to be associated with cumulative rather than a critical period of exposure during the first 2 yr.\n\nCONCLUSIONS:\nA robust and dose-dependent association was found between antibiotic use in the first 2 yr of life and asthma at age 7.5 yr but did not appear to be mediated through an association with atopy." + }, + "questions": [ + { + "id": "a1d94c6a-3e85-4316-8da3-d661bfcccc1d", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1388, + "text": "antibiotic use in the first 2 yr of life" + } + ] + } + ] +} \ No newline at end of file diff --git a/112ce6bc-992a-4795-8ca5-775bfbf4712a.json b/112ce6bc-992a-4795-8ca5-775bfbf4712a.json new file mode 100644 index 0000000000000000000000000000000000000000..108e793c97819d2169155a146404e011cf3665b0 --- /dev/null +++ b/112ce6bc-992a-4795-8ca5-775bfbf4712a.json @@ -0,0 +1,43 @@ +{ + "id": "112ce6bc-992a-4795-8ca5-775bfbf4712a", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "23897126", + "text": "OBJECTIVE:\nTo estimate familial aggregation of rheumatoid arthritis (RA) in 3 large population-representative samples and to test if familial aggregation is affected by rheumatoid factor (RF)/anti-citrullinated protein antibody (ACPA) status, type of relative, sex, and age at onset of RA.\n\nMETHODS:\nA register-based nested case-control study was performed in the Swedish total population. Data on patients with RA were ascertained through the nationwide Swedish Patient Register (n = 88,639), the clinical Swedish Rheumatology Quality Register (n = 11,519), and the Epidemiological Investigation of Rheumatoid Arthritis case-control study (n = 2,871). Data on first- and second-degree relatives were obtained through the Swedish Multigeneration Register. Familial risks were calculated using conditional logistic regression.\n\nRESULTS:\nConsistent across data sources, the familial odds ratio for RA was ∼3 in first-degree relatives of RA patients and 2 in second-degree relatives. Familial risks were similar among siblings, parents, and offspring. Familial aggregation was not modified by sex, but was higher in RA patients with early-onset disease and in RF/ACPA-positive RA patients. The observed familial risks were consistent with a heritability of ∼50% for ACPA-positive RA and ∼20% for ACPA-negative RA.\n\nCONCLUSION:\nThe pattern of risks suggests that familial factors influence RA in men and women equally and that these factors are of less importance for late-onset RA. Familial factors are more important for seropositive RA, but there is significant familial overlap between seropositive RA and seronegative RA. Even if the familial risk is assumed to be completely due to genetics, the observed risks suggest that heritability of RA is lower than previously reported, in particular for ACPA-negative RA." + }, + "questions": [ + { + "id": "493c4671-e046-4f87-b7c0-cb9cd58b98c9", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 23, + "text": "familial aggregation" + }, + { + "answer_start": 1200, + "text": "familial risks" + }, + { + "answer_start": 981, + "text": "Familial risks were similar among siblings, parents, and offspring" + } + ] + } + ] +} \ No newline at end of file diff --git a/115b1453-6b15-4f89-88ed-4e74759220b2.json b/115b1453-6b15-4f89-88ed-4e74759220b2.json new file mode 100644 index 0000000000000000000000000000000000000000..f18d246497fd843af45c0ca05221c077f9904e2b --- /dev/null +++ b/115b1453-6b15-4f89-88ed-4e74759220b2.json @@ -0,0 +1,42 @@ +{ + "id": "115b1453-6b15-4f89-88ed-4e74759220b2", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "18501234", + "text": "PURPOSE:\nThe study compares the risk of incident diabetes associated with fasting plasma glucose levels in the normal range, controlling for other risk factors.\n\nMETHODS:\nWe identified 46,578 members of Kaiser Permanente Northwest who had fasting plasma glucose levels less than 100 mg/dL between January 1, 1997, and December 31, 2000, and who did not previously have diabetes or impaired fasting glucose. After assigning subjects to 1 of 4 categories (\u003c85, 85-89, 90-94, or 95-99 mg/dL), we followed them until they developed diabetes, died, or left the health plan, or until April 30, 2007. We used Cox regression analysis to estimate the risk of incident diabetes, adjusted for age, sex, body mass index, blood pressure, lipids, smoking, cardiovascular disease, and hypertension.\n\nRESULTS:\nSubjects developed diabetes at a rate of less than 1% per year during a mean follow-up of 81.0 months. Each milligram per deciliter of fasting plasma glucose increased diabetes risk by 6% (hazard ratio [HR] 1.06, 95% confidence interval [CI], 1.05-1.07, P \u003c .0001) after controlling for other risk factors. Compared with those with fasting plasma glucose levels less than 85 mg/dL, subjects with glucose levels of 95 to 99 mg/dL were 2.33 times more likely to develop diabetes (HR 2.33; 95% CI, 1.95-2.79; P \u003c .0001). Subjects in the 90 to 94 mg/dL group were 49% more likely to progress to diabetes (HR 1.49; 95% CI, 1.23-1.79; P \u003c.0001). All other risk factors except sex were significantly associated with a diabetes diagnosis.\n\nCONCLUSIONS:\nThe strong independent association between the level of normal fasting plasma glucose and the incidence of diabetes after controlling for other risk factors suggests that diabetes risk increases as fasting plasma glucose levels increase, even within the currently accepted normal range." + }, + "questions": [ + { + "id": "f19c26a2-4af7-4fdd-b15d-396e1b8b5fc0", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 897, + "text": "Each milligram per deciliter of fasting plasma glucose" + }, + { + "answer_start": 1176, + "text": "subjects with glucose levels of 95 to 99 mg/dL" + }, + { + "answer_start": 1312, + "text": "Subjects in the 90 to 94 mg/dL group" + } + ] + } + ] +} \ No newline at end of file diff --git a/116922a9-f469-4251-b6a5-a36e0b08801b.json b/116922a9-f469-4251-b6a5-a36e0b08801b.json new file mode 100644 index 0000000000000000000000000000000000000000..1e4c2d44f92cc2fae701886e6a88b183cd1a238a --- /dev/null +++ b/116922a9-f469-4251-b6a5-a36e0b08801b.json @@ -0,0 +1,40 @@ +{ + "id": "116922a9-f469-4251-b6a5-a36e0b08801b", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "19800047", + "text": "Chronic obstructive pulmonary disease (COPD) is the fourth leading cause of death worldwide and is influenced by both genetic determinants and smoking. We identified genomic regions from 56 lung-tissue gene-expression microarrays and used them to select 889 SNPs to be tested for association with COPD. We genotyped SNPs in 389 severe COPD cases from the National Emphysema Treatment Trial and 424 cigarette-smoking controls from the Normative Aging Study. A total of 71 autosomal SNPs demonstrated at least nominal significance with COPD susceptibility (p = 3.4 x 10(-6) to 0.05). These 71 SNPs were evaluated in a family-based study of 127 probands with severe, early-onset COPD and 822 of their family members in the Boston Early-Onset COPD Study. We combined p values from the case-control and family-based analyses, setting p = 5.60 x 10(-5) as a conservative threshold for significance. Three SNPs in the iron regulatory protein 2 (IREB2) gene met this stringent threshold for significance, and four other IREB2 SNPs demonstrated combined p \u003c 0.02. We demonstrated replication of association for these seven IREB2 SNPs (all p values \u003c or = 0.02) in a family-based study of 3117 subjects from the International COPD Genetics Network; combined p values across all cohorts for the main phenotype of interest ranged from 1.6 x 10(-7) to 6.4 x 10(-4). IREB2 protein and mRNA were increased in lung-tissue samples from COPD subjects in comparison to controls. In summary, gene-expression and genetic-association results have implicated IREB2 as a COPD susceptibility gene." + }, + "questions": [ + { + "id": "08dcc626-6a58-4451-91c4-191bed3551db", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 1353, + "text": "IREB2 protein" + }, + { + "answer_start": 1536, + "text": "IREB2" + } + ] + } + ] +} \ No newline at end of file diff --git a/125ce4cc-ee01-457a-9f57-41046f5b092d.json b/125ce4cc-ee01-457a-9f57-41046f5b092d.json new file mode 100644 index 0000000000000000000000000000000000000000..fa293c592399bfbeefde7dc3e8231132b0eec3eb --- /dev/null +++ b/125ce4cc-ee01-457a-9f57-41046f5b092d.json @@ -0,0 +1,37 @@ +{ + "id": "125ce4cc-ee01-457a-9f57-41046f5b092d", + "disease": { + "id": "M2023_04_26_16_38_52", + "names": [ + "Migraine" + ], + "dbLinks": { + "icd10": [ + "G43" + ], + "icd11": [ + "8A80" + ], + "mesh": [ + "C10.228.140.546.399.750" + ] + }, + "description": "Migraine is a chronic neurological disorder characterized by recurrent episodes of unilateral, pulsatile headaches associated with autonomic symptoms such as nausea, vomiting, photophobia, and phonophobia. The pathophysiology of migraine is multifactorial and involves complex interactions between genetic, environmental, and neurochemical factors that modulate cerebral vascular tone and nociception. Migraine attacks can be triggered by a variety of factors, including stress, hormonal changes, sleep disturbances, and certain foods or medications. Treatment options for migraine include pharmacotherapy for acute attacks, preventive medications for frequent or severe headaches, and lifestyle modifications to avoid triggers. In refractory cases, interventional therapies such as nerve blocks or neuromodulation techniques may be considered." + }, + "article": { + "id": "3404480", + "text": "We have studied the association between migraine and major depression in a group of 133 probands with major depression, a group of 82 normal community controls and 400 interviewed first-degree relatives of the probands and controls. There was a significant association between depression and migraine among both the probands and the relatives. We also found that concomitant symptoms of anxiety were prominent among the depressed persons with migraine. Both depression and migraine were strongly familial but their association did not appear to be highly transmissible. Rather, our data suggested that depression may either be a sequela of migraine or the diathesis which results in both migraine and depression." + }, + "questions": [ + { + "id": "7b735d6f-646f-4fc8-9831-c696e272cd95", + "text": "what are the risk factors of Migraine?", + "answers": [ + { + "answer_start": 277, + "text": "depression" + } + ] + } + ] +} \ No newline at end of file diff --git a/126f2585-0b2b-44f8-9676-81ce41451731.json b/126f2585-0b2b-44f8-9676-81ce41451731.json new file mode 100644 index 0000000000000000000000000000000000000000..21c8a3f463f2f1b3b975148ce87b8720d9ea2854 --- /dev/null +++ b/126f2585-0b2b-44f8-9676-81ce41451731.json @@ -0,0 +1,42 @@ +{ + "id": "126f2585-0b2b-44f8-9676-81ce41451731", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "12441324", + "text": "BACKGROUND:\nPrevious studies have demonstrated that ingestion of arsenic in drinking water is a strong risk factor for several forms of cancer, including bladder cancer. It is not known whether arsenic-related cancers are genetically similar to cancers in unexposed individuals or what mechanisms of carcinogenesis may underlie their formation. This study was designed to compare chromosomal alterations in bladder cancers of arsenic-exposed individuals to provide insight into the mechanism of how arsenic may induce or promote cancer.\n\nMETHODS:\nA case-case study was conducted in Argentina and Chile examining chromosomal alterations in bladder tumor DNA in 123 patients who had been exposed to arsenic in their drinking water. Patients were placed into one of four arsenic exposure categories according to their average 5-year peak arsenic exposure. Patients were also classified as ever smokers or never smokers. Comparative genomic hybridization was used to identify chromosomal alterations throughout the genome. All statistical tests were two-sided.\n\nRESULTS:\nThe total number of chromosomal alterations was higher in individuals exposed to higher arsenic levels (5.7 +/- 5.1, 5.6 +/- 5.1, 7.3 +/- 7.4, and 9.1 +/- 6.5 [mean +/- standard deviation] chromosomal alterations per tumor with increasing arsenic exposure; P(trend) =.02, adjusted for stage and grade). The trend was stronger in high-grade (G2-G3) tumors (6.3 +/- 5.5, 8.3 +/- 4.7, 10.3 +/- 7.8, and 10.5 +/- 6.4 alterations per tumor; P(trend) =.01) than it was in low-grade (G1) tumors (3.5 +/- 3.1, 1.1 +/- 1.1, 2.5 +/- 2.5, and 3.6 +/- 3.2 alterations per tumor; P(trend) =.79). The mean number of chromosomal alterations also increased with tumor stage and grade (P(trend)\u003c.001) independently of arsenic exposure but was not associated with smoking history. Deletion of part or all of chromosome 17p (P(trend)\u003c.001) showed the strongest association with arsenic exposure.\n\nCONCLUSIONS:\nBladder tumors in patients with higher levels of arsenic exposure showed higher levels of chromosomal instability. Most of the chromosomal alterations associated with arsenic exposure were also associated with tumor stage and grade, raising the possibility that bladder tumors from arsenic-exposed patients may behave more aggressively than tumors from unexposed patients." + }, + "questions": [ + { + "id": "dae01f3c-0fcd-45e6-bcfb-fdf56e194cc9", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 1976, + "text": "patients with higher levels of arsenic exposure" + }, + { + "answer_start": 2124, + "text": " arsenic exposure" + }, + { + "answer_start": 1295, + "text": "increasing arsenic exposure" + } + ] + } + ] +} \ No newline at end of file diff --git a/1274df29-3d1a-41e4-935f-639f4f8729e4.json b/1274df29-3d1a-41e4-935f-639f4f8729e4.json new file mode 100644 index 0000000000000000000000000000000000000000..5d4781c86e8ee0037a1594d73fac323f0b53bd15 --- /dev/null +++ b/1274df29-3d1a-41e4-935f-639f4f8729e4.json @@ -0,0 +1,58 @@ +{ + "id": "1274df29-3d1a-41e4-935f-639f4f8729e4", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "23890780", + "text": "BACKGROUND:\nAssociations between circulating concentrations of oestrogens, progesterone, and androgens with breast cancer and related risk factors in premenopausal women are not well understood. We aimed to characterise these associations with a pooled analysis of data from seven studies.\n\nMETHODS:\nIndividual participant data for prediagnostic sex hormone and sex hormone-binding globulin (SHBG) concentrations were contributed from seven prospective studies. We restricted analyses to women who were premenopausal and younger than 50 years at blood collection, and to women with breast cancer diagnosed before age 50 years. We estimated odds ratios (ORs) with 95% CIs for breast cancer associated with hormone concentrations by conditional logistic regression in cases and controls matched for age, date of blood collection, and day of cycle, with stratification by study and further adjustment for cycle phase. We examined associations of hormones with risk factors for breast cancer in control women by comparing geometric mean hormone concentrations in categories of these risk factors, adjusted for study, age, phase of menstrual cycle, and body-mass index (BMI). All statistical tests were two-sided.\n\nFINDINGS:\nWe included data for up to 767 women with breast cancer and 1699 controls in the risk analyses. Breast cancer risk was associated with a doubling in concentrations of oestradiol (OR 1·19, 95% CI 1·06-1·35), calculated free oestradiol (1·17, 1·03-1·33), oestrone (1·27, 1·05-1·54), androstenedione (1·30, 1·10-1·55), dehydroepiandrosterone sulphate (1·17, 1·04-1·32), testosterone (1·18, 1·03-1·35), and calculated free testosterone (1·08, 0·97-1·21). Breast cancer risk was not associated with luteal phase progesterone (doubling in concentration OR 1·00, 95% CI 0·92-1·09), and adjustment for other factors had little effect on any of these ORs. Cross-sectional analyses in control women showed several associations of sex hormones with breast cancer risk factors.\n\nINTERPRETATION:\nCirculating oestrogens and androgens are positively associated with the risk for breast cancer in premenopausal women." + }, + "questions": [ + { + "id": "fe91b342-6c3b-4d09-8aa0-988495fa9c62", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1357, + "text": "doubling in concentrations of oestradiol" + }, + { + "answer_start": 1427, + "text": "calculated free oestradiol" + }, + { + "answer_start": 1473, + "text": "oestrone" + }, + { + "answer_start": 1500, + "text": " androstenedione" + }, + { + "answer_start": 1536, + "text": "dehydroepiandrosterone sulphate" + }, + { + "answer_start": 1587, + "text": "testosterone" + }, + { + "answer_start": 2003, + "text": "Circulating oestrogens and androgens" + } + ] + } + ] +} \ No newline at end of file diff --git a/129ebf8c-6e7f-4221-9fda-f63d23907055.json b/129ebf8c-6e7f-4221-9fda-f63d23907055.json new file mode 100644 index 0000000000000000000000000000000000000000..2987202e0d6427a74b0f0fd5f2b0c57621810dc6 --- /dev/null +++ b/129ebf8c-6e7f-4221-9fda-f63d23907055.json @@ -0,0 +1,39 @@ +{ + "id": "129ebf8c-6e7f-4221-9fda-f63d23907055", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "1395752", + "text": "To determine the possibility that asymptomatic bronchial hyperresponsiveness (BHR) develops into symptomatic asthma, a two-year follow-up study was conducted in 81 students (48 male, 33 female; 11 to 17 years) who were found to have BHR in a 3,067 population survey (BHR group). Eighty-eight age-matched students (48 male, 40 female) with normal bronchial responsiveness served as control subjects. Daily symptom cards were recorded. Peak expiratory flow rate was measured for 24 h when symptoms occurred. Histamine inhalation tests were performed at the beginning of the study and at the end of the first and the second year. In the BHR group, 58 students remained bronchial hyperresponsive at the end of follow-up. Nine of 31 students with initially diagnosed bronchial asthma had their symptoms relieved entirely, but ten asymptomatic students developed asthma. The incidence of newly diagnosed asthma (12.5 percent in the BHR group or 20 percent in the asymptomatic BHR group) and the total percentage of diagnosed asthma (39.5 percent) in the BHR group were significantly higher than those (2.27 percent, 2.27 percent) in the control group. FVC and FEV1 showed no significant difference between two groups. PD20 FEV1 values in newly diagnosed asthmatics were significantly lower than those in asymptomatic students both at the beginning (3.05 +/- 1.56 mumol vs 6.14 +/- 1.60 mumol, p \u003c 0.05) or the end (3.47 +/- 1.73 mumol vs 6.55 +/- 1.51 mumol, p \u003c 0.05). The percentage of early respiratory illness was significantly higher in those with newly diagnosed asthma (80 percent) than in asymptomatic students (22.3 percent), but atopic index and the percentage of parental asthma showed no difference between two groups. In nine asthmatics whose symptoms were relieved entirely in the two-year follow-up, PD20 FEV1 was undetectable within the cumulative dose of 7.8 mumol of histamine in three students and rose from 4.58 +/- 1.85 mumol to 7.62 +/- 1.02 mumol in the remaining six. The higher the BHR, the more likely the students developed asthma. About 45 percent of asymptomatic students with PD20 \u003c or = 3.2 mumol developed asthma in the following two years and 80 percent of them had a history of early respiratory illness, suggesting that they may have subclinical or potential asthma." + }, + "questions": [ + { + "id": "52873524-3416-4030-a8eb-d5c1f15295b2", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1048, + "text": "BHR" + }, + { + "answer_start": 2001, + "text": "BHR" + } + ] + } + ] +} \ No newline at end of file diff --git a/12c9a0bd-1547-4262-b430-d5e302bf107b.json b/12c9a0bd-1547-4262-b430-d5e302bf107b.json new file mode 100644 index 0000000000000000000000000000000000000000..f9056a6c01cdbfe37fa46b45f2f32cba54654aa3 --- /dev/null +++ b/12c9a0bd-1547-4262-b430-d5e302bf107b.json @@ -0,0 +1,40 @@ +{ + "id": "12c9a0bd-1547-4262-b430-d5e302bf107b", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "15249443", + "text": "BACKGROUND:\nFor several years, asthma and COPD have been regarded as distinct entities, with distinct clinical courses. However, despite distinctive physiologic features at the time of diagnosis, and different risk factors, the two diseases over time may develop features that are quite similar.\n\nSTUDY OBJECTIVE:\nTo evaluate the association between physician-diagnosed asthma and the subsequent development of COPD in a cohort of 3,099 adult subjects from Tucson, AZ.\n\nDESIGN AND METHODS:\nA prospective observational study. Participants completed up to 12 standard respiratory questionnaires and 11 spirometry lung function measurements over a period of 20 years. Survival curves (with time to development of COPD as the dependent variable) were compared between subjects with asthma and subjects without asthma at the initial survey.\n\nRESULTS:\nSubjects with active asthma (n = 192) had significantly higher hazard ratios than inactive (n = 156) or nonasthmatic subjects (n = 2751) for acquiring COPD. As compared with nonasthmatics, active asthmatics had a 10-times-higher risk for acquiring symptoms of chronic bronchitis (95% confidence interval [CI], 4.94 to 20.25), 17-times-higher risk of receiving a diagnosis of emphysema (95% CI, 8.31 to 34.83), and 12.5-times-higher risk of fulfilling COPD criteria (95% CI, 6.84 to 22.84), even after adjusting for smoking history and other potential confounders.\n\nCONCLUSIONS:\nPhysician-diagnosed asthma is significantly associated with an increased risk for CB, emphysema, and COPD." + }, + "questions": [ + { + "id": "469ac7de-a52e-499a-aada-cfd077000d62", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 1424, + "text": "Physician-diagnosed asthma" + }, + { + "answer_start": 1035, + "text": "active asthmatics" + } + ] + } + ] +} \ No newline at end of file diff --git a/13765be1-2ba0-40a7-8584-1aedde831e27.json b/13765be1-2ba0-40a7-8584-1aedde831e27.json new file mode 100644 index 0000000000000000000000000000000000000000..a036ad4935c91e087453078e68520c0722120931 --- /dev/null +++ b/13765be1-2ba0-40a7-8584-1aedde831e27.json @@ -0,0 +1,45 @@ +{ + "id": "13765be1-2ba0-40a7-8584-1aedde831e27", + "disease": { + "id": "M2023_04_26_16_38_52", + "names": [ + "Migraine" + ], + "dbLinks": { + "icd10": [ + "G43" + ], + "icd11": [ + "8A80" + ], + "mesh": [ + "C10.228.140.546.399.750" + ] + }, + "description": "Migraine is a chronic neurological disorder characterized by recurrent episodes of unilateral, pulsatile headaches associated with autonomic symptoms such as nausea, vomiting, photophobia, and phonophobia. The pathophysiology of migraine is multifactorial and involves complex interactions between genetic, environmental, and neurochemical factors that modulate cerebral vascular tone and nociception. Migraine attacks can be triggered by a variety of factors, including stress, hormonal changes, sleep disturbances, and certain foods or medications. Treatment options for migraine include pharmacotherapy for acute attacks, preventive medications for frequent or severe headaches, and lifestyle modifications to avoid triggers. In refractory cases, interventional therapies such as nerve blocks or neuromodulation techniques may be considered." + }, + "article": { + "id": "23808359", + "text": "BACKGROUND:\nDisturbances in sleep are common among migraineurs, particularly those with frequent (ie, chronic) migraine. Examination of specific types of sleep disturbance and behaviors among episodic migraineurs, however, has not been sufficiently explored. Further, few studies have investigated whether sleep disturbance is attributable to comorbid affective symptomatology.\n\nOBJECTIVES:\nThe present case-control study sought to (1) assess sleep quality, daytime sleepiness, and sleep hygiene among a large sample of episodic migraineurs; (2) quantify relations between sleep disturbance and headache-related variables; and (3) determine if these relations remain after accounting for comorbid depression and anxiety.\n\nMETHODS:\nTwo hundred ninety-two undergraduate students (69.9% female, mean age = 19.19, standard deviation [SD] = 3.21 years) completed measures of sleep quality, daytime sleepiness, and sleep hygiene along with well-validated measures of depression and anxiety symptomatology. Those screening positive for migraine were subsequently administered a structured diagnostic interview to verify diagnosis of migraine consistent with the International Classification of Headache Disorders, 2nd edition. Episodic migraineurs and non-migraine controls were compared on the sleep disturbance variables, and among those with migraine, relations with headache frequency, severity, and disability were quantified with linear regression analyses.\n\nRESULTS:\nSeventy-eight (26.7%) participants met International Classification of Headache Disorders, 2nd edition criteria for episodic migraine. Compared with participants without migraine, episodic migraineurs reported poorer sleep quality (mean = 8.90 [SD = 3.39] vs 6.63 [SD = 3.02], P \u003c .0001), with 85.9% reporting clinically significant poor sleep quality (vs 62.0% of controls). Poor sleep quality was significantly associated with headache frequency and headache-related disability, accounting for proportions of variance (14.8% in frequency and 18.2% in disability, both P ≤ .001) similar to those attributable to depression and anxiety. These relationships remained significant after controlling for these affective symptoms, in which sleep quality accounted for 5.3% and 5.8% of unique variance in frequency and disability, respectively (P \u003c .05). By comparison, daytime sleepiness and poor sleep hygiene were not consistently associated with migraine or migraine-related variables.\n\nCONCLUSIONS:\nConsistent with prior studies on chronic migraine, poor sleep quality is uniquely associated with episodic migraine, and this relationship is not solely attributable to comorbid psychiatric symptomatology. Sleep quality should be preferentially assessed (vs sleepiness and sleep hygiene) when subjective self-report measures of insomnia are used in clinical headache settings. Future studies should supplement these findings by evaluating the efficacy of interventions that specifically target sleep quality and insomnia (eg, stimulus control, sleep restriction) among episodic migraineurs." + }, + "questions": [ + { + "id": "b52c9f8a-975f-40b8-aebf-c62ec7dd31dc", + "text": "what are the risk factors of Migraine?", + "answers": [ + { + "answer_start": 2516, + "text": "poor sleep quality" + }, + { + "answer_start": 1677, + "text": "poorer sleep quality" + }, + { + "answer_start": 1843, + "text": "Poor sleep quality" + } + ] + } + ] +} \ No newline at end of file diff --git a/13e5edba-789c-42bf-8102-814d2f6939fb.json b/13e5edba-789c-42bf-8102-814d2f6939fb.json new file mode 100644 index 0000000000000000000000000000000000000000..dfc46536f48ec2f371aabe229f9e2282e6dbd110 --- /dev/null +++ b/13e5edba-789c-42bf-8102-814d2f6939fb.json @@ -0,0 +1,35 @@ +{ + "id": "13e5edba-789c-42bf-8102-814d2f6939fb", + "disease": { + "id": "H00056", + "names": [ + "Alzheimer disease", + "Dementia due to Alzheimer disease" + ], + "dbLinks": { + "icd10": [ + "G30" + ], + "mesh": [ + "D000544" + ] + }, + "category": "Neurodegenerative disease" + }, + "article": { + "id": "18349428", + "text": "Air pollution is a serious environmental problem. We investigated whether residency in cities with high air pollution is associated with neuroinflammation/neurodegeneration in healthy children and young adults who died suddenly. We measured mRNA cyclooxygenase-2, interleukin-1beta, and CD14 in target brain regions from low (n = 12) or highly exposed residents (n = 35) aged 25.1 +/- 1.5 years. Upregulation of cyclooxygenase-2, interleukin-1beta, and CD14 in olfactory bulb, frontal cortex, substantia nigrae and vagus nerves; disruption of the blood-brain barrier; endothelial activation, oxidative stress, and inflammatory cell trafficking were seen in highly exposed subjects. Amyloid beta42 (Abeta42) immunoreactivity was observed in 58.8% of apolipoprotein E (APOE) 3/3 \u003c 25 y, and 100% of the APOE 4 subjects, whereas alpha-synuclein was seen in 23.5% of \u003c 25 y subjects. Particulate material (PM) was seen in olfactory bulb neurons, and PM \u003c 100 nm were observed in intraluminal erythrocytes from lung, frontal, and trigeminal ganglia capillaries. Exposure to air pollution causes neuroinflammation, an altered brain innate immune response, and accumulation of Abeta42 and alpha-synuclein starting in childhood. Exposure to air pollution should be considered a risk factor for Alzheimer's and Parkinson's diseases, and carriers of the APOE 4 allele could have a higher risk of developing Alzheimer's disease if they reside in a polluted environment." + }, + "questions": [ + { + "id": "bf624ae5-cb88-4e19-81eb-a4b8bb52b7ba", + "text": "What are the risk factors of Alzheimer disease?", + "answers": [ + { + "answer_start": 1221, + "text": "Exposure to air pollution" + } + ] + } + ] +} \ No newline at end of file diff --git a/141a7b68-ec2a-467f-96c8-202d39e4f148.json b/141a7b68-ec2a-467f-96c8-202d39e4f148.json new file mode 100644 index 0000000000000000000000000000000000000000..fd3a3671b8f3bcd2bd773aec16af1a05c25c2b41 --- /dev/null +++ b/141a7b68-ec2a-467f-96c8-202d39e4f148.json @@ -0,0 +1,35 @@ +{ + "id": "141a7b68-ec2a-467f-96c8-202d39e4f148", + "disease": { + "id": "H00056", + "names": [ + "Alzheimer disease", + "Dementia due to Alzheimer disease" + ], + "dbLinks": { + "icd10": [ + "G30" + ], + "mesh": [ + "D000544" + ] + }, + "category": "Neurodegenerative disease" + }, + "article": { + "id": "28017827", + "text": "INTRODUCTION:\nThe presence of cerebrovascular pathology may increase the risk of clinical diagnosis of Alzheimer's disease (AD).\n\nMETHODS:\nWe examined excess risk of incident clinical diagnosis of AD (probable and possible AD) posed by the presence of lacunes and large infarcts beyond AD pathology using data from the Statistical Modeling of Aging and Risk of Transition study, a consortium of longitudinal cohort studies with more than 2000 autopsies. We created six mutually exclusive pathology patterns combining three levels of AD pathology (low, moderate, or high AD pathology) and two levels of vascular pathology (without lacunes and large infarcts or with lacunes and/or large infarcts).\n\nRESULTS:\nThe coexistence of lacunes and large infarcts results in higher likelihood of clinical diagnosis of AD only when AD pathology burden is low.\n\nDISCUSSION:\nOur results reinforce the diagnostic importance of AD pathology in clinical AD. Further harmonization of assessment approaches for vascular pathologies is required." + }, + "questions": [ + { + "id": "5e03abd2-096d-4a24-a4ff-008962a4357e", + "text": "What are the risk factors of Alzheimer disease?", + "answers": [ + { + "answer_start": 711, + "text": "coexistence of lacunes and large infarcts" + } + ] + } + ] +} \ No newline at end of file diff --git a/143e2668-926b-4793-9957-8bd6a408ecdc.json b/143e2668-926b-4793-9957-8bd6a408ecdc.json new file mode 100644 index 0000000000000000000000000000000000000000..97ff949c430d0a1689b1a5167b1be4546e8a2fdf --- /dev/null +++ b/143e2668-926b-4793-9957-8bd6a408ecdc.json @@ -0,0 +1,34 @@ +{ + "id": "143e2668-926b-4793-9957-8bd6a408ecdc", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "9833970", + "text": "Blackfoot disease is an endemic peripheral vascular disease found among people in a limited area on the southwest coast of Taiwan, where artesian well water has a high concentration of arsenic and was used since the turn of this century. This is an important public health problem and was noted by the authorities, who began improving the water supply in such communities in 1956. This enabled us to test the relationship between arsenic and malignant tumors using a specific exposed community. Study subjects were divided into four groups according to age (under or over 40 yr) and gender. Two methods were used for the estimation of the age-adjusted mortality rate ratios. First using the first time interval (1971-1973) as the standard, the mortality rate ratio for all malignant tumors was estimated from this interval through to the last interval (1992-1994) using Poisson regression. Cancers that were found to be related to arsenic in previous reports, such as liver, lung, bladder, kidney, and skin cancers, were examined and other malignant tumors except these cancers were also assessed. The same calculations were performed for all of Chiayi and Tainan counties, excluding the study areas, which were used as the local reference, and for the general population of Taiwan, which was used as a national reference group. Second, mortality rate ratios for the study area were compared to the local and national reference for the same time intervals for each disease category. From our results, significantly declining trends for mortality rate ratios of all malignant tumors with 1971-1973 as the standard were found for the study areas, especially in females. A decrease of mortality rate ratios from malignant cancers, compared to the local or national references, was found in those aged over 40 yr for both sexes. The decreases are mainly due to a fall in internal and skin cancer mortality rates. In conclusion, our results suggest that the improvement of drinking water supply to eliminate arsenic exposure from artesian well water decreased the mortality incidence of arsenic-related cancers in blackfoot disease endemic communities." + }, + "questions": [ + { + "id": "60886618-d012-4ab7-81f9-d37aa4605648", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 163, + "text": "high concentration of arsenic" + } + ] + } + ] +} \ No newline at end of file diff --git a/1454f8f7-1bac-4b98-a253-a87aad3dee4c.json b/1454f8f7-1bac-4b98-a253-a87aad3dee4c.json new file mode 100644 index 0000000000000000000000000000000000000000..4e8087b3623f6c183ebf80e360b569b5ca44152b --- /dev/null +++ b/1454f8f7-1bac-4b98-a253-a87aad3dee4c.json @@ -0,0 +1,42 @@ +{ + "id": "1454f8f7-1bac-4b98-a253-a87aad3dee4c", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "26936410", + "text": "OBJECTIVE:\nTo determine the association between exposure to radiotherapy for the treatment of prostate cancer and subsequent second malignancies (second primary cancers).\n\nDESIGN:\nSystematic review and meta-analysis of observational studies.\n\nDATA SOURCES:\nMedline and Embase up to 6 April 2015 with no restrictions on year or language.\n\nSTUDY SELECTION:\nComparative studies assessing the risk of second malignancies in patients exposed or unexposed to radiotherapy in the course of treatment for prostate cancer were selected by two reviewers independently with any disagreement resolved by consensus.\n\nDATA EXTRACTION AND SYNTHESIS:\nTwo reviewers independently extracted study characteristics and outcomes. Risk of bias was assessed with the Newcastle-Ottawa scale. Outcomes were synthesized with random effects models and Mantel-Haenszel weighting. Unadjusted odds ratios and multivariable adjusted hazard ratios, when available, were pooled.\n\nMAIN OUTCOME MEASURES:\nSecond cancers of the bladder, colorectal tract, rectum, lung, and hematologic system.\n\nRESULTS:\nOf 3056 references retrieved, 21 studies were selected for analysis. Most included studies were large multi-institutional reports but had moderate risk of bias. The most common type of radiotherapy was external beam; 13 studies used patients treated with surgery as controls and eight used patients who did not undergo radiotherapy as controls. The length of follow-up among studies varied. There was increased risk of cancers of the bladder (four studies; adjusted hazard ratio 1.67, 95% confidence interval 1.55 to 1.80), colorectum (three studies; 1.79, 1.34 to 2.38), and rectum (three studies; 1.79, 1.34 to 2.38), but not cancers of the hematologic system (one study; 1.64, 0.90 to 2.99) or lung (two studies; 1.45, 0.70 to 3.01), after radiotherapy compared with the risk in those unexposed to radiotherapy. The odds of a second cancer varied depending on type of radiotherapy: treatment with external beam radiotherapy was consistently associated with increased odds while brachytherapy was not. Among the patients who underwent radiotherapy, from individual studies, the highest absolute rates reported for bladder, colorectal, and rectal cancers were 3.8%, 4.2%, and 1.2%, respectively, while the lowest reported rates were 0.1%, 0.3%, and 0.3%.\n\nCONCLUSION:\nRadiotherapy for prostate cancer was associated with higher risks of developing second malignancies of the bladder, colon, and rectum compared with patients unexposed to radiotherapy, but the reported absolute rates were low. Further studies with longer follow-up are required to confirm these findings." + }, + "questions": [ + { + "id": "e946fdcf-b480-40ec-8f18-5425b3b2a73b", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 2336, + "text": "Radiotherapy for prostate cancer" + }, + { + "answer_start": 1810, + "text": "radiotherapy" + }, + { + "answer_start": 1952, + "text": "treatment with external beam radiotherapy" + } + ] + } + ] +} \ No newline at end of file diff --git a/145634c7-ddff-48da-be6e-d6534fec4158.json b/145634c7-ddff-48da-be6e-d6534fec4158.json new file mode 100644 index 0000000000000000000000000000000000000000..9e13c63d329abd1d05ac70c8a8b32129ebf6fbc5 --- /dev/null +++ b/145634c7-ddff-48da-be6e-d6534fec4158.json @@ -0,0 +1,34 @@ +{ + "id": "145634c7-ddff-48da-be6e-d6534fec4158", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "25271602", + "text": "BACKGROUND:\nThe relationship between the risk of celiac disease and both the age at which gluten is introduced to a child's diet and a child's early dietary pattern is unclear.\n\nMETHODS:\nWe randomly assigned 832 newborns who had a first-degree relative with celiac disease to the introduction of dietary gluten at 6 months (group A) or 12 months (group B). The HLA genotype was determined at 15 months of age, and serologic screening for celiac disease was evaluated at 15, 24, and 36 months and at 5, 8, and 10 years. Patients with positive serologic findings underwent intestinal biopsies. The primary outcome was the prevalence of celiac disease autoimmunity and of overt celiac disease among the children at 5 years of age.\n\nRESULTS:\nOf the 707 participants who remained in the trial at 36 months, 553 had a standard-risk or high-risk HLA genotype and completed the study. At 2 years of age, significantly higher proportions of children in group A than in group B had celiac disease autoimmunity (16% vs. 7%, P=0.002) and overt celiac disease (12% vs. 5%, P=0.01). At 5 years of age, the between-group differences were no longer significant for autoimmunity (21% in group A and 20% in group B, P=0.59) or overt disease (16% and 16%, P=0.78 by the log-rank test). At 10 years, the risk of celiac disease autoimmunity was far higher among children with high-risk HLA than among those with standard-risk HLA (38% vs. 19%, P=0.001), as was the risk of overt celiac disease (26% vs. 16%, P=0.05). Other variables, including breast-feeding, were not associated with the development of celiac disease.\n\nCONCLUSIONS:\nNeither the delayed introduction of gluten nor breast-feeding modified the risk of celiac disease among at-risk infants, although the later introduction of gluten was associated with a delayed onset of disease. A high-risk HLA genotype was an important predictor of disease. (Funded by the Fondazione Celiachia of the Italian Society for Celiac Disease; CELIPREV ClinicalTrials.gov number, NCT00639444.)." + }, + "questions": [ + { + "id": "ce34ef38-1e85-4fa7-98fd-4b1e2b0db5ee", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 1826, + "text": "high-risk HLA genotype" + } + ] + } + ] +} \ No newline at end of file diff --git a/147284b4-9423-41fe-83c0-3b6bd37ea1a8.json b/147284b4-9423-41fe-83c0-3b6bd37ea1a8.json new file mode 100644 index 0000000000000000000000000000000000000000..685003ba2aef7037b31470e92e6a1c2440d37924 --- /dev/null +++ b/147284b4-9423-41fe-83c0-3b6bd37ea1a8.json @@ -0,0 +1,70 @@ +{ + "id": "147284b4-9423-41fe-83c0-3b6bd37ea1a8", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "17720018", + "text": "BACKGROUND:\nIndividuals with diabetes are at higher risk of myocardial infarction than non-diabetics. However, much less is known about the incidence of, and risk factors for, development of diabetes and impaired fasting glucose in patients who have had a myocardial infarction. We set out to estimate this incidence and investigate whether lifestyle factors such as dietary habits might alter this risk.\n\nMETHODS:\nWe used prospectively obtained data for 8291 Italian patients with a myocardial infarction within the previous 3 months, who were free of diabetes (determined by medication use, a physician-reported diagnosis, or fasting glucose \u003e or =7 mmol/L) at baseline. Incidence of new-onset diabetes (new diabetes medication or fasting glucose \u003e or =7 mmol/L) and impaired fasting glucose (fasting glucose \u003e or =6.1 mmol/L and \u003c7 mmol/L) were assessed at follow-up at 0.5, 1.0, 1.5, 2.5, and 3.5 years. Baseline data for body-mass index (BMI), other risk factors, dietary habits, and medications were updated during follow-up. A Mediterranean diet score was assigned according to consumption of cooked and raw vegetables, fruit, fish, and olive oil. Associations of demographic, clinical, and lifestyle risk-factors with incidence of diabetes and impaired fasting glucose were assessed with multivariable Cox proportional hazards.\n\nFINDINGS:\nDuring 26 795 person-years (mean follow-up 3.2 years [SD 0.9]), 998 individuals (12%) developed new-onset diabetes (incidence 37 cases per 1000 person-years). Of the 7533 without impaired fasting glucose at baseline, 2514 (33%) developed new-onset impaired fasting glucose or diabetes (incidence 123 cases per 1000 person-years), rising to 3859 (62%) of 6229 with the lower cutoff for impaired fasting glucose of 5.6 mmol/L (incidence 321 cases per 1000 person-years). Independent risk factors for new-onset diabetes or impaired fasting glucose included older age, hypertension, use of beta-blockers, lipid-lowering medications (protective), and diuretic use. Independent lifestyle risk-factors included higher BMI, greater BMI gain during follow-up, current smoking, a lower Mediterranean dietary score, and wine consumption of more than 1 L/day. Data for physical activity were unavailable, but inability to perform exercise testing was associated with higher incidence of diabetes and impaired fasting glucose.\n\nINTERPRETATION:\nCompared with population-based cohorts, patients with a recent myocardial infarction had a higher annual incidence rate of impaired fasting glucose (1.8 vs 27.5% in our study) and diabetes (0.8-1.6% compared with 3.7%) in this study. Thus, our results indicate that myocardial infarction could be a prediabetes risk equivalent. Smoking cessation, prevention of weight gain, and consumption of typical Mediterranean foods might lower this risk, which emphasises the need for guidance on diet and other lifestyle factors for patients who have had a myocardial infarction." + }, + "questions": [ + { + "id": "584fbf14-39db-4580-bc56-fc260fd64d7c", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 2418, + "text": "patients with a recent myocardial infarction" + }, + { + "answer_start": 1901, + "text": "older age" + }, + { + "answer_start": 1912, + "text": "hypertension" + }, + { + "answer_start": 1926, + "text": "use of beta-blockers" + }, + { + "answer_start": 1993, + "text": "diuretic use" + }, + { + "answer_start": 2051, + "text": "higher BMI" + }, + { + "answer_start": 2063, + "text": "greater BMI gain" + }, + { + "answer_start": 2098, + "text": "current smoking" + }, + { + "answer_start": 2117, + "text": "lower Mediterranean dietary score" + }, + { + "answer_start": 2156, + "text": "wine consumption of more than 1 L/day" + } + ] + } + ] +} \ No newline at end of file diff --git a/15250763-59b4-4114-b2a9-1e4fc03a8e3a.json b/15250763-59b4-4114-b2a9-1e4fc03a8e3a.json new file mode 100644 index 0000000000000000000000000000000000000000..afaf69d1cdda62512166f3cfd3f35264c63414ee --- /dev/null +++ b/15250763-59b4-4114-b2a9-1e4fc03a8e3a.json @@ -0,0 +1,38 @@ +{ + "id": "15250763-59b4-4114-b2a9-1e4fc03a8e3a", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "15893180", + "text": "OBJECTIVES:\nWe sought to determine the predictive ability of total white blood cell (WBC) count and its subtypes for risk of death or myocardial infarction (MI).\n\nBACKGROUND:\nAn elevated WBC count has been associated with cardiovascular risk, but which leukocyte subtypes carry this risk is uncertain.\n\nMETHODS:\nConsecutive patients without acute MI who were assessed angiographically for coronary artery disease (CAD) and were followed up long-term were studied. The predictive ability for death/MI of quartile (Q) 4 versus Q1 total WBC, neutrophil (N), lymphocyte (L), and monocyte (M) counts and N/L ratio were assessed using Cox regressions.\n\nRESULTS:\nA total of 3,227 patients was studied. Mean age was 63 years; 63% of patients were male, and 65% had CAD. In multivariable modeling entering standard risk factors, presentation, and CAD severity, the total WBC (hazard ratio [HR] 1.4, p = 0.01) and M (HR 1.3, p \u003c 0.02) were weaker and N (HR 1.8, p \u003c 0.001), L (HR 0.51, p \u003c 0.001), and N/L ratio (HR 2.2, p \u003c 0.001) were independent predictors of death/MI. When WBC variables were entered together, N/L ratio and M were retained as independent predictors. Risk associations persisted in analyses restricted to CAD patients or including acute MI patients.\n\nCONCLUSIONS:\nTotal WBC count is confirmed to be an independent predictor of death/MI in patients with or at high risk for CAD, but greater predictive ability is provided by high N (Q4 \u003e6.6 x 10(3)/microl) or low L counts. The greatest risk prediction is given by the N/L ratio, with Q4 versus Q1 (\u003e4.71 versus \u003c1.96) increasing the hazard 2.2-fold. These findings have important implications for CAD risk assessment." + }, + "questions": [ + { + "id": "c33c5f3a-55e9-4272-b581-68839f6a7eb9", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1275, + "text": "Total WBC" + }, + { + "answer_start": 1105, + "text": "N/L ratio" + } + ] + } + ] +} \ No newline at end of file diff --git a/15632bb0-df93-4e27-832e-2be8739c2af2.json b/15632bb0-df93-4e27-832e-2be8739c2af2.json new file mode 100644 index 0000000000000000000000000000000000000000..f4873d9cfecfbc192fb3f874c9deaae76789f4fd --- /dev/null +++ b/15632bb0-df93-4e27-832e-2be8739c2af2.json @@ -0,0 +1,34 @@ +{ + "id": "15632bb0-df93-4e27-832e-2be8739c2af2", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "23316283", + "text": "BACKGROUND:\nGlycemic index (GI) and glycemic load (GL) have been associated with coronary heart disease (CHD) risk in some but not all cohort studies. We therefore assessed the association of GI and GL with CHD risk in prospective cohorts.\n\nMETHODS AND RESULTS:\nWe searched MEDLINE, EMBASE, and CINAHL (through April 5, 2012) and identified all prospective cohorts assessing associations of GI and GL with incidence of CHD. Meta-analysis of observational studies in epidemiology (MOOSE) methodologies were used. Relative measures of risk, comparing the group with the highest exposure (mean GI of cohorts=84.4 GI units, range 79.9 to 91; mean GL of cohorts=224.8, range 166 to 270) to the reference group (mean GI=72.3 GI units, range 68.1 to 77; mean GL=135.4, range 83 to 176), were pooled using random-effects models, expressed as relative risk (RR) with heterogeneity assessed by χ(2) and quantified by I(2). Subgroups included sex and duration of follow-up. Ten studies (n=240 936) were eligible. Pooled analyses showed an increase in CHD risk for the highest GI quantile compared with the lowest, with RR=1.11 (95% confidence interval [CI] 0.99 to 1.24) and for GL, RR=1.27 (95% CI 1.09 to 1.49), both with evidence of heterogeneity (I(2)\u003e42%, P\u003c0.07). Subgroup analyses revealed only a significant modification by sex, with the female cohorts showing significance for GI RR=1.26 (95% CI 1.12 to 1.41) and for GL RR=1.55 (95% CI 1.18 to 2.03).\n\nCONCLUSIONS:\nHigh GI and GL diets were significantly associated with CHD events in women but not in men. Further studies are required to determine the relationship between GI and GL with CHD in men." + }, + "questions": [ + { + "id": "589fa03b-a929-429e-919b-6af7d645eca6", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1464, + "text": "High GI and GL diets" + } + ] + } + ] +} \ No newline at end of file diff --git a/16072262-95b1-49bf-9896-6ecba09326c4.json b/16072262-95b1-49bf-9896-6ecba09326c4.json new file mode 100644 index 0000000000000000000000000000000000000000..d46768d6e7ffbbf1953ed3bf3b6bbbca9791fb8f --- /dev/null +++ b/16072262-95b1-49bf-9896-6ecba09326c4.json @@ -0,0 +1,46 @@ +{ + "id": "16072262-95b1-49bf-9896-6ecba09326c4", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "14583769", + "text": "Animal experiments and human ecological studies suggest that dietary fat intake is associated with a risk of breast cancer, but individual-based studies have given contradictory results. We have carried out a meta-analysis of this association to include all papers published up to July 2003. Case-control and cohort studies that examined the association of dietary fat, or fat-containing foods, with risk of breast cancer were identified. A total of 45 risk estimates for total fat intake were obtained. Descriptive data from each study were extracted with an estimate of relative risk and its associated 95% confidence interval (CI), and were analysed using the random effects model of DerSimonian and Laird. The summary relative risk, comparing the highest and lowest levels of intake of total fat, was 1.13 (95% CI: 1.03-1.25). Cohort studies (N=14) had a summary relative risk of 1.11 (95% CI: 0.99-1.25) and case-control studies (N=31) had a relative risk of 1.14 (95% CI 0.99-1.32). Significant summary relative risks were also found for saturated fat (RR, 1.19; 95% CI: 1.06-1.35) and meat intake (RR, 1.17; 95% CI 1.06-1.29). Combined estimates of risk for total and saturated fat intake, and for meat intake, all indicate an association between higher intakes and an increased risk of breast cancer. Case-control and cohort studies gave similar results." + }, + "questions": [ + { + "id": "010d1299-2362-482b-95c3-6890fe4a8f93", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1044, + "text": "saturated fat" + }, + { + "answer_start": 1092, + "text": "meat intake" + }, + { + "answer_start": 1165, + "text": "total and saturated fat intake" + }, + { + "answer_start": 1205, + "text": "meat intake" + } + ] + } + ] +} \ No newline at end of file diff --git a/161155f4-41e9-4378-b8d2-79ce6e15c1f9.json b/161155f4-41e9-4378-b8d2-79ce6e15c1f9.json new file mode 100644 index 0000000000000000000000000000000000000000..f8917633a95f3db4857a13fdafc12d1171b9dd8f --- /dev/null +++ b/161155f4-41e9-4378-b8d2-79ce6e15c1f9.json @@ -0,0 +1,37 @@ +{ + "id": "161155f4-41e9-4378-b8d2-79ce6e15c1f9", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "29510753", + "text": "BACKGROUND:\nObesity and physical activity (PA) are predictors of colon (CC) and rectal (RC) cancers. Prolonged sitting is also emerging as a potential predictor for these cancers. Little knowledge exists about the interactive effects of obesity, PA and prolonged sitting on cancer risk. This analysis assessed independent and interactive effects of PA, body mass index (BMI) and sitting time on CC and RC risks.\n\nMETHODS:\nThis analysis used data from a prospective study of 226,584 participants aged 45 years and over in New South Wales (NSW), Australia, who joined the 45 and Up study between 2006 and 2009. Baseline data were linked with data relating to mortality, cancer registration, hospital admission and Department of Human Services to December 2010. Multivariable Cox regression was used to estimate adjusted hazard ratios (referred to as relative risks, RRs) and 95% confidence intervals (Cis). Statistical significance was defined as p \u003c 0.05.\n\nRESULTS:\nThere were 846 and 369 ascertained cases of CC and RC. BMI was positively associated with CC risk (p = 0.003, P-trend = 0.0006) but not with RC. CC risk was increased in participants in the highest BMI quartile (≥29.4-≤50 kg/m) compared to the lowest (15- \u003c 23.6 kg/m), (RR = 1.32, 95% CI:1.08-1.63). PA was associated with CC risk (p = 0.02) but not with RC. Specifically, CC risk was lower in individuals partaking in any amount of vigorous activity (time/week) compared to participants with no engagement (RR = 0.78, 95% CI:0.65-0.93). Sitting time was not associated with CC or RC. We found no evidence of interactive effects of PA, BMI and prolonged sitting on cancer risk.\n\nCONCLUSION:\nThis evidence suggests that a healthy weight and vigorous activity are essential to reduce CC risk since these factors may be independent of each other." + }, + "questions": [ + { + "id": "fe2b7a2b-a3a9-4e43-b8ab-ac1aefb708bf", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1154, + "text": " highest BMI quartile (≥29.4-≤50 kg/m)" + } + ] + } + ] +} \ No newline at end of file diff --git a/16388330-1b9b-4f91-af7c-6bb72d7949f2.json b/16388330-1b9b-4f91-af7c-6bb72d7949f2.json new file mode 100644 index 0000000000000000000000000000000000000000..7ed90f88c2d974e46d6d7dd33d108f30cef0596a --- /dev/null +++ b/16388330-1b9b-4f91-af7c-6bb72d7949f2.json @@ -0,0 +1,34 @@ +{ + "id": "16388330-1b9b-4f91-af7c-6bb72d7949f2", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "12885485", + "text": "Pooled analyses of cohort studies show no relation between fat intake and breast-cancer risk. However, food-frequency questionnaire (FFQ) methods used in these studies are prone to measurement error. We assessed diet with an FFQ and a detailed 7-day food diary in 13070 women between 1993 and 1997. We compared 168 breast-cancer cases incident by 2000 with four matched controls. Risk of breast cancer was associated with saturated-fat intake measured with the food diary (hazard ratio 1.22 [95% CI 1.06-1.40], p=0.005, per quintile increase in energy-adjusted fat intake), but not with saturated fat measured with the FFQ (1.10 [0.94-1.29], p=0.23). Dietary measurement error might explain the absence of a significant association between dietary fat and breast-cancer risk in cohort studies." + }, + "questions": [ + { + "id": "3e2725ab-1964-4fd0-83bd-5ac3b4071aad", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 422, + "text": "saturated-fat intake" + } + ] + } + ] +} \ No newline at end of file diff --git a/175e9fd7-097a-4b10-af20-ecabf54dc388.json b/175e9fd7-097a-4b10-af20-ecabf54dc388.json new file mode 100644 index 0000000000000000000000000000000000000000..68546f0d13a87bf444f9f1f560eca696abf4dc34 --- /dev/null +++ b/175e9fd7-097a-4b10-af20-ecabf54dc388.json @@ -0,0 +1,35 @@ +{ + "id": "175e9fd7-097a-4b10-af20-ecabf54dc388", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "30086135", + "text": "BACKGROUND:\nObservational studies on pubertal timing and asthma, mainly performed in females, have provided conflicting results about a possible association of early puberty with higher risk of adult asthma, possibly due to residual confounding. To overcome issues of confounding, we used Mendelian randomisation (MR), i.e., genetic variants were used as instrumental variables to estimate causal effects of early puberty on post-pubertal asthma in both females and males.\n\nMETHODS AND FINDINGS:\nMR analyses were performed in UK Biobank on 243,316 women using 254 genetic variants for age at menarche, and on 192,067 men using 46 variants for age at voice breaking. Age at menarche, recorded in years, was categorised as early (\u003c12), normal (12-14), or late (\u003e14); age at voice breaking was recorded and analysed as early (younger than average), normal (about average age), or late (older than average). In females, we found evidence for a causal effect of pubertal timing on asthma, with an 8% increase in asthma risk for early menarche (odds ratio [OR] 1.08; 95% CI 1.04 to 1.12; p = 8.7 × 10(-5)) and an 8% decrease for late menarche (OR 0.92; 95% CI 0.89 to 0.97; p = 3.4 × 10(-4)), suggesting a continuous protective effect of increasing age at puberty. In males, we found very similar estimates of causal effects, although with wider confidence intervals (early voice breaking: OR 1.07; 95% CI 1.00 to 1.16; p = 0.06; late voice breaking: OR 0.93; 95% CI 0.87 to 0.99; p = 0.03). We detected only modest pleiotropy, and our findings showed robustness when different methods to account for pleiotropy were applied. BMI may either introduce pleiotropy or lie on the causal pathway; secondary analyses excluding variants associated with BMI yielded similar results to those of the main analyses. Our study relies on self-reported exposures and outcomes, which may have particularly affected the power of the analyses on age at voice breaking.\n\nCONCLUSIONS:\nThis large MR study provides evidence for a causal detrimental effect of early puberty on asthma, and does not support previous observational findings of a U-shaped relationship between pubertal timing and asthma. Common biological or psychological mechanisms associated with early puberty might explain the similarity of our results in females and males, but further research is needed to investigate this. Taken together with evidence for other detrimental effects of early puberty on health, our study emphasises the need to further investigate and address the causes of the secular shift towards earlier puberty observed worldwide." + }, + "questions": [ + { + "id": "b5cec4e8-9a5d-46e3-b0e5-070cd8fef8df", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 2033, + "text": "early puberty" + } + ] + } + ] +} \ No newline at end of file diff --git a/17b214c1-38a2-4b51-a66c-cea67a2ac56f.json b/17b214c1-38a2-4b51-a66c-cea67a2ac56f.json new file mode 100644 index 0000000000000000000000000000000000000000..3a553b09248af9478e246d5f3265163840f64e23 --- /dev/null +++ b/17b214c1-38a2-4b51-a66c-cea67a2ac56f.json @@ -0,0 +1,39 @@ +{ + "id": "17b214c1-38a2-4b51-a66c-cea67a2ac56f", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "31626886", + "text": "BACKGROUND:\nWhile cutaneous melanomas (CM) account for greater than 90% of all melanomas, noncutaneous melanomas (NCM) are more aggressive and associated with worse outcomes. The shared progenitor cell type among CM and NCM suggests that patients with a history of CM may be at higher risk for subsequent NCM.\n\nOBJECTIVE:\nTo determine whether patients with a history of CM demonstrate an increased risk of second primary cutaneous, ocular, oral, or vaginal/exocervical melanoma compared with the general population.\n\nMETHODS:\nThis was a population-based retrospective cohort study using the Surveillance, Epidemiology, and End Results database. We calculated standardized incidence ratios (SIRs) and excess absolute risks of second primary cutaneous, ocular, oral, and vaginal/exocervical melanoma in patients with a history of CM.\n\nRESULTS:\nPatients with prior CM (n = 169,841) were more likely than the general population to develop a second primary CM (SIR, 8.17; 95% confidence interval [CI], 8.01-8.33), ocular melanoma (SIR, 1.99; 95% CI, 1.54-2.53), oral melanoma (SIR, 6.87; 95% CI, 2.23-16.04), and vaginal/exocervical melanoma (SIR, 10.17; 95% CI, 4.65-19.30).\n\nLIMITATIONS:\nThis study is limited by possible under-reporting of CM in cancer registries.\n\nCONCLUSION:\nIn caring for patients with a history of CM, physicians should be vigilant not only about risk of recurrence but also about second primary CM and NCM." + }, + "questions": [ + { + "id": "2933c777-de0b-4ae2-9c73-30223cc43b09", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 842, + "text": "Patients with prior CM" + }, + { + "answer_start": 18, + "text": "cutaneous melanomas (CM)" + } + ] + } + ] +} \ No newline at end of file diff --git a/17d59181-ee4b-4125-86f7-6ef57167fae3.json b/17d59181-ee4b-4125-86f7-6ef57167fae3.json new file mode 100644 index 0000000000000000000000000000000000000000..6c976c96fac50eb681f64ac0db58f671906fd1bf --- /dev/null +++ b/17d59181-ee4b-4125-86f7-6ef57167fae3.json @@ -0,0 +1,32 @@ +{ + "id": "17d59181-ee4b-4125-86f7-6ef57167fae3", + "disease": { + "id": "M2023_04_26_16_49_01", + "names": [ + "Metabolic syndrome" + ], + "dbLinks": { + "mesh": [ + "C18.452.394.968.500.570", + "C18.452.625" + ] + }, + "description": "Metabolic syndrome is a complex constellation of metabolic derangements that increase the risk of atherosclerotic cardiovascular disease, type 2 diabetes, and all-cause mortality. The key features of metabolic syndrome include central obesity, insulin resistance, dyslipidemia, and hypertension. These abnormalities are believed to arise from a combination of genetic predisposition and environmental factors, such as sedentary behavior, poor dietary habits, and chronic stress. Diagnosis of metabolic syndrome requires meeting three or more established criteria, based on standardized guidelines. Management of metabolic syndrome involves a comprehensive approach, including lifestyle modifications such as weight loss, physical activity, and dietary changes, as well as pharmacotherapy to address underlying risk factors such as hypertension, dyslipidemia, and hyperglycemia. Early intervention and aggressive management of metabolic syndrome are critical to preventing or delaying the onset of complications and improving long-term health outcomes." + }, + "article": { + "id": "25048195", + "text": "The mechanisms that predispose to hypertension, coronary artery disease (CAD), and type 2 diabetes (T2D) in individuals of normal weight are poorly understood. In contrast, in monogenic primary lipodystrophy-a reduction in subcutaneous adipose tissue-it is clear that it is adipose dysfunction that causes severe insulin resistance (IR), hypertension, CAD, and T2D. We aimed to test the hypothesis that common alleles associated with IR also influence the wider clinical and biochemical profile of monogenic IR. We selected 19 common genetic variants associated with fasting insulin-based measures of IR. We used hierarchical clustering and results from genome-wide association studies of eight nondisease outcomes of monogenic IR to group these variants. We analyzed genetic risk scores against disease outcomes, including 12,171 T2D cases, 40,365 CAD cases, and 69,828 individuals with blood pressure measurements. Hierarchical clustering identified 11 variants associated with a metabolic profile consistent with a common, subtle form of lipodystrophy. A genetic risk score consisting of these 11 IR risk alleles was associated with higher triglycerides (β = 0.018; P = 4 × 10(-29)), lower HDL cholesterol (β = -0.020; P = 7 × 10(-37)), greater hepatic steatosis (β = 0.021; P = 3 × 10(-4)), higher alanine transaminase (β = 0.002; P = 3 × 10(-5)), lower sex-hormone-binding globulin (β = -0.010; P = 9 × 10(-13)), and lower adiponectin (β = -0.015; P = 2 × 10(-26)). The same risk alleles were associated with lower BMI (per-allele β = -0.008; P = 7 × 10(-8)) and increased visceral-to-subcutaneous adipose tissue ratio (β = -0.015; P = 6 × 10(-7)). Individuals carrying ≥17 fasting insulin-raising alleles (5.5% population) were slimmer (0.30 kg/m(2)) but at increased risk of T2D (odds ratio [OR] 1.46; per-allele P = 5 × 10(-13)), CAD (OR 1.12; per-allele P = 1 × 10(-5)), and increased blood pressure (systolic and diastolic blood pressure of 1.21 mmHg [per-allele P = 2 × 10(-5)] and 0.67 mmHg [per-allele P = 2 × 10(-4)], respectively) compared with individuals carrying ≤9 risk alleles (5.5% population). Our results provide genetic evidence for a link between the three diseases of the \"metabolic syndrome\" and point to reduced subcutaneous adiposity as a central mechanism." + }, + "questions": [ + { + "id": "5e70f8df-cc73-49be-9af8-f3d5fdca12ee", + "text": "What is a risk factor for Metabolic Syndrome?", + "answers": [ + { + "answer_start": 1654, + "text": "Individuals carrying ≥17 fasting insulin-raising alleles" + } + ] + } + ] +} \ No newline at end of file diff --git a/17eb9d7f-cc83-4380-acdf-e3a2e318ccfb.json b/17eb9d7f-cc83-4380-acdf-e3a2e318ccfb.json new file mode 100644 index 0000000000000000000000000000000000000000..09a8ab5fc572388443651efac17d486f90b84d7c --- /dev/null +++ b/17eb9d7f-cc83-4380-acdf-e3a2e318ccfb.json @@ -0,0 +1,38 @@ +{ + "id": "17eb9d7f-cc83-4380-acdf-e3a2e318ccfb", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "20800156", + "text": "BACKGROUND:\nLactation has been associated with improvements in maternal glucose metabolism.\n\nMETHODS:\nWe explored the relationships between lactation and risk of type 2 diabetes in a well-characterized, population-representative cohort of women, aged 40-78 years, who were members of a large integrated health care delivery organization in California and enrolled in the Reproductive Risk factors for Incontinence Study at Kaiser (RRISK), between 2003 and 2008. Multivariable logistic regression was used to control for age, parity, race, education, hysterectomy, physical activity, tobacco and alcohol use, family history of diabetes, and body mass index while examining the impact of duration, exclusivity, and consistency of lactation on risk of having developed type 2 diabetes.\n\nRESULTS:\nOf 2233 women studied, 1828 were mothers; 56% had breastfed an infant for \u003e or =1 month. In fully adjusted models, the risk of type 2 diabetes among women who consistently breastfed all of their children for \u003e or =1 month remained similar to that of women who had never given birth (odds ratio [OR] 1.01; 95% confidence interval [CI], 0.56-1.81). In contrast, mothers who had never breastfed an infant were more likely to have developed type 2 diabetes than nulliparous women (OR 1.93; 95% CI, 1.14-3.27) [corrected]. Mothers who never exclusively breastfed were more likely to have developed type 2 diabetes than mothers who exclusively breastfed for 1-3 months (OR 1.52; 95% CI, 1.11-2.10).\n\nCONCLUSIONS:\nRisk of type 2 diabetes increases when term pregnancy is followed by \u003c1 month of lactation, independent of physical activity and body mass index in later life. Mothers should be encouraged to exclusively breastfeed all of their infants for at least 1 month." + }, + "questions": [ + { + "id": "65613fd4-4ee5-4e42-8087-ffd743eaa835", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1311, + "text": "Mothers who never exclusively breastfed" + }, + { + "answer_start": 1539, + "text": "term pregnancy is followed by \u003c1 month of lactation" + } + ] + } + ] +} \ No newline at end of file diff --git a/194ce44e-43e3-42a6-aac7-b1e54ea9856a.json b/194ce44e-43e3-42a6-aac7-b1e54ea9856a.json new file mode 100644 index 0000000000000000000000000000000000000000..9902c45c41be4cd7cf4c69b55ad0760c6c0a2ac9 --- /dev/null +++ b/194ce44e-43e3-42a6-aac7-b1e54ea9856a.json @@ -0,0 +1,35 @@ +{ + "id": "194ce44e-43e3-42a6-aac7-b1e54ea9856a", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "24872541", + "text": "Indoor tanning is carcinogenic to humans. Individuals report that they tan indoors before planning to be in the sun to prevent sunburns, but whether skin cancer is subsequently reduced is unknown. Using a population-based case-control study, we calculated the association between melanoma and indoor tanning after excluding exposed participants reporting indoor tanning-related burns, stratified by their number of lifetime sunburns (0, 1-2, 3-5, \u003e5). Confounding was addressed using propensity score analysis methods. All statistical tests were two-sided. We observed increased risk of melanoma across all sunburn categories for participants who had tanned indoors without burning compared with those who never tanned indoors, including those who reported zero lifetime sunburns (odds ratio = 3.87; 95% confidence interval = 1.68 to 8.91; P = .002). These data provide evidence that indoor tanning is a risk factor for melanoma even among persons who reported never experiencing burns from indoor tanning or outdoor sun exposure." + }, + "questions": [ + { + "id": "7996c178-86df-452f-99e8-eb9b1c5ec890", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 884, + "text": "indoor tanning" + } + ] + } + ] +} \ No newline at end of file diff --git a/195f7924-ab38-4ee8-94cd-7530a9554b6c.json b/195f7924-ab38-4ee8-94cd-7530a9554b6c.json new file mode 100644 index 0000000000000000000000000000000000000000..66e04d7259c2b24e27f3bde618f0533bd81c6260 --- /dev/null +++ b/195f7924-ab38-4ee8-94cd-7530a9554b6c.json @@ -0,0 +1,46 @@ +{ + "id": "195f7924-ab38-4ee8-94cd-7530a9554b6c", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "28486582", + "text": "The prevalence of binge drinking in the United States is rising. While alcohol is a risk factor for breast cancer, less is known about the impact of episodic heavy drinking. In 2003-2009, women aged 35-74 years who were free of breast cancer were enrolled in the Sister Study (n = 50,884). Residents of the United States or Puerto Rico who had a sister with breast cancer were eligible. Multivariable Cox regression was used to estimate adjusted hazard ratios and 95% confidence intervals for breast cancer. During follow-up (mean = 6.4 years), 1,843 invasive breast cancers were diagnosed. Increased breast cancer risk was observed for higher lifetime alcohol intake (for ≥230 drinks/year vs. \u003c60 drinks/year, hazard ratio (HR) = 1.35, 95% confidence interval (CI): 1.15, 1.58). Relative to low-level drinkers (\u003c60 drinks/year), hazard ratios were increased for ever binge drinking (HR = 1.29, 95% CI: 1.15, 1.45) or blacking out (HR = 1.39, 95% CI: 1.17, 1.64). Compared with low-level drinkers who never binged, moderate drinkers (60-229 drinks/year) who binged had a higher risk (HR = 1.25, 95% CI: 1.08, 1.44). There was evidence of effect modification between moderate lifetime drinking and binging (relative excess risk due to interaction = 0.33, 95% CI: 0.10, 0.57). Our findings support the established association between lifetime alcohol intake and breast cancer and provide evidence for an increased risk associated with heavy episodic drinking, especially among moderate lifetime drinkers." + }, + "questions": [ + { + "id": "a4e7bb0a-4d56-4fb9-88c2-95debbe367b4", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 637, + "text": "higher lifetime alcohol intake (for ≥230 drinks/year vs. \u003c60 drinks/year" + }, + { + "answer_start": 863, + "text": "ever binge drinking" + }, + { + "answer_start": 918, + "text": "blacking out" + }, + { + "answer_start": 1332, + "text": "lifetime alcohol intake" + } + ] + } + ] +} \ No newline at end of file diff --git a/19712c99-d7d7-46fd-8062-25188399818f.json b/19712c99-d7d7-46fd-8062-25188399818f.json new file mode 100644 index 0000000000000000000000000000000000000000..e9da52ce7cd84ad8c0e709bd921d15439fd5240f --- /dev/null +++ b/19712c99-d7d7-46fd-8062-25188399818f.json @@ -0,0 +1,80 @@ +{ + "id": "19712c99-d7d7-46fd-8062-25188399818f", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "29650248", + "text": "BACKGROUND:\nAlthough exposure to cigarette smoking and air pollution is common, the current prevalence of chronic obstructive pulmonary disease (COPD) is unknown in the Chinese adult population. We conducted the China Pulmonary Health (CPH) study to assess the prevalence and risk factors of COPD in China.\n\nMETHODS:\nThe CPH study is a cross-sectional study in a nationally representative sample of adults aged 20 years or older from ten provinces, autonomous regions, and municipalities in mainland China. All participants underwent a post-bronchodilator pulmonary function test. COPD was diagnosed according to 2017 Global Initiative for Chronic Obstructive Lung Disease (GOLD) criteria.\n\nFINDINGS:\nBetween June, 2012, and May, 2015, 57 779 individuals were invited to participate, of whom 50 991 (21 446 men and 29 545 women) had reliable post-bronchodilator results and were included in the final analysis. The overall prevalence of spirometry-defined COPD was 8·6% (95% CI 7·5-9·9), accounting for 99·9 (95% CI 76·3-135·7) million people with COPD in China. Prevalence was higher in men (11·9%, 95% CI 10·2-13·8) than in women (5·4%, 4·6-6·2; p\u003c0·0001 for sex difference) and in people aged 40 years or older (13·7%, 12·1-15·5) than in those aged 20-39 years (2·1%, 1·4-3·2; p\u003c0·0001 for age difference). Only 12·0% (95% CI 8·1-17·4) of people with COPD reported a previous pulmonary function test. Risk factors for COPD included smoking exposure of 20 pack-years or more (odds ratio [OR] 1·95, 95% CI 1·53-2·47), exposure to annual mean particulate matter with a diameter less than 2·5 μm of 50-74 μg/m (1·85, 1·23-2·77) or 75 μg/m or higher (2·00, 1·36-2·92), underweight (body-mass index \u003c18·5 kg/m; 1·43, 1·03-1·97), sometimes childhood chronic cough (1·48, 1·14-1·93) or frequent cough (2·57, 2·01-3·29), and parental history of respiratory diseases (1·40, 1·23-1·60). A lower risk of COPD was associated with middle or high school education (OR 0·76, 95% CI 0·64-0·90) and college or higher education (0·47, 0·33-0·66).\n\nINTERPRETATION:\nSpirometry-defined COPD is highly prevalent in the Chinese adult population. Cigarette smoking, ambient air pollution, underweight, childhood chronic cough, parental history of respiratory diseases, and low education are major risk factors for COPD. Prevention and early detection of COPD using spirometry should be a public health priority in China to reduce COPD-related morbidity and mortality.\n\nFUNDING:\nMinistry of Health and Ministry of Science and Technology of China." + }, + "questions": [ + { + "id": "12f20d42-81e6-4fb3-a2b7-011e62e7b91f", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 2125, + "text": "Cigarette smoking" + }, + { + "answer_start": 2144, + "text": "ambient air pollution" + }, + { + "answer_start": 2167, + "text": "underweight" + }, + { + "answer_start": 2180, + "text": "childhood chronic cough" + }, + { + "answer_start": 2205, + "text": "parental history of respiratory diseases" + }, + { + "answer_start": 2251, + "text": "low education" + }, + { + "answer_start": 1435, + "text": "smoking exposure of 20 pack-years or more" + }, + { + "answer_start": 1519, + "text": "exposure to annual mean particulate matter with a diameter less than 2·5 μm of 50-74 μg/m" + }, + { + "answer_start": 1667, + "text": "underweight (body-mass index \u003c18·5 kg/m" + }, + { + "answer_start": 1726, + "text": "sometimes childhood chronic cough" + }, + { + "answer_start": 1781, + "text": "frequent cough" + }, + { + "answer_start": 1819, + "text": "parental history of respiratory diseases" + } + ] + } + ] +} \ No newline at end of file diff --git a/19cb5b7c-d031-498c-bfa2-56611d88615d.json b/19cb5b7c-d031-498c-bfa2-56611d88615d.json new file mode 100644 index 0000000000000000000000000000000000000000..3a2bd8b746e33c766b244fc136400c98bf8f9076 --- /dev/null +++ b/19cb5b7c-d031-498c-bfa2-56611d88615d.json @@ -0,0 +1,40 @@ +{ + "id": "19cb5b7c-d031-498c-bfa2-56611d88615d", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "9620904", + "text": "Severe alpha-1-antitrypsin deficiency is the only proven genetic risk factor for chronic obstructive pulmonary disease (COPD). We have assembled a cohort of 44 probands with severe, early-onset COPD, who do not have severe alpha-1-antitrypsin deficiency. A surprisingly high prevalence of females (79.6%) was found. Assessment of the risk to relatives of these early-onset COPD probands for airflow obstruction and chronic bronchitis was performed to determine whether significant familial aggregation for COPD, independent of alpha-1-antitrypsin deficiency, could be demonstrated. First- degree relatives of early-onset COPD probands had significantly lower FEV1 and FEV1/FVC values than control subjects (p \u003c 0.01), despite similar pack-years of smoking. Reduced spirometric values in first-degree relatives of early-onset COPD probands were found only in current or ex-cigarette smokers. The mean FEV1 in current or ex-smoking first-degree relatives was 76.1 +/- 20.9% predicted compared to 89.2 +/- 14.4% predicted in current or ex-smoking control subjects (p \u003c 0.01); in lifelong nonsmokers, the mean FEV1 was 93.4% predicted for both control subjects and first-degree relatives of early-onset COPD probands. Generalized estimating equations, adjusting for age and pack-years of smoking, demonstrated increased odds of reduced FEV1 and chronic bronchitis in current or ex-smoking first-degree relatives of early-onset COPD probands. Using a new method to estimate relative risk from relative odds, we estimate that the relative risks for FEV1 below 60%, FEV1 below 80%, and chronic bronchitis are each approximately three in current or ex-smoking first-degree relatives of early-onset COPD probands. The increased risk to relatives of early-onset COPD probands for reduced FEV1 and chronic bronchitis, limited to current or ex-smokers, suggests genetic risk factor(s) for COPD that are expressed in response to cigarette smoking." + }, + "questions": [ + { + "id": "4700d9d8-2388-4f33-bc83-205f6f8624ed", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 1727, + "text": "relatives of early-onset COPD probands" + }, + { + "answer_start": 908, + "text": "current or ex-smoking first-degree relatives" + } + ] + } + ] +} \ No newline at end of file diff --git a/1ac8e817-6d61-401c-917b-4688f21d651b.json b/1ac8e817-6d61-401c-917b-4688f21d651b.json new file mode 100644 index 0000000000000000000000000000000000000000..339120e8298ecb390f10a0faa1e28a97eceebba2 --- /dev/null +++ b/1ac8e817-6d61-401c-917b-4688f21d651b.json @@ -0,0 +1,51 @@ +{ + "id": "1ac8e817-6d61-401c-917b-4688f21d651b", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "14558078", + "text": "OBJECTIVE:\nTo evaluate the prevalence and predictive value of anti-cyclic citrullinated peptide (anti-CCP) antibodies in individuals who subsequently developed rheumatoid arthritis (RA) and to determine the relationship to rheumatoid factor (RF) of any isotype.\n\nMETHODS:\nA case-control study was nested within the Northern Sweden Health and Disease Study and the Maternity cohorts of Northern Sweden. Patients with RA were identified among blood donors whose samples had been taken years before the onset of symptoms. Control subjects matched for age, sex, date of sampling, and residential area were selected randomly from the same cohorts. Anti-CCP antibody and RFs were determined using enzyme immunoassays.\n\nRESULTS:\nEighty-three individuals with RA were identified as having donated blood before presenting with any symptoms of joint disease (median 2.5 years [interquartile range 1.1-4.7] before RA). In samples obtained before the onset of RA, the prevalence of autoantibodies was 33.7% for anti-CCP, 16.9% for IgG-RF, 19.3% for IgM-RF, and 33.7% for IgA-RF (all highly significant compared with controls). The sensitivities for detecting these autoantibodies \u003e1.5 years and \u003c/=1.5 years before the appearance of any RA symptoms were 25% and 52% for anti-CCP, 15% and 30% for IgM-RF, 12% and 27% for IgG-RF, and 29% and 39% for IgA-RF. In conditional logistic regression models, anti-CCP antibody and IgA-RF were found to be significant predictors of RA.\n\nCONCLUSION:\nAnti-CCP antibody and RFs of all isotypes predated the onset of RA by several years. The presence of anti-CCP and IgA-RF predicted the development of RA, with anti-CCP antibody having the highest predictive value. This indicates that citrullination and the production of anti-CCP and RF autoantibodies are early processes in RA." + }, + "questions": [ + { + "id": "40810d58-2d4e-477f-90fc-e56b2014849e", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 999, + "text": "anti-CCP" + }, + { + "answer_start": 1019, + "text": "IgG-RF" + }, + { + "answer_start": 1037, + "text": "IgM-RF" + }, + { + "answer_start": 1476, + "text": "Anti-CCP antibody" + }, + { + "answer_start": 1498, + "text": "RFs of all isotypes" + } + ] + } + ] +} \ No newline at end of file diff --git a/1b1356a2-590d-47fe-80da-5db0f671bfa9.json b/1b1356a2-590d-47fe-80da-5db0f671bfa9.json new file mode 100644 index 0000000000000000000000000000000000000000..c8748d4030ed163d94e982a217125698c0182b4c --- /dev/null +++ b/1b1356a2-590d-47fe-80da-5db0f671bfa9.json @@ -0,0 +1,43 @@ +{ + "id": "1b1356a2-590d-47fe-80da-5db0f671bfa9", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "24492409", + "text": "BACKGROUND:\nAccumulating evidence implicates early life factors in the aetiology of non-communicable diseases, including asthma/wheezing disorders. We undertook a systematic review investigating risks of asthma/wheezing disorders in children born preterm, including the increasing numbers who, as a result of advances in neonatal care, now survive very preterm birth.\n\nMETHODS AND FINDINGS:\nTwo reviewers independently searched seven online databases for contemporaneous (1 January 1995-23 September 2013) epidemiological studies investigating the association between preterm birth and asthma/wheezing disorders. Additional studies were identified through reference and citation searches, and contacting international experts. Quality appraisal was undertaken using the Effective Public Health Practice Project instrument. We pooled unadjusted and adjusted effect estimates using random-effects meta-analysis, investigated \"dose-response\" associations, and undertook subgroup, sensitivity, and meta-regression analyses to assess the robustness of associations. We identified 42 eligible studies from six continents. Twelve were excluded for population overlap, leaving 30 unique studies involving 1,543,639 children. Preterm birth was associated with an increased risk of wheezing disorders in unadjusted (13.7% versus 8.3%; odds ratio [OR] 1.71, 95% CI 1.57-1.87; 26 studies including 1,500,916 children) and adjusted analyses (OR 1.46, 95% CI 1.29-1.65; 17 studies including 874,710 children). The risk was particularly high among children born very preterm (\u003c32 wk gestation; unadjusted: OR 3.00, 95% CI 2.61-3.44; adjusted: OR 2.81, 95% CI 2.55-3.12). Findings were most pronounced for studies with low risk of bias and were consistent across sensitivity analyses. The estimated population-attributable risk of preterm birth for childhood wheezing disorders was ≥3.1%. Key limitations related to the paucity of data from low- and middle-income countries, and risk of residual confounding.\n\nCONCLUSIONS:\nThere is compelling evidence that preterm birth-particularly very preterm birth-increases the risk of asthma. Given the projected global increases in children surviving preterm births, research now needs to focus on understanding underlying mechanisms, and then to translate these insights into the development of preventive interventions.\n\nREVIEW REGISTRATION:\nPROSPERO CRD42013004965." + }, + "questions": [ + { + "id": "d9ff9d69-f49a-41bd-a7e9-99f0e6fbe5dd", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 2041, + "text": "preterm birth" + }, + { + "answer_start": 2068, + "text": "very preterm birth" + }, + { + "answer_start": 1533, + "text": "children born very preterm (\u003c32 wk gestation" + } + ] + } + ] +} \ No newline at end of file diff --git a/1b295633-6f10-41d8-91fc-6fb841c1920e.json b/1b295633-6f10-41d8-91fc-6fb841c1920e.json new file mode 100644 index 0000000000000000000000000000000000000000..8f112cebd2e228fc0e79a8e76f77ad01c3fb1b0f --- /dev/null +++ b/1b295633-6f10-41d8-91fc-6fb841c1920e.json @@ -0,0 +1,39 @@ +{ + "id": "1b295633-6f10-41d8-91fc-6fb841c1920e", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "17030233", + "text": "BACKGROUND:\nAccumulating evidence suggests that reduced duration of pregnancy predicts increased risk of asthma, but the studies published have been inconsistent.\n\nOBJECTIVE:\nWe sought to synthesize the evidence on the relation between preterm delivery and the risk of asthma later in life and to assess differences between the studies as potential sources for heterogeneity of the results.\n\nMETHODS:\nWe conducted a MEDLINE search (until the end of May 2005). The outcome was asthma. The determinant of interest was preterm delivery defined as a gestational age of less than 37 weeks.\n\nRESULTS:\nWe identified 19 articles that provided estimates for the meta-analysis. The summary effect estimates for asthma (fixed-effects odds ratio, 1.074 [95% CI, 1.072-1.075]; heterogeneity P = .000; random-effects odds ratio, 1.366 [95% CI, 1.303-1.432]) showed an increased risk in relation to preterm delivery, with substantial heterogeneity between study-specific estimates. The effect of preterm delivery on asthma was stronger in cross-sectional studies; studies with broad outcome criteria, a small sample size, and a younger study population; and studies conducted in English-speaking populations, outside Europe, and published more recently. In metaregression, adjusting for other determinants, the effect estimate was significantly associated only with the mean age of the study population.\n\nCONCLUSIONS:\nThe weight of evidence shows that preterm babies have an increased risk of asthma compared with term babies.\n\nCLINICAL IMPLICATIONS:\nRecognition of prematurity as a determinant of asthma emphasizes the importance of active treatment of physiologic airflow obstruction and a need for special preventive measures against known environmental determinants of asthma in preterm babies." + }, + "questions": [ + { + "id": "eab683f8-0817-4dfe-a912-b61859924488", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1437, + "text": "preterm babies" + }, + { + "answer_start": 884, + "text": "preterm delivery" + } + ] + } + ] +} \ No newline at end of file diff --git a/1b2a60c9-852c-4b9c-8d96-c35caa0aa7ab.json b/1b2a60c9-852c-4b9c-8d96-c35caa0aa7ab.json new file mode 100644 index 0000000000000000000000000000000000000000..10fb903e038bbc3f3656adf018c844db383ebde0 --- /dev/null +++ b/1b2a60c9-852c-4b9c-8d96-c35caa0aa7ab.json @@ -0,0 +1,34 @@ +{ + "id": "1b2a60c9-852c-4b9c-8d96-c35caa0aa7ab", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "9552903", + "text": "OBJECTIVE:\nTo compare risk of myocardial infarction associated with smoking in men and women, taking into consideration differences in smoking behaviour and a number of potential confounding variables.\n\nDESIGN:\nProspective cohort study with follow up of myocardial infarction.\n\nSETTING:\nPooled data from three population studies conducted in Copenhagen.\n\nSUBJECTS:\n11,472 women and 13,191 men followed for a mean of 12.3 years.\n\nMAIN OUTCOME MEASURES:\nFirst admission to hospital or death caused by myocardial infarction.\n\nRESULTS:\n1251 men and 512 women had a myocardial infarction during follow up. Compared with non-smokers, female current smokers had a relative risk of myocardial infarction of 2.24 (range 1.85-2.71) and male smokers 1.43 (1.26-1.62); ratio 1.57 (1.25-1.97). Relative risk of myocardial infarction increased with tobacco consumption in both men and women and was higher in inhalers than in non-inhalers. The risks associated with smoking, measured by both current and accumulated tobacco exposure, were consistently higher in women than in men and did not depend on age. This sex difference was not affected by adjustment for arterial blood pressure, total and high density lipoprotein cholesterol concentrations, triglyceride concentrations, diabetes, body mass index, height, alcohol intake, physical activity, and level of education.\n\nCONCLUSION:\nWomen may be more sensitive than men to some of the harmful effects of smoking. Interactions between components of smoke and hormonal factors that may be involved in development of ischaemic heart disease should be examined further." + }, + "questions": [ + { + "id": "4ce4304c-193f-4181-9662-115e71a9c59d", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 835, + "text": "tobacco consumption in both men and women" + } + ] + } + ] +} \ No newline at end of file diff --git a/1b41fbdc-a994-4b7c-afff-c01dd9a9282b.json b/1b41fbdc-a994-4b7c-afff-c01dd9a9282b.json new file mode 100644 index 0000000000000000000000000000000000000000..cf526dda50c65d2c48cd62dcf2863dcab4634f08 --- /dev/null +++ b/1b41fbdc-a994-4b7c-afff-c01dd9a9282b.json @@ -0,0 +1,43 @@ +{ + "id": "1b41fbdc-a994-4b7c-afff-c01dd9a9282b", + "disease": { + "id": "H01633", + "names": [ + "High blood pressure", + "Hypertension" + ], + "dbLinks": { + "icd10": [ + "I10" + ], + "mesh": [ + "D006973" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "15477381", + "text": "Epidemiological studies have demonstrated a positive relationship between heavy alcohol use and hypertension, but few studies have directly addressed the role of drinking pattern. This study was designed to investigate the association of current alcohol consumption and aspects of drinking pattern with hypertension risk in a sample of 2609 white men and women from western New York, aged 35 to 80 years, and free from other cardiovascular diseases. Hypertension was defined by systolic blood pressure \u003e or =140 mm Hg or diastolic blood pressure \u003e or =90 mm Hg or use of antihypertensive medication. Odds ratios (95% confidence intervals) were computed after adjustment for several covariates. Compared with lifetime abstainers, participants reporting drinking on a daily basis (1.75 [1.13 to 2.72]) or mostly without food (1.64 [1.08 to 2.51]) exhibited significantly higher risk of hypertension. When analyses were restricted to current drinkers, daily drinkers and participants consuming alcohol without food exhibited a significantly higher risk of hypertension compared with those drinking less than weekly (1.65 [1.18 to 2.30]) and those drinking mostly with food (1.49 [1.10 to 2.00]), respectively. After additional adjustment for the amount of alcohol consumed in the past 30 days, the results were follows: 0.90 (0.58 to 1.41) for daily drinkers and 1.41 (1.04 to 1.91) for drinkers without food. For predominant beverage preference, no consistent association with hypertension risk was found across the various types of beverages considered (beer, wine, and liquor). In conclusion, drinking outside meals appears to have a significant effect on hypertension risk independent of the amount of alcohol consumed." + }, + "questions": [ + { + "id": "92d9793a-cbc0-46e6-ae9e-906e464d9813", + "text": "What are the risk factors for Hypertension?", + "answers": [ + { + "answer_start": 752, + "text": "drinking on a daily basis" + }, + { + "answer_start": 1384, + "text": "drinkers without food" + }, + { + "answer_start": 1593, + "text": "drinking outside meals" + } + ] + } + ] +} \ No newline at end of file diff --git a/1bc348b7-44fd-44dc-a3ca-72429c58b970.json b/1bc348b7-44fd-44dc-a3ca-72429c58b970.json new file mode 100644 index 0000000000000000000000000000000000000000..ae8cabcb3904ac05ed3dc5c081503b70cd4ed117 --- /dev/null +++ b/1bc348b7-44fd-44dc-a3ca-72429c58b970.json @@ -0,0 +1,42 @@ +{ + "id": "1bc348b7-44fd-44dc-a3ca-72429c58b970", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "8625126", + "text": "BACKGROUND:\nThe pattern of second cancers after treatment for cervical cancer provides important information on the risk of radiation-induced malignancies. Large numbers of women survive many years and can be studied for late effects.\n\nMETHODS:\nIncident second cancers in 86,193 patients with cervical cancer reported to 13 population-based cancer registries in 5 countries were evaluated to estimate the risk of second cancer among very long term survivors.\n\nRESULTS:\nOverall, 7543 second cancers were observed versus 6015 cancers expected based on population rates (observed/expected = 1.2). Lung cancer accounted for nearly half of the excess cancers. Among the 49,828 women treated with radiation, 3750 survived 30 or more years and a two-fold risk of cancers of heavily irradiated organs was seen. Most of the excess cancers were of the rectum, vagina, vulva, ovary, and bladder. Patterns of risk over time since treatment were consistent with a radiation etiology. Significant increases of nonchronic lymphocytic leukemia and cancers of the bone and kidney were also linked to radiotherapy. Women treated surgically were also at significant risk of second cancers, in all likelihood related to cigarette smoking and risk factors similar to those of cervical cancer.\n\nCONCLUSIONS:\nCurative therapy for cervical cancer results in large numbers of long term survivors who develop second cancers very late in life. Radiation is an important cause of this increase and there is no evidence that risk returns to normal levels." + }, + "questions": [ + { + "id": "6cfd59fa-a4e4-451a-9a31-83167d94d7e7", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 767, + "text": "heavily irradiated organs" + }, + { + "answer_start": 672, + "text": "women treated with radiation" + }, + { + "answer_start": 1286, + "text": "Curative therapy for cervical cancer" + } + ] + } + ] +} \ No newline at end of file diff --git a/1c071b59-3d1b-4770-bca8-3195bb20db40.json b/1c071b59-3d1b-4770-bca8-3195bb20db40.json new file mode 100644 index 0000000000000000000000000000000000000000..9e8f57a0eb24833b4b6e0d7062fe03588977db0d --- /dev/null +++ b/1c071b59-3d1b-4770-bca8-3195bb20db40.json @@ -0,0 +1,42 @@ +{ + "id": "1c071b59-3d1b-4770-bca8-3195bb20db40", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "7615824", + "text": "The increased prevalence of non-insulin-dependent diabetes mellitus (NIDDM) among women with polycystic ovary syndrome (PCOS) has been ascribed to the insulin resistance characteristic of PCOS. This study was undertaken to determine the role of defects in insulin secretion as well as familial factors to the predisposition to NIDDM seen in PCOS. We studied three groups of women: PCOS with a family history of NIDDM (PCOS FHx POS; n = 11), PCOS without a family history of NIDDM (PCOS FHx NEG; n = 13), and women without PCOS who have a family history of NIDDM (NON-PCOS FHx POS; n = 8). Beta cell function was evaluated during a frequently sampled intravenous glucose tolerance test, by a low dose graded glucose infusion, and by the ability of the beta cell to be entrained by an oscillatory glucose infusion. PCOS FHx POS women were significantly less likely to demonstrate appropriate beta cell compensation for the degree of insulin resistance. The ability of the beta cell to entrain, as judged by the spectral power for insulin secretion rate, was significantly reduced in PCOS FHx POS subjects. In conclusion, a history of NIDDM in a first-degree relative appears to define a subset of PCOS subjects with a greater prevalence of insulin secretory defects. The risk of developing NIDDM imparted by insulin resistance in PCOS may be enhanced by these defects in insulin secretion." + }, + "questions": [ + { + "id": "5b7ae41a-0f02-48bb-bb80-2d63c8dab15e", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 28, + "text": "non-insulin-dependent diabetes mellitus (NIDDM)" + }, + { + "answer_start": 82, + "text": "women with polycystic ovary syndrome (PCOS)" + }, + { + "answer_start": 1328, + "text": "PCOS" + } + ] + } + ] +} \ No newline at end of file diff --git a/1c32adf3-428e-4627-a066-bc9f80cec2e7.json b/1c32adf3-428e-4627-a066-bc9f80cec2e7.json new file mode 100644 index 0000000000000000000000000000000000000000..5d3206f5f40a0bdc03c6ba4f521bbbcd710e714b --- /dev/null +++ b/1c32adf3-428e-4627-a066-bc9f80cec2e7.json @@ -0,0 +1,38 @@ +{ + "id": "1c32adf3-428e-4627-a066-bc9f80cec2e7", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "2024123", + "text": "Although bladder cancers are very common, little is known about their molecular pathogenesis. In this study, invasive bladder cancers were evaluated for the presence of gene mutations in the p53 suppressor gene. Of 18 tumors evaluated, 11 (61 percent) were found to have genetic alterations of p53. The alterations included ten point mutations resulting in single amino acid substitutions, and one 24-base pair deletion. In all but one case, the mutations were associated with chromosome 17p allelic deletions, leaving the cells with only mutant forms of the p53 gene products. Through the use of the polymerase chain reaction and oligomer-specific hybridization, p53 mutations were identified in 1 to 7 percent of the cells within the urine sediment of each of three patients tested. The p53 mutations are the first genetic alterations demonstrated to occur in a high proportion of primary invasive bladder cancers. Detection of such mutations ex vivo has clinical implications for monitoring individuals whose tumor cells are shed extracorporeally." + }, + "questions": [ + { + "id": "af650dc7-3805-47af-bd72-66f464b23654", + "text": "What are the risk factors of Bladder Cancer?", + "answers": [ + { + "answer_start": 789, + "text": "p53 mutations" + }, + { + "answer_start": 539, + "text": "mutant forms of the p53 gene products" + } + ] + } + ] +} \ No newline at end of file diff --git a/1c59e1c4-d3f2-448b-be3a-1d3707f95575.json b/1c59e1c4-d3f2-448b-be3a-1d3707f95575.json new file mode 100644 index 0000000000000000000000000000000000000000..b15a5519e828e38d5acbfd1c4dda358a1e6601e0 --- /dev/null +++ b/1c59e1c4-d3f2-448b-be3a-1d3707f95575.json @@ -0,0 +1,59 @@ +{ + "id": "1c59e1c4-d3f2-448b-be3a-1d3707f95575", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "14559875", + "text": "BACKGROUND:\nAlthough sun exposure is an established cause of cutaneous malignant melanoma, possible interactions with host factors remain incompletely understood. Here we report the first results from a large prospective cohort study of pigmentation factors and sun exposure in relation to melanoma risk.\n\nMETHODS:\nThe Women's Lifestyle and Health Cohort Study included 106 379 women from Norway and Sweden who were aged 30-50 years in 1991 or 1992 when they completed an extensive questionnaire on personal characteristics and exposures. Linkages to national registries ensured complete follow-up through December 31, 1999. Poisson regression models were used to estimate relative risks (RRs). All statistical tests were two-sided.\n\nRESULTS:\nDuring an average follow-up of 8.1 years, 187 cases of melanoma were diagnosed. Risk of melanoma was statistically significantly associated with increasing body surface area (RR for \u003e or =1.79 m2 versus \u003c or =1.61 m2 = 1.60, 95% confidence interval [CI] = 1.03 to 2.48; P(trend) =.02), number of large asymmetric nevi on the legs (RR for \u003e or =7 nevi versus 0 nevi = 5.29, 95% CI = 2.33 to 12.01; P(trend)\u003c.001), hair color (RR for red versus dark brown or black = 4.05, 95% CI = 2.11 to 7.76; P(trend)\u003c.001), sunburns per year at ages 10-19, 20-29, and 30-39 years (P(trend)\u003c.001, P(trend) =.03, and P(trend) =.05, respectively), and use of a device that emits artificial light (solarium) one or more times per month (P =.04).\n\nCONCLUSIONS:\nOur results confirm previous findings that hair color, number of nevi on the legs, and history of sunburn are risk factors for melanoma and suggest that use of a solarium is also associated with melanoma risk. Adolescence and early adulthood appear to be among the most sensitive age periods for the effects of sunburn and solarium use on melanoma risk. However, it may be too early to see the full effect of adult exposures in this cohort." + }, + "questions": [ + { + "id": "ead053ab-c6c1-4bd8-ba3c-713847ebfe70", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 888, + "text": "increasing body surface area" + }, + { + "answer_start": 1029, + "text": "number of large asymmetric nevi on the legs" + }, + { + "answer_start": 1156, + "text": "hair color" + }, + { + "answer_start": 1253, + "text": "sunburns per year at ages 10-19, 20-29, and 30-39 years" + }, + { + "answer_start": 1528, + "text": "hair color" + }, + { + "answer_start": 1540, + "text": "number of nevi on the legs" + }, + { + "answer_start": 1572, + "text": "history of sunburn" + } + ] + } + ] +} \ No newline at end of file diff --git a/1c9c69e4-40ec-4e4a-ba28-a9e2e465c386.json b/1c9c69e4-40ec-4e4a-ba28-a9e2e465c386.json new file mode 100644 index 0000000000000000000000000000000000000000..55cb3e0ce6aff74e486d2df070abbec9316856a0 --- /dev/null +++ b/1c9c69e4-40ec-4e4a-ba28-a9e2e465c386.json @@ -0,0 +1,42 @@ +{ + "id": "1c9c69e4-40ec-4e4a-ba28-a9e2e465c386", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "32530506", + "text": "BACKGROUND:\nInsulin resistance is associated with higher all-cause and cancer-specific mortality in postmenopausal women. However, to the authors' knowledge, information regarding insulin resistance and breast cancer mortality risk is limited. Therefore, the authors examined associations between insulin resistance and breast cancer incidence and mortality in a subsample of Women's Health Initiative participants.\n\nMETHODS:\nA total of 22,837 postmenopausal women with fasting baseline glucose and insulin levels were followed for incident breast cancer and breast cancer mortality. Breast cancers were verified by medical record review and serial National Death Index linkage-enhanced mortality findings. Insulin resistance was estimated using the homeostatic model assessment of insulin resistance (HOMA-IR). Multivariable Cox proportional hazards models were used to compute hazard ratios (HRs) with 95% confidence intervals (95% CIs) for quartile comparisons. Outcomes included breast cancer incidence, deaths from breast cancer, and deaths after breast cancer (breast cancer followed by death from any cause).\n\nRESULTS:\nDuring a median of 19.8 years of follow-up of 1328 breast cancer cases, there were 512 deaths reported, 151 of which were from breast cancer. Breast cancer incidence was higher in women in the highest HOMA-IR quartile (HR, 1.34; 95% CI, 1.12-1.61 [P for trend = .003]). Although HOMA-IR was not found to be associated with risk of death from breast cancer (HR, 1.04; 95% CI, 0.60-1.79), women in the highest versus those in the lowest HOMA-IR quartile were at a higher risk of death after breast cancer (HR, 1.78; 95% CI, 1.32-2.39 [P for trend \u003c.001]).\n\nCONCLUSIONS:\nHigher levels of insulin resistance in postmenopausal women are associated with higher breast cancer incidence and higher all-cause mortality after breast cancer." + }, + "questions": [ + { + "id": "1c609977-bbd0-4a39-90d8-2aa6956f1333", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1694, + "text": "Higher levels of insulin resistance in postmenopausal women" + }, + { + "answer_start": 1305, + "text": " women in the highest HOMA-IR quartile" + }, + { + "answer_start": 750, + "text": "homeostatic model assessment of insulin resistance (HOMA-IR)" + } + ] + } + ] +} \ No newline at end of file diff --git a/1ca9372b-a660-4e0a-a4ce-ac27bc8f8c0b.json b/1ca9372b-a660-4e0a-a4ce-ac27bc8f8c0b.json new file mode 100644 index 0000000000000000000000000000000000000000..bdd6110142c4e6fdf8010245737e04a2d3d2e7dc --- /dev/null +++ b/1ca9372b-a660-4e0a-a4ce-ac27bc8f8c0b.json @@ -0,0 +1,38 @@ +{ + "id": "1ca9372b-a660-4e0a-a4ce-ac27bc8f8c0b", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "1535181", + "text": "OBJECTIVES:\nIndividual epidemiological investigations into the association between chlorination by-products in drinking water and cancer have been suggestive but inconclusive. Enough studies exist to provide the basis for a meaningful meta-analysis.\n\nMETHODS:\nAn extensive literature search was performed to identify pertinent case-control studies and cohort studies. Consumption of chlorinated water, surface water, or water with high levels of chloroform was used as a surrogate for exposure to chlorination by-products. Relative risk estimates were abstracted from the individual studies and pooled.\n\nRESULTS:\nA simple meta-analysis of all cancer sites yielded a relative risk estimate for exposure to chlorination by-products of 1.15 (95% CI: 1.09, 1.20). Pooled relative risk estimates for organ-specific neoplasms were 1.21 (95% CI: 1.09, 1.34) for bladder cancer and 1.38 (95% CI: 1.01, 1.87) for rectal cancer. When studies that adjusted for potential confounders were pooled separately, estimates of relative risks did not change substantially.\n\nCONCLUSIONS:\nThe results of this meta-analysis suggest a positive association between consumption of chlorination by-products in drinking water and bladder and rectal cancer in humans." + }, + "questions": [ + { + "id": "b8977c3b-0aa7-4759-95b6-e2fc74619de8", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 693, + "text": "exposure to chlorination by-products" + }, + { + "answer_start": 1141, + "text": "consumption of chlorination by-products in drinking water" + } + ] + } + ] +} \ No newline at end of file diff --git a/1d6087ff-dbdd-4364-a531-5a27df521a5d.json b/1d6087ff-dbdd-4364-a531-5a27df521a5d.json new file mode 100644 index 0000000000000000000000000000000000000000..9ecb3b98b70cb4d4982cb2c78750f198c6f473f6 --- /dev/null +++ b/1d6087ff-dbdd-4364-a531-5a27df521a5d.json @@ -0,0 +1,42 @@ +{ + "id": "1d6087ff-dbdd-4364-a531-5a27df521a5d", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "21148114", + "text": "Four authoritative reviews of active smoking and breast cancer have been published since 2000, but only one considered data after 2002 and conclusions varied. Three reviews of secondhand smoke (SHS) and breast cancer (2004-2006) each came to different conclusions. With 30 new studies since 2002, further review was deemed desirable. An Expert Panel was convened by four Canadian agencies, the Ontario Tobacco Research Unit, the Public Health Agency of Canada, Physicians for a Smoke-Free Canada and the Canadian Partnership Against Cancer to comprehensively examine the weight of evidence from epidemiological and toxicological studies and understanding of biological mechanisms regarding the relationship between tobacco smoke and breast cancer. This article summarises the panel's full report (http://www.otru.org/pdf/special/expert_panel_tobacco_breast_cancer.pdf). There are 20 known or suspected mammary carcinogens in tobacco smoke, and recognised biological mechanisms that explain how exposure to these carcinogens could lead to breast cancer. Results from the nine cohort studies reporting exposure metrics more detailed than ever/never and ex/current smoker show that early age of smoking commencement, higher pack-years and longer duration of smoking increase breast cancer risk 15% to 40%. Three meta-analyses report 35% to 50% increases in breast cancer risk for long-term smokers with N-acetyltransferase 2 gene (NAT2) slow acetylation genotypes. The active smoking evidence bolsters support for three meta-analyses that each reported about a 65% increase in premenopausal breast cancer risk among never smokers exposed to SHS. The Panel concluded that: 1) the association between active smoking and breast cancer is consistent with causality and 2) the association between SHS and breast cancer among younger, primarily premenopausal women who have never smoked is consistent with causality." + }, + "questions": [ + { + "id": "b41b6d32-a0eb-41d4-82e5-465a9a03254c", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1696, + "text": "active smoking" + }, + { + "answer_start": 176, + "text": "secondhand smoke (SHS)" + }, + { + "answer_start": 1789, + "text": "SHS" + } + ] + } + ] +} \ No newline at end of file diff --git a/1d8af62a-5c71-4de3-b616-c911c36a9176.json b/1d8af62a-5c71-4de3-b616-c911c36a9176.json new file mode 100644 index 0000000000000000000000000000000000000000..ffa4e5bedd13d7963c70f13cfc0630cc001e7e2d --- /dev/null +++ b/1d8af62a-5c71-4de3-b616-c911c36a9176.json @@ -0,0 +1,41 @@ +{ + "id": "1d8af62a-5c71-4de3-b616-c911c36a9176", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "15952101", + "text": "BACKGROUND \u0026 AIMS:\nType 2 diabetes mellitus might increase the risk of colorectal cancer on the basis of chronic hyperinsulinemia and hyperglycemia. However, epidemiologic evidence for this association is inconclusive. We conducted a population-based study to clarify this association.\n\nMETHODS:\nWe conducted a case-control study in the United Kingdom General Practice Research Database. Cases included all patients with incident colorectal cancer diagnoses (n = 10,447). Up to 10 control subjects were selected for each case, matching on year of birth, enrollment date, and duration of database follow-up. The exposure of interest was type 2 diabetes mellitus. Odds ratios (ORs) were calculated by using conditional logistic regression.\n\nRESULTS:\nA prior diagnosis of type 2 diabetes mellitus was associated with a modestly increased risk of colorectal cancer (OR, 1.42; 95% confidence interval [CI], 1.25-1.62). The association between type 2 diabetes mellitus and colorectal cancer was observed in both men (OR, 1.36; 95% CI, 1.16-1.61) and women (OR, 1.38; 95% CI, 1.14-1.67). The risk increase was observed in both colon (OR, 1.45; 95% CI, 1.25-1.70) and rectal (OR, 1.34; 95% CI, 1.08-1.68) cancers.\n\nCONCLUSIONS:\nType 2 diabetes mellitus is associated with an increased risk of colorectal cancer. The risk increase is present in both sexes, as well as in both colonic and rectal cancers." + }, + "questions": [ + { + "id": "e36412d8-c206-400c-b57d-01826c4f7463", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 748, + "text": "A prior diagnosis of type 2 diabetes mellitus" + }, + { + "answer_start": 1220, + "text": "Type 2 diabetes mellitus" + } + ] + } + ] +} \ No newline at end of file diff --git a/1da0f201-c056-44d1-9d01-1a15bae606e3.json b/1da0f201-c056-44d1-9d01-1a15bae606e3.json new file mode 100644 index 0000000000000000000000000000000000000000..3060112487bcfb02e703d6d08edf72957b4da394 --- /dev/null +++ b/1da0f201-c056-44d1-9d01-1a15bae606e3.json @@ -0,0 +1,34 @@ +{ + "id": "1da0f201-c056-44d1-9d01-1a15bae606e3", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "16763645", + "text": "Mortality from bladder cancer has shown downward trends over the last 2 decades in several western European countries (albeit 10-15 years later than similar trends in the US), but is still increasing in some eastern European countries. Tobacco smoking and occupational exposure to aromatic amines are the two major established environmental risk factors for bladder cancer. Controlling exposure to these factors has been an important contributor to the reduction in bladder cancer mortality, particularly among men. Diet could influence bladder carcinogenesis, as many compounds contained in foods--and their metabolites--are excreted through the urinary tract. Fruit and vegetable consumption was inversely related with bladder cancer in many studies, but no consistent association has emerged between intake of related micronutrients and reduced risk of bladder cancer. Other widely investigated lifestyle habits are probably not associated with risk of developing bladder cancer (e.g. coffee consumption, artificial sweetener use, hair dyes) or are difficult to assess (e.g. fluid intake). Infections and stones in the urinary tract might cause chronic irritation of the bladder epithelium, and thus increase bladder cancer risk. First-degree relatives of bladder cancer patients have a 50-100% increased relative risk of developing the disease, a risk that could be even higher when the proband is diagnosed at an early age." + }, + "questions": [ + { + "id": "5b15d837-3ae4-477c-9720-c0ee41703abe", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 1233, + "text": "First-degree relatives of bladder cancer patients" + } + ] + } + ] +} \ No newline at end of file diff --git a/1da1c8ea-5822-41ec-a0de-f4218d16846f.json b/1da1c8ea-5822-41ec-a0de-f4218d16846f.json new file mode 100644 index 0000000000000000000000000000000000000000..71e0f3a3a604a2359c7e960bfc6f7b93e71b409f --- /dev/null +++ b/1da1c8ea-5822-41ec-a0de-f4218d16846f.json @@ -0,0 +1,46 @@ +{ + "id": "1da1c8ea-5822-41ec-a0de-f4218d16846f", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "17259486", + "text": "OBJECTIVE:\nWe sought to estimate the rate of progression from newly acquired (incident) impaired fasting glucose (IFG) to diabetes under the old and new IFG criteria and to identify predictors of progression to diabetes.\n\nRESEARCH DESIGN AND METHODS:\nWe identified 5,452 members of an HMO with no prior history of diabetes, with at least two elevated fasting glucose tests (100-125 mg/dl) measured between 1 January 1994 and 31 December 2003, and with a normal fasting glucose test before the two elevated tests. All data were obtained from electronic records of routine clinical care. Subjects were followed until they developed diabetes, died, left the health plan, or until 31 December 2005.\n\nRESULTS:\nOverall, 8.1% of subjects whose initial abnormal fasting glucose was 100-109 mg/dl (added IFG subjects) and 24.3% of subjects whose initial abnormal fasting glucose was 110-125 mg/dl (original IFG subjects) developed diabetes (P \u003c 0.0001). Added IFG subjects who progressed to diabetes did so within a mean of 41.4 months, a rate of 1.34% per year. Original IFG subjects converted at a rate of 5.56% per year after an average of 29.0 months. A steeper rate of increasing fasting glucose; higher BMI, blood pressure, and triglycerides; and lower HDL cholesterol predicted diabetes development.\n\nCONCLUSIONS:\nTo our knowledge, these are the first estimates of diabetes incidence from a clinical care setting when the date of IFG onset is approximately known under the new criterion for IFG. The older criterion was more predictive of diabetes development. Many newly identified IFG patients progress to diabetes in \u003c3 years, which is the currently recommended screening interval." + }, + "questions": [ + { + "id": "c9861689-8fb6-4101-81e9-deb51d63c9b5", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 88, + "text": "impaired fasting glucose (IFG)" + }, + { + "answer_start": 722, + "text": "subjects whose initial abnormal fasting glucose was 100-109 mg/dl" + }, + { + "answer_start": 822, + "text": "subjects whose initial abnormal fasting glucose was 110-125 mg/dl" + }, + { + "answer_start": 1570, + "text": "identified IFG patients" + } + ] + } + ] +} \ No newline at end of file diff --git a/1deff1e2-61c8-4d50-9260-4547d6734d86.json b/1deff1e2-61c8-4d50-9260-4547d6734d86.json new file mode 100644 index 0000000000000000000000000000000000000000..4d814c471e1e3e5ae2fc7c95cfaa07026946388a --- /dev/null +++ b/1deff1e2-61c8-4d50-9260-4547d6734d86.json @@ -0,0 +1,37 @@ +{ + "id": "1deff1e2-61c8-4d50-9260-4547d6734d86", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "24496701", + "text": "Recent studies have suggested that Helicobacter pylori (H. pylori) constitutes a risk for the development of colonic neoplasia. Hypergastrinemia can be induced by H. pylori infection, and gastrin can act as putative promoter of colorectal carcinogenesis. Aim of our study was to assess whether H. pylori infection and/or increased serum gastrin levels are associated with the occurrence of colonic neoplasms. For this, we reviewed prospectively collected data of 377 patients with a minimum age of 50 years who underwent colonoscopy. H. pylori and CagA status were determined by serology. Serum gastrin levels were measured in fasting state by commercially available assay. In H. pylori infected patients (n = 138; 36.6%), the overall prevalence of colonic neoplasms was more frequent compared to H. pylori negative patients (n = 239; 63.4%) (OR = 2.73, 95% CI: 1.76-4.24). H. pylori infection occurred more frequently in patients with hyperplastic polyps (OR = 2.66, 95% CI: 1.23-5.74) and adenomas presenting with low grade intraepithelial neoplasia (IEN) (OR = 1.85, 95% CI: 1.14-2.99). Attributable risk for adenomas with high grade IEN and colorectal adenocarcinoma (n = 14) was not assessed due to the low number of cases. The expression of CagA was also associated with an increased risk for colonic neoplasms (OR = 2.25, 95% CI: 1.29-3.94). Hypergastrinemia did not increase the risk for any colonic neoplasms and there was no difference in basal serum gastrin levels between H. pylori positive and negative patients. In conclusion, H. pylori infection, including CagA expression is associated with an increased risk for the development of colonic neoplasm." + }, + "questions": [ + { + "id": "5ed2ed7b-1339-4d03-933b-78e5547b896f", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1541, + "text": "H. pylori infection, including CagA expression" + } + ] + } + ] +} \ No newline at end of file diff --git a/1e7bcc22-6cc7-468c-8330-175f1cd990f8.json b/1e7bcc22-6cc7-468c-8330-175f1cd990f8.json new file mode 100644 index 0000000000000000000000000000000000000000..2d679357d073eae060e56b1b89a8be3863f93206 --- /dev/null +++ b/1e7bcc22-6cc7-468c-8330-175f1cd990f8.json @@ -0,0 +1,36 @@ +{ + "id": "1e7bcc22-6cc7-468c-8330-175f1cd990f8", + "disease": { + "id": "M2023_04_26_16_49_01", + "names": [ + "Metabolic syndrome" + ], + "dbLinks": { + "mesh": [ + "C18.452.394.968.500.570", + "C18.452.625" + ] + }, + "description": "Metabolic syndrome is a complex constellation of metabolic derangements that increase the risk of atherosclerotic cardiovascular disease, type 2 diabetes, and all-cause mortality. The key features of metabolic syndrome include central obesity, insulin resistance, dyslipidemia, and hypertension. These abnormalities are believed to arise from a combination of genetic predisposition and environmental factors, such as sedentary behavior, poor dietary habits, and chronic stress. Diagnosis of metabolic syndrome requires meeting three or more established criteria, based on standardized guidelines. Management of metabolic syndrome involves a comprehensive approach, including lifestyle modifications such as weight loss, physical activity, and dietary changes, as well as pharmacotherapy to address underlying risk factors such as hypertension, dyslipidemia, and hyperglycemia. Early intervention and aggressive management of metabolic syndrome are critical to preventing or delaying the onset of complications and improving long-term health outcomes." + }, + "article": { + "id": "17646581", + "text": "BACKGROUND:\nConsumption of soft drinks has been linked to obesity in children and adolescents, but it is unclear whether it increases metabolic risk in middle-aged individuals.\n\nMETHODS AND RESULTS:\nWe related the incidence of metabolic syndrome and its components to soft drink consumption in participants in the Framingham Heart Study (6039 person-observations, 3470 in women; mean age 52.9 years) who were free of baseline metabolic syndrome. Metabolic syndrome was defined as the presence of \u003e or = 3 of the following: waist circumference \u003e or = 35 inches (women) or \u003e or = 40 inches (men); fasting blood glucose \u003e or = 100 mg/dL; serum triglycerides \u003e or = 150 mg/dL; blood pressure \u003e or = 135/85 mm Hg; and high-density lipoprotein cholesterol \u003c 40 mg/dL (men) or \u003c 50 mg/dL (women). Multivariable models included adjustments for age, sex, physical activity, smoking, dietary intake of saturated fat, trans fat, fiber, magnesium, total calories, and glycemic index. Cross-sectionally, individuals consuming \u003e or = 1 soft drink per day had a higher prevalence of metabolic syndrome (odds ratio [OR], 1.48; 95% CI, 1.30 to 1.69) than those consuming \u003c 1 drink per day. On follow-up (mean of 4 years), new-onset metabolic syndrome developed in 717 of 4033 participants (17.8%) consuming \u003c 1 drink/day and in 433 of 2006 persons (21.6%) [corrected] consuming \u003e or = 1 soft drink/day [corrected] Consumption of \u003e or = 1 soft drink per day was associated with increased odds of developing metabolic syndrome (OR, 1.44; 95% CI, 1.20 to 1.74), obesity (OR, 1.31; 95% CI, 1.02 to 1.68), increased waist circumference (OR, 1.30; 95% CI, 1.09 to 1.56), impaired fasting glucose (OR, 1.25; 95% CI, 1.05 to 1.48), higher blood pressure (OR, 1.18; 95% CI, 0.96 to 1.44), hypertriglyceridemia (OR, 1.25; 95% CI, 1.04 to 1.51), and low high-density lipoprotein cholesterol (OR, 1.32; 95% CI 1.06 to 1.64).\n\nCONCLUSIONS:\nIn middle-aged adults, soft drink consumption is associated with a higher prevalence and incidence of multiple metabolic risk factors." + }, + "questions": [ + { + "id": "e3274023-222f-4e21-bb04-bc2bf5550fb7", + "text": "What is a risk factor for Metabolic Syndrome?", + "answers": [ + { + "answer_start": 1933, + "text": "soft drink consumption" + }, + { + "answer_start": 1397, + "text": "Consumption of \u003e or = 1 soft drink per day" + } + ] + } + ] +} \ No newline at end of file diff --git a/1f4ca3ab-620d-4114-9d38-7af90d48a020.json b/1f4ca3ab-620d-4114-9d38-7af90d48a020.json new file mode 100644 index 0000000000000000000000000000000000000000..259d4d9910adba2e9f0d187b61f16e98f5e2d2e2 --- /dev/null +++ b/1f4ca3ab-620d-4114-9d38-7af90d48a020.json @@ -0,0 +1,38 @@ +{ + "id": "1f4ca3ab-620d-4114-9d38-7af90d48a020", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "11468199", + "text": "BACKGROUND:\nFew studies have examined the effects of paternal and maternal history of myocardial infarction (MI), including age at MI, on cardiovascular disease (CVD) risk, particularly among women.\n\nMETHODS AND RESULTS:\nWe prospectively studied 22 071 men from the Physicians' Health Study and 39 876 women from the Women's Health Study with data on parental history and age at MI. Among men, 2654 CVD cases developed over 13.0 years; among women, 563 CVD cases occurred over 6.2 years. Compared with men with no parental history, only maternal, only paternal, and both maternal and paternal history of MI conferred relative risks (RRs) of CVD of 1.71, 1.40, and 1.85; among women, the respective RRs were 1.46, 1.15, and 2.05. For men, maternal age at MI of \u003c50, 50 to 59, 60 to 69, 70 to 79, and \u003e/=80 years had RRs of 1.00, 1.88, 1.88, 1.67, and 1.17; for women, the RRs for maternal age at MI of \u003c50, 50 to 59, and \u003e/=60 years were 2.57, 1.33, and 1.52. Paternal age at MI of \u003c50, 50 to 59, 60 to 69, 70 to 79, and \u003e/=80 years in men had RRs of 2.19, 1.64, 1.42, 1.16, and 0.92; in women, for paternal age at MI of \u003c50, 50 to 59, and \u003e/=60 years, the RRs were 1.63, 1.33, and 1.13.\n\nCONCLUSIONS:\nAn early history of parental MI (\u003c60 years) conferred a greater risk of CVD than did MI at older ages. However, an increased risk of CVD remained for maternal age at MI of 70 to 79 years in men and \u003e/=60 years in women, which suggests that any maternal history of MI may be important." + }, + "questions": [ + { + "id": "0555ffad-7a6b-43b5-840a-943a27c64395", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1204, + "text": "early history of parental MI (\u003c60 years)" + }, + { + "answer_start": 1441, + "text": "any maternal history of MI" + } + ] + } + ] +} \ No newline at end of file diff --git a/20742b5a-0ced-4466-aeb2-31e129205981.json b/20742b5a-0ced-4466-aeb2-31e129205981.json new file mode 100644 index 0000000000000000000000000000000000000000..c6a7fff2e5eb191556d2a1754f71cefdab161b3e --- /dev/null +++ b/20742b5a-0ced-4466-aeb2-31e129205981.json @@ -0,0 +1,39 @@ +{ + "id": "20742b5a-0ced-4466-aeb2-31e129205981", + "disease": { + "id": "H01633", + "names": [ + "High blood pressure", + "Hypertension" + ], + "dbLinks": { + "icd10": [ + "I10" + ], + "mesh": [ + "D006973" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "23492672", + "text": "AIMS:\nTo explore the causal effect of long-term alcohol consumption on coronary heart disease risk factors.\n\nMETHODS AND RESULTS:\nWe used variants in ADH1B and ADH1C genes as instrumental variables (IV) to estimate the causal effect of long-term alcohol consumption on body mass index (BMI), blood pressure (BP), lipids, fibrinogen, and glucose. Analyses were undertaken in 54 604 Danes (mean age 56 years). Both confounder-adjusted multivariable and IV analyses suggested that a greater alcohol consumption among those who drank any alcohol resulted in a higher BP [mean difference in SBP per doubling of alcohol consumption among drinkers: 0.76 mmHg (95% CI: 0.63, 0.90) from multivariable analyses and 0.94 mmHg (-3.03, 4.69) from IV analyses; P-value for difference in these results = 0.95]. The positive association of alcohol with HDLc in the multivariable analyses [4.9% (4.7, 5.1)] appeared stronger than in the IV analyses [1.5% (-4.5, 7.4)], and the weak inverse association with fibrinogen in the multivariable analysis [-2.0% (-2.1, -1.8)] was not present in the IV analyses [0.6% (-3.8, 5.0)], but statistically the results for both of these could not be reliably distinguished from each other (P-values 0.21 and 0.32, respectively). The weak inverse association of alcohol with BMI [-0.13 kg/m(2) (-0.16, -0.10)] and with triglycerides [-0.4% (-0.7, 0.4)] in multivariable analyses were in contrast to the strong positive association of alcohol with BMI [1.37 kg/m(2) (0.59, 2.15)] and the strong inverse association with triglycerides [-14.9% (-25.6, -4.3)] in IV analyses; P = 0.006 and 0.01, respectively, for difference between the two. Alcohol was not associated with non-HDLc or glucose.\n\nCONCLUSION:\nOur results show adverse effects of long-term alcohol consumption on BP and BMI. We also found novel evidence for a potentially beneficial effect on triglyceride levels, which needs further replication." + }, + "questions": [ + { + "id": "30862d21-be4c-4161-85f9-e5413e392e78", + "text": "What are the risk factors for Hypertension?", + "answers": [ + { + "answer_start": 1757, + "text": "long-term alcohol consumption" + }, + { + "answer_start": 480, + "text": "greater alcohol consumption among those who drank any alcohol" + } + ] + } + ] +} \ No newline at end of file diff --git a/20b65f48-eeea-4a86-ab4b-487d2ccab9f2.json b/20b65f48-eeea-4a86-ab4b-487d2ccab9f2.json new file mode 100644 index 0000000000000000000000000000000000000000..c47f6cea19ddfe0f1e09faef2fe7a19c33d0ed61 --- /dev/null +++ b/20b65f48-eeea-4a86-ab4b-487d2ccab9f2.json @@ -0,0 +1,38 @@ +{ + "id": "20b65f48-eeea-4a86-ab4b-487d2ccab9f2", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "29069505", + "text": "BACKGROUND:\nRegion II in northern Chile (population 442 570) experienced a sudden major increase in arsenic water concentrations in 1958 in the main city of Antofagasta, followed by a major reduction in exposure when an arsenic removal plant was installed in 1970. It provides a unique opportunity to study latency effects of exposure to arsenic, and this is the first study with mortality data up to 40 years after exposure reduction.\n\nMETHODS:\nWe previously identified high mortality rates in Region II up to the year 2000. Here we present rate ratios (RRs) for Region II compared with all the rest of Chile from 2001 to 2010, and with unexposed Region V (population 1 539 852) for all years from 1950 to 2010. All statistical tests were one-sided.\n\nRESULTS:\nFrom 2001 to 2010, comparing Region II with the rest of Chile, lung and bladder mortality were still greatly elevated (RR = 3.38, 95% confidence interval [CI] = 3.19 to 3.58, P \u003c .001 for lung cancer in men; RR = 2.41, 95% CI = 2.20 to 2.64, P \u003c .001 for lung cancer in women; RR = 4.79, 95% CI = 4.20 to 5.46, P \u003c .001 for bladder cancer in men; RR = 6.43, 95% CI = 5.49 to 7.54, P \u003c .001 for bladder cancer in women). Kidney cancer mortality was also elevated (RR = 1.75, 95% CI = 1.49 to 2.05, P \u003c .001 for men; RR = 2.09, 95% CI = 1.69 to 2.57, P \u003c .001 for women). Earlier short latency acute myocardial infarction mortality increases had subsided.\n\nCONCLUSIONS:\nLung, bladder, and kidney cancer mortality due to arsenic exposure have very long latencies, with increased risks manifesting 40 years after exposure reduction. Our findings suggest that arsenic in drinking water may involve one of the longest cancer latencies for a human carcinogen." + }, + "questions": [ + { + "id": "ba287c01-0bf8-43a0-8b39-527bee8d39c1", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 1479, + "text": "arsenic exposure" + }, + { + "answer_start": 1616, + "text": "arsenic in drinking water" + } + ] + } + ] +} \ No newline at end of file diff --git a/20cd5251-84ec-433c-b86e-6de5746525b9.json b/20cd5251-84ec-433c-b86e-6de5746525b9.json new file mode 100644 index 0000000000000000000000000000000000000000..14f31fed5e583f185f06b8d80d0fccee3a06f55d --- /dev/null +++ b/20cd5251-84ec-433c-b86e-6de5746525b9.json @@ -0,0 +1,39 @@ +{ + "id": "20cd5251-84ec-433c-b86e-6de5746525b9", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "19174392", + "text": "OBJECTIVES:\nTo assess whether smoking is a risk factor for developing rheumatoid arthritis (RA).\n\nDESIGN:\nMeta-analysis.\n\nDATA SOURCES:\nwere observational studies that examined the association between smoking history and the risk of developing RA identified through Medline and EMBASE (from 1966 to December 2006), relevant books and a reference search. Two authors independently extracted the following: authors' names, publication year, sample size, participant characteristics, odds ratios (OR) or relative risks, adjustment factors, study design and area where the study was conducted. Data syntheses were based upon random effects model. Summarised syntheses effects were expressed by OR.\n\nRESULTS:\nSixteen studies were selected from among 433 articles. For men, summary OR for ever, current and past smokers were 1.89 (95% CI 1.56 to 2.28), 1.87 (1.49 to 2.34) and 1.76 (1.33 to 2.31), respectively. For rheumatoid factor-positive (RF+) RA, summary OR for ever, current and past smokers were 3.02 (2.35 to 3.88), 3.91 (2.78 to 5.50) and 2.46 (1.74 to 3.47), respectively. Summary OR for 20 or more pack-years of smoking was 2.31 (1.55 to 3.41). For women, summary OR for ever, current and past smokers were 1.27 (1.12 to 1.44), 1.31 (1.12 to 1.54) and 1.22 (1.06 to 1.40), respectively. For RF+ RA, summary OR for ever, current and past smokers were 1.34 (0.99 to 1.80), 1.29 (0.94 to 1.77) and 1.21 (0.83 to 1.77). Summary OR for 20 or more pack-years of smoking was 1.75 (1.52 to 2.02).\n\nCONCLUSION:\nSmoking is a risk factor for RA, especially RF+ RA men and heavy smokers." + }, + "questions": [ + { + "id": "f1c2759f-d806-4ace-84cd-a74703b5eb00", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 1508, + "text": "Smoking" + }, + { + "answer_start": 1320, + "text": "ever, current and past smokers" + } + ] + } + ] +} \ No newline at end of file diff --git a/20d36cd7-2dcd-4a37-bf3b-dc54f566e5ce.json b/20d36cd7-2dcd-4a37-bf3b-dc54f566e5ce.json new file mode 100644 index 0000000000000000000000000000000000000000..e6bde365e29ab3d67948246e67b7b5eca140bab6 --- /dev/null +++ b/20d36cd7-2dcd-4a37-bf3b-dc54f566e5ce.json @@ -0,0 +1,38 @@ +{ + "id": "20d36cd7-2dcd-4a37-bf3b-dc54f566e5ce", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "9032046", + "text": "BACKGROUND:\nRecent studies have shown a direct relation between serum estrogen levels assessed at a single point in time and the risk of breast cancer, but no evidence links estrogen levels assessed repeatedly over an extended interval to the risk of breast cancer. Bone mass has been proposed as a marker of cumulative exposure to estrogen in women. We therefore studied the association between bone mass and the incidence of breast cancer.\n\nMETHODS:\nBetween 1967 and 1970, 1373 women who were 47 to 80 years old and had no history of breast cancer underwent posteroanterior hand radiography in the Framingham Study. We used radiogrametry to measure the cortical width of each woman's second metacarpal. Participants were followed until the end of 1993. All incident cases of breast cancer were confirmed by pathological reports. We used a Cox proportional-hazards model to examine the relation of metacarpal bone mass to the risk of postmenopausal breast cancer.\n\nRESULTS:\nPostmenopausal breast cancer developed in 91 subjects. Incidence rates per 1000 person-years increased from 2.0 among the women in the lowest age-specific quartile of metacarpal bone mass to 2.6, 2.7, and 7.0 among the women in the second, third, and highest quartiles, respectively. After adjustments for age and other potential confounding factors, the rate ratios for the risk of breast cancer were 1.0, 1.3, 1.3, and 3.5 from the lowest quartile to the highest (P for trend, \u003c0.001).\n\nCONCLUSIONS:\nWomen in the highest quartile of bone mass are at higher risk for postmenopausal breast cancer than those in the lowest quartile. The mechanisms underlying this relation are not understood, but cumulative exposure to estrogen may play a part." + }, + "questions": [ + { + "id": "44c331e0-079d-4ee2-9d8c-b002629f3818", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1477, + "text": "Women in the highest quartile of bone mass" + }, + { + "answer_start": 1110, + "text": "lowest age-specific quartile of metacarpal bone mass to 2.6, 2.7, and 7.0 among the women in the second, third, and highest quartiles" + } + ] + } + ] +} \ No newline at end of file diff --git a/219fa2d2-1cf7-423c-91d1-f77d7e587c5a.json b/219fa2d2-1cf7-423c-91d1-f77d7e587c5a.json new file mode 100644 index 0000000000000000000000000000000000000000..8ad3e40d5534ef995347e74c7993c66b9f332aa8 --- /dev/null +++ b/219fa2d2-1cf7-423c-91d1-f77d7e587c5a.json @@ -0,0 +1,42 @@ +{ + "id": "219fa2d2-1cf7-423c-91d1-f77d7e587c5a", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "26954518", + "text": "BACKGROUND:\nEarly-life physical fitness has rarely been examined in relation to type 2 diabetes mellitus (DM) in adulthood because of the lengthy follow-up required. Elucidation of modifiable risk factors at young ages may help facilitate earlier and more effective interventions.\n\nOBJECTIVE:\nTo examine aerobic capacity and muscle strength at age 18 years in relation to risk for type 2 DM in adulthood.\n\nDESIGN:\nNational cohort study.\n\nSETTING:\nSweden.\n\nPARTICIPANTS:\n1 534 425 military conscripts from 1969 to 1997 (97% to 98% of all men aged 18 years nationwide) without prior type 2 DM.\n\nMEASUREMENTS:\nAerobic capacity and muscle strength (measured in watts and newtons per kilogram of body weight, respectively) were examined in relation to type 2 DM identified from outpatient and inpatient diagnoses from 1987 to 2012 (maximum age, 62 years).\n\nRESULTS:\n34 008 men were diagnosed with type 2 DM in 39.4 million person-years of follow-up. Low aerobic capacity and muscle strength were independently associated with increased risk for type 2 DM. The absolute difference in cumulative incidence of type 2 DM between the lowest and highest tertiles of both aerobic capacity and strength was 0.22% at 20 years of follow-up (95% CI, 0.20% to 0.25%), 0.76% at 30 years (CI, 0.71% to 0.81%), and 3.97% at 40 years (CI, 3.87% to 4.06%). Overall, the combination of low aerobic capacity and muscle strength was associated with a 3-fold risk for type 2 DM (adjusted hazard ratio, 3.07 [CI, 2.88 to 3.27]; P \u003c 0.001), with a positive additive interaction (P \u003c 0.001). These associations were seen even among men with normal body mass index.\n\nLIMITATION:\nThis cohort did not include women and did not measure physical fitness at older ages.\n\nCONCLUSION:\nIn this large cohort of Swedish male military conscripts, low aerobic capacity and muscle strength at age 18 years were associated with increased long-term risk for type 2 DM, even among those with normal body mass index.\n\nPRIMARY FUNDING SOURCE:\nNational Institutes of Health." + }, + "questions": [ + { + "id": "0b71f17d-9050-4a1b-8c5c-03be08201b4e", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 945, + "text": "Low aerobic capacity and muscle strength" + }, + { + "answer_start": 1344, + "text": "the combination of low aerobic capacity and muscle strength" + }, + { + "answer_start": 1805, + "text": " low aerobic capacity and muscle strength at age 18 years" + } + ] + } + ] +} \ No newline at end of file diff --git a/22200b92-b954-488f-9605-af8a3f7f66bc.json b/22200b92-b954-488f-9605-af8a3f7f66bc.json new file mode 100644 index 0000000000000000000000000000000000000000..ca70b0df00e59e232c1a3d5f68023ef6ba1c69f1 --- /dev/null +++ b/22200b92-b954-488f-9605-af8a3f7f66bc.json @@ -0,0 +1,41 @@ +{ + "id": "22200b92-b954-488f-9605-af8a3f7f66bc", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "8919279", + "text": "Bile acid composition was assessed in 50 patients with colorectal cancer as compared to that in a control group of 50 subjects. The two groups were age- and sex-matched. The overall bile acid values were similar in both groups, while the relative concentrations of primary and secondary bile acids were different, a significant increase in the patients with colorectal cancer being observed. This finding thus seems to confirm the existence of a link between colorectal cancer and cholelithiasis. Both conditions share common risk factors, such as alterations in cholesterol metabolism and bile acid composition." + }, + "questions": [ + { + "id": "36ee3c6a-1a3a-4c2f-8973-cca5ce1bce81", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 548, + "text": "alterations in cholesterol metabolism" + }, + { + "answer_start": 590, + "text": "bile acid composition" + } + ] + } + ] +} \ No newline at end of file diff --git a/23551061-9b0b-43c1-a014-abc384c3b454.json b/23551061-9b0b-43c1-a014-abc384c3b454.json new file mode 100644 index 0000000000000000000000000000000000000000..c713932147d88b8a87f3f3d836ddf0f1e1c0b81b --- /dev/null +++ b/23551061-9b0b-43c1-a014-abc384c3b454.json @@ -0,0 +1,58 @@ +{ + "id": "23551061-9b0b-43c1-a014-abc384c3b454", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "15364185", + "text": "BACKGROUND:\nAlthough more than 80% of the global burden of cardiovascular disease occurs in low-income and middle-income countries, knowledge of the importance of risk factors is largely derived from developed countries. Therefore, the effect of such factors on risk of coronary heart disease in most regions of the world is unknown.\n\nMETHODS:\nWe established a standardised case-control study of acute myocardial infarction in 52 countries, representing every inhabited continent. 15152 cases and 14820 controls were enrolled. The relation of smoking, history of hypertension or diabetes, waist/hip ratio, dietary patterns, physical activity, consumption of alcohol, blood apolipoproteins (Apo), and psychosocial factors to myocardial infarction are reported here. Odds ratios and their 99% CIs for the association of risk factors to myocardial infarction and their population attributable risks (PAR) were calculated.\n\nFINDINGS:\nSmoking (odds ratio 2.87 for current vs never, PAR 35.7% for current and former vs never), raised ApoB/ApoA1 ratio (3.25 for top vs lowest quintile, PAR 49.2% for top four quintiles vs lowest quintile), history of hypertension (1.91, PAR 17.9%), diabetes (2.37, PAR 9.9%), abdominal obesity (1.12 for top vs lowest tertile and 1.62 for middle vs lowest tertile, PAR 20.1% for top two tertiles vs lowest tertile), psychosocial factors (2.67, PAR 32.5%), daily consumption of fruits and vegetables (0.70, PAR 13.7% for lack of daily consumption), regular alcohol consumption (0.91, PAR 6.7%), and regular physical activity (0.86, PAR 12.2%), were all significantly related to acute myocardial infarction (p\u003c0.0001 for all risk factors and p=0.03 for alcohol). These associations were noted in men and women, old and young, and in all regions of the world. Collectively, these nine risk factors accounted for 90% of the PAR in men and 94% in women.\n\nINTERPRETATION:\nAbnormal lipids, smoking, hypertension, diabetes, abdominal obesity, psychosocial factors, consumption of fruits, vegetables, and alcohol, and regular physical activity account for most of the risk of myocardial infarction worldwide in both sexes and at all ages in all regions. This finding suggests that approaches to prevention can be based on similar principles worldwide and have the potential to prevent most premature cases of myocardial infarction." + }, + "questions": [ + { + "id": "2c196643-7862-4c29-86f2-756826751c2e", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1893, + "text": "Abnormal lipids" + }, + { + "answer_start": 1910, + "text": "smoking" + }, + { + "answer_start": 1919, + "text": "hypertension" + }, + { + "answer_start": 1933, + "text": "diabetes" + }, + { + "answer_start": 1943, + "text": "abdominal obesity" + }, + { + "answer_start": 1962, + "text": "psychosocial factors" + }, + { + "answer_start": 1021, + "text": "raised ApoB/ApoA1 ratio" + } + ] + } + ] +} \ No newline at end of file diff --git a/23f6aa91-264f-4d05-89e0-11d02c6b9d8f.json b/23f6aa91-264f-4d05-89e0-11d02c6b9d8f.json new file mode 100644 index 0000000000000000000000000000000000000000..364644f28105219e6c0870bf9067b83712ba89fa --- /dev/null +++ b/23f6aa91-264f-4d05-89e0-11d02c6b9d8f.json @@ -0,0 +1,45 @@ +{ + "id": "23f6aa91-264f-4d05-89e0-11d02c6b9d8f", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "30380096", + "text": "BACKGROUND:\nInvestigations of the associations with colorectal cancer have yielded conflicting results. The aim of our study was to synthesize the research on colorectal cancer risks in BRCA mutation carriers by means of a systematic review and quantitatively by means of meta-analyses overall and in subgroups of BRCA mutation carriers.\n\nMETHODS:\nWe searched PubMed/MEDLINE, Embase, Cochrane, Scopus, and ProQuest Dissertation \u0026 Theses. Unadjusted odds ratios (ORs) were used to derive pooled estimates of colorectal cancer risk overall and in subgroups defined by mutation type (BRCA1 or BRCA2), cancer type (colorectal or colon cancer), study design (age-sex-adjusted or crude), and ascertainment method (ascertained or inferred genotyping). The associations were evaluated using random-effect models. All statistical tests were two-sided.\n\nRESULTS:\nEighteen studies were included in the systematic review: five cohort studies with ascertained BRCA mutation, six cohort studies involving pedigree analysis, five case-control studies, and two kin-cohort studies. Of these, 14 were used in the meta-analysis, which revealed a statistically significant increased risk of colorectal cancer in overall BRCA mutation carriers (OR = 1.24, 95% confidence interval (CI) = 1.02 to 1.51, P = .03). In subgroup meta-analyses by BRCA type, BRCA1 mutation was associated with increased risk of colorectal cancer (OR = 1.49, 95% CI = 1.19 to 1.85, P \u003c .001), but BRCA2 was not (OR = 1.10, 95% CI = 0.77 to 1.58, P = .61). In subgroup meta-analyses of studies reporting estimates adjusted for age and sex, an increased risk of colorectal cancer for BRCA1 (OR = 1.56, 95% CI = 1.23 to 1.98, P \u003c .001), but not for BRCA2 (OR = 1.09, 95% CI = 0.75 to 1.58, P = .66) was observed. Analyses stratified by ascertainment method found no association between BRCA mutation and colorectal cancer risk.\n\nCONCLUSION:\nThe meta-analysis results provide clinicians and health-care regulatory agencies with evidence of the increased risk of colorectal cancer in BRCA1 mutation carriers, but not in BRCA2." + }, + "questions": [ + { + "id": "7f16ab72-d2ca-41bc-8808-3915da676bef", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 2033, + "text": "BRCA1 mutation carriers, but not in BRCA2" + }, + { + "answer_start": 1330, + "text": "BRCA1" + }, + { + "answer_start": 1636, + "text": "BRCA1" + } + ] + } + ] +} \ No newline at end of file diff --git a/240be164-5d18-4c82-bc69-63ebc50b20d3.json b/240be164-5d18-4c82-bc69-63ebc50b20d3.json new file mode 100644 index 0000000000000000000000000000000000000000..f223e9651e83f68326122156e2edd4a12852fee3 --- /dev/null +++ b/240be164-5d18-4c82-bc69-63ebc50b20d3.json @@ -0,0 +1,39 @@ +{ + "id": "240be164-5d18-4c82-bc69-63ebc50b20d3", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "19134022", + "text": "BACKGROUND:\nRecent data in mice suggest that acid suppression during pregnancy yields offspring with type 2 T helper-dominant immunity, suggesting a predisposition for allergy.\n\nOBJECTIVE:\nTo determine the association of in utero exposure to acid-suppressive medications and the subsequent development of allergic diseases in children.\n\nMETHODS:\nWe studied a population-based observational cohort formed by linking data from three Swedish national healthcare registers: the Medical Birth Register, the Hospital Discharge Register, and the Swedish Prescribed Drug Register. Main outcome measures included a hospital discharge diagnosis of an allergic disease or prescription for asthma medications, epinephrine auto-injectors, antihistamines or steroid ointments in children. Data were analysed using the Mantel-Haenszel procedure.\n\nRESULTS:\nTwenty-nine thousand four hundred and ninety (5.03%) children had a discharge diagnosis of allergy or prescriptions for allergy medications. Five thousand six hundred and forty-five (0.96%) children had been exposed to acid suppression therapy during pregnancy; of these, 405 (0.07%) were treated for allergic diseases. Exposure to acid-suppressive medications in utero was associated with an increased odds ratio (OR) for developing allergy (OR 1.43, 95% confidence interval (95% CI) 1.29-1.59). We observed this association irrespective of the type of drug, time of exposure during pregnancy, and maternal history of allergy. The use of maternal acid-suppressive medication was associated with an increased OR for the development of childhood asthma (3.7% in the population at large vs. 5.6% in exposed children, OR 1.51, 95% CI 1.35-1.69), but not for other allergic diseases.\n\nCONCLUSION:\nThese data provide first evidence of a significant association between in utero exposure to acid-suppressive drugs and the risk of developing childhood asthma." + }, + "questions": [ + { + "id": "599d8103-cb1c-46f2-be86-13037c96f9f1", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1469, + "text": "The use of maternal acid-suppressive medication" + }, + { + "answer_start": 1805, + "text": "in utero exposure to acid-suppressive drugs" + } + ] + } + ] +} \ No newline at end of file diff --git a/246bae70-7436-4965-a933-3a8d864b1869.json b/246bae70-7436-4965-a933-3a8d864b1869.json new file mode 100644 index 0000000000000000000000000000000000000000..48f89ecb1bd971540c852ef6b1e714b9dcec2ba1 --- /dev/null +++ b/246bae70-7436-4965-a933-3a8d864b1869.json @@ -0,0 +1,36 @@ +{ + "id": "246bae70-7436-4965-a933-3a8d864b1869", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "25431272", + "text": "The aim of the present study was to analyse the interaction between asthma and smoking in the risk of adult airway obstruction, accounting for atopy. In the European Community Respiratory Health Survey, 15 668 persons aged 20-56 years underwent spirometry in 1991-1993 and 9 years later (n=8916). Risk of airway obstruction and lung function decline associated with smoking and early-onset (\u003c10 years of age) and late-onset (\u003e10 years of age) asthma were analysed with generalised estimating equation models and random-effect linear models, adjusting for covariates. Interaction of asthma with smoking was expressed as relative excess risk due to interaction (RERI). A 20-fold increase in adult airway obstruction was found among those with early-onset asthma independently of smoking status (never-smokers: OR 21.0, 95% CI 12.7-35; current smokers: OR 23.7, 95% CI 13.9-40.6). Late-onset asthma was associated with airway obstruction, with a stronger association among current smokers (OR 25.6, 95% CI 15.6-41.9) than among never-smokers (OR 11.2, 95% CI 6.8-18.6) (RERI 12.02, 95% CI 1.96-22.07). Stratifying by atopy, the association between smoking and asthma was most pronounced among nonatopics. Early- and late-onset asthma were associated with 10-20-fold increased risk of adult airway obstruction. Smoking increased the risk of adult airway obstruction in subjects with asthma onset after age 10 years. Investigation of measures potentially preventive of chronic obstructive pulmonary disease development following asthma is urgently needed." + }, + "questions": [ + { + "id": "a16bb409-eb65-4c1e-bc72-d757a3c609aa", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 1202, + "text": "Early- and late-onset asthma" + } + ] + } + ] +} \ No newline at end of file diff --git a/24ba1081-ca97-4b26-a27e-fa45e4b37d2a.json b/24ba1081-ca97-4b26-a27e-fa45e4b37d2a.json new file mode 100644 index 0000000000000000000000000000000000000000..b7005512c87c94a6210926f285d7cdae298444cb --- /dev/null +++ b/24ba1081-ca97-4b26-a27e-fa45e4b37d2a.json @@ -0,0 +1,40 @@ +{ + "id": "24ba1081-ca97-4b26-a27e-fa45e4b37d2a", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "10413721", + "text": "BACKGROUND:\nEnzymes that contribute to the local detoxification in alveoli and bronchioles have an important role in the defence mechanism against tobacco smoke. It has been suggested that genetic susceptibility to smoking injury may confer a risk for the development of chronic obstructive pulmonary disease (COPD). The polymorphisms in glutathione S-transferase P1 (GSTP1), a xenobiotic metabolising enzyme, were investigated in patients with COPD.\n\nMETHODS:\nPolymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) were performed to genotype GSTP1 polymorphisms in exon 5 (Ile105Val) and exon 6 (Ala114Val). Blood samples were taken from 53 patients with COPD and 50 control subjects at the Tokyo University Hospital, the Juntendo University Hospital, and the Tokyo Kenbikyoin Clinic for use in the study.\n\nRESULTS:\nThe proportion of GSTP1/Ile105 homozygotes was significantly higher in the patients with COPD than in the control subjects (79% vs 52%). The odds ratio for GSTP1/Ile105 homozygotes versus all other genotypes was 3.5 (95% CI 2.7 to 4.6) for COPD. Polymorphism at residue 114 of GSTP1 was not found in either group.\n\nCONCLUSIONS:\nGenetic polymorphism of exon 5 of GSTP1 may be associated with COPD because the GSTP1/Ile105 genotype is predominantly found in COPD. It is suggested that the GSTP1/Ile105 genotype may be less protective against xenobiotics in tobacco smoke." + }, + "questions": [ + { + "id": "245c9aa5-6d47-4a94-84e1-2f149ae09883", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 864, + "text": "GSTP1/Ile105 homozygotes" + }, + { + "answer_start": 1174, + "text": "Genetic polymorphism of exon 5 of GSTP1" + } + ] + } + ] +} \ No newline at end of file diff --git a/24e10978-6233-4404-bc35-e521cf4ca8f6.json b/24e10978-6233-4404-bc35-e521cf4ca8f6.json new file mode 100644 index 0000000000000000000000000000000000000000..84c07358f08365f66f772fc8ab6b58cc352213e4 --- /dev/null +++ b/24e10978-6233-4404-bc35-e521cf4ca8f6.json @@ -0,0 +1,39 @@ +{ + "id": "24e10978-6233-4404-bc35-e521cf4ca8f6", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "24648197", + "text": "BACKGROUND:\nThe understanding of the role of smoking exposure in the induction of wheezing and asthma in children is important for prevention.\n\nMETHODS:\nA systematic review of literature and a meta-analysis were conducted to identify studies on unselected prospective birth cohorts. The effect of exposure to maternal/parental smoking on the induction of current wheezing or asthma was evaluated in children aged 6 months, \u003c6 years, and ≥6 years. Pooled odds ratios (OR) with 95% confidence intervals (CI) were estimated.\n\nRESULTS:\nWe identified 43 papers. Exposure to maternal prenatal smoking was associated with an increased risk of wheezing in \u003c6-year-olds (OR 1.36; 95% CI: 1.19-1.55) and of wheezing or asthma in ≥6-year-olds (OR: 1.22, 95% CI: 1.03-1.44). A positive association (OR: 1.24, 95% CI: 1.11-1.38) was also found in the only three studies that evaluated exposure to maternal prenatal smoking alone. Postnatal exposures to maternal/parental smoking were associated with wheezing in \u003c6-year-olds (OR: 1.21; 95% CI: 1.13-1.31 and OR: 1.30; 95% CI: 1.13-1.51), although it was often impossible to separate the role of postnatal from that of prenatal exposure; data in schoolchildren are limited and this precluded a meta-analysis. No clear association was found between exclusive postnatal exposure and wheezing or asthma.\n\nCONCLUSIONS:\nWe confirmed an important role of prenatal exposure to maternal smoking on the induction of wheezing and asthma in offspring, particularly in the first years of life. More studies with a consistent number of subjects only exposed to smoke postnatally are needed to better investigate the harmful effects on the induction of wheezing or asthma, particularly in schoolchildren." + }, + "questions": [ + { + "id": "1e0c0eef-2a19-4acc-85a3-18ae0faaadef", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 569, + "text": "maternal prenatal smoking" + }, + { + "answer_start": 1385, + "text": "prenatal exposure to maternal smoking" + } + ] + } + ] +} \ No newline at end of file diff --git a/24e446c0-83c0-486c-9bfe-932a792db495.json b/24e446c0-83c0-486c-9bfe-932a792db495.json new file mode 100644 index 0000000000000000000000000000000000000000..99c7cdede56b179ade2904b860439b829520d652 --- /dev/null +++ b/24e446c0-83c0-486c-9bfe-932a792db495.json @@ -0,0 +1,38 @@ +{ + "id": "24e446c0-83c0-486c-9bfe-932a792db495", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "15451783", + "text": "BACKGROUND:\nChronic inflammation represents an essential feature of the atherosclerotic process. Lipoprotein-associated phospholipase A2 (Lp-PLA2), an enzyme mainly produced by monocytes/macrophages, generates potent proinflammatory products.\n\nMETHODS AND RESULTS:\nPlasma concentrations of Lp-PLA2 were determined by ELISA in 934 apparently healthy men aged 45 to 64 years sampled from the general population in 1984 and followed up until 1998. During this period, 97 men experienced a coronary event diagnosed according to the MONICA (MONItoring of trends and determinants in CArdiovascular disease) protocol. Baseline levels of Lp-PLA2 were higher in subjects who experienced an event than in event-free subjects (295+/-113 versus 263+/-79 ng/mL, P\u003c0.01). Lp-PLA2 was positively correlated with total cholesterol (R=0.30, P\u003c0.0001) and age (R=0.12, P=0.001), was only slightly correlated with HDL cholesterol (R=0.09, P=0.005) and C-reactive protein R=0.06, P=0.06), but was not correlated with body mass index or blood pressure. In a Cox model, a 1-SD increase in Lp-PLA2 was associated with risk of future coronary events (hazard ratio [HR] 1.37, 95% CI 1.16 to 1.62). After controlling for potential confounders, the HR was attenuated but remained statistically significant (HR 1.23, 95% CI 1.02 to 1.47). Further inclusion of C-reactive protein in the model did not appreciably affect its predictive ability (HR 1.21, 95% CI 1.01 to 1.45).\n\nCONCLUSIONS:\nElevated levels of Lp-PLA2 appeared to be predictive of future coronary events in apparently healthy middle-aged men with moderately elevated total cholesterol, independent of CRP. This suggests that Lp-PLA2 and CRP may be additive in their ability to predict risk of coronary heart disease." + }, + "questions": [ + { + "id": "429bfef1-d1d0-4385-a582-99b910e755b9", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1460, + "text": "Elevated levels of Lp-PLA2" + }, + { + "answer_start": 611, + "text": "Baseline levels of Lp-PLA2" + } + ] + } + ] +} \ No newline at end of file diff --git a/24fc4fe3-cbee-4433-be7b-e36a584fae46.json b/24fc4fe3-cbee-4433-be7b-e36a584fae46.json new file mode 100644 index 0000000000000000000000000000000000000000..5ea00974484666d564ccc5fa9f49ca1a1ee29c10 --- /dev/null +++ b/24fc4fe3-cbee-4433-be7b-e36a584fae46.json @@ -0,0 +1,43 @@ +{ + "id": "24fc4fe3-cbee-4433-be7b-e36a584fae46", + "disease": { + "id": "H00056", + "names": [ + "Alzheimer disease", + "Dementia due to Alzheimer disease" + ], + "dbLinks": { + "icd10": [ + "G30" + ], + "mesh": [ + "D000544" + ] + }, + "category": "Neurodegenerative disease" + }, + "article": { + "id": "12160362", + "text": "BACKGROUND:\nPresence of the apolipoprotein E (apoE) epsilon4 allele, which is involved in cholesterol metabolism, is the most important genetic risk factor for Alzheimer disease. Elevated midlife values for total cholesterol level and blood pressure have been implicated recently as risk factors for Alzheimer disease.\n\nOBJECTIVE:\nTo study the relative importance and the putative relationship among the apoE epsilon4 allele, midlife total cholesterol level, and midlife blood pressure as risk factors for late-life Alzheimer disease.\n\nDESIGN:\nProspective population-based study.\n\nSETTING:\nKuopio and Joensuu, eastern Finland.\n\nPARTICIPANTS:\nParticipants were derived from random population surveys from 1972, 1977, 1982, and 1987. A total of 1449 persons (73%), 65 to 79 years of age, participated in the reexamination in 1998 (mean follow-up, 21 years).\n\nMEASUREMENTS:\nMidlife blood pressure and total cholesterol level, apoE genotype, and development of Alzheimer disease during follow-up.\n\nRESULTS:\nThe apoE epsilon4 allele was an independent risk factor for Alzheimer disease, even after adjustment for midlife vascular risk factors and other confounders (odds ratio, 2.1 [95% CI, 1.1 to 4.1]). Similarly, elevated midlife values for serum total cholesterol level (odds ratio, 2.8 [CI, 1.2 to 6.7]) and systolic blood pressure (odds ratio, 2.6 [CI, 1.1 to 6.6]) were independent risk factors for Alzheimer disease, even after adjustment for apoE genotype and other confounding factors.\n\nCONCLUSIONS:\nThe association between the apoE epsilon4 allele and Alzheimer disease does not seem to be mediated by vascular factors. The apoE epsilon4 allele, elevated midlife total cholesterol level, and high midlife systolic blood pressure are independent risk factors for Alzheimer disease. The risk for Alzheimer disease from treatable factors--elevated total cholesterol level and blood pressure--appears to be greater than that from the apoE epsilon4 allele." + }, + "questions": [ + { + "id": "ea19f423-b0ac-4454-be75-3df08c8f71d8", + "text": "What are the risk factors of Alzheimer disease?", + "answers": [ + { + "answer_start": 28, + "text": "apolipoprotein E (apoE) epsilon4 allele" + }, + { + "answer_start": 1652, + "text": "elevated midlife total cholesterol level" + }, + { + "answer_start": 1698, + "text": "high midlife systolic blood pressure" + } + ] + } + ] +} \ No newline at end of file diff --git a/25ed4b3f-0cc3-4bab-a476-05fe7f68b267.json b/25ed4b3f-0cc3-4bab-a476-05fe7f68b267.json new file mode 100644 index 0000000000000000000000000000000000000000..e8456176fd9451adfa294faf932c97f17e211a85 --- /dev/null +++ b/25ed4b3f-0cc3-4bab-a476-05fe7f68b267.json @@ -0,0 +1,46 @@ +{ + "id": "25ed4b3f-0cc3-4bab-a476-05fe7f68b267", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "11118026", + "text": "Study of parental transmission of diabetes provides insight into the relative contributions of underlying maternal and paternal influences. We estimated risk for type 2 diabetes and milder degrees of glucose intolerance associated with parental diabetes among subjects of the population-based Framingham Offspring Study, in which participants are primarily Caucasian and at relatively low risk for diabetes and for which both parental and offspring phenotypes were ascertained by direct examination. Parental diabetes, assessed over 40 years of biennial follow-up, was defined by use of hypoglycemic drug therapy or a casual plasma glucose level \u003e or = 11.1 mmol/l at any examination. Offspring glucose tolerance, assessed over 20 years of quadrennial follow-up, was defined by fasting plasma glucose levels \u003e or = 7.8 mmol/l at any two examinations, use of hypoglycemic drug therapy at any examination, or with a 75-g oral glucose tolerance test (1980 World Health Organization criteria) at the most recent examination. We calculated odds ratios (ORs) and 95% CIs for offspring glucose tolerance status using generalized estimating equations to account for differential correlations within and between families. The 2,527 offspring came from 1,303 nuclear families, of which 77.6% had two or more siblings per family and in which the prevalence of parental diabetes was 24.6%. The mean offspring age was 54 years (range 26-82), 53% were women, 8.6% had diabetes, 11.4% had impaired glucose tolerance, 76.3% had no parental diabetes, 10.5% had maternal diabetes, 11.5% had paternal diabetes, and 1.7% had bilineal diabetes. Relative to individuals without parental diabetes, the age-adjusted ORs (95% CI) for offspring type 2 diabetes or abnormal glucose tolerance (fasting plasma glucose \u003e or = 6.1 mmol/l or 2-h postchallenge glucose tolerance \u003e or = 7.8 mmol/l) among individuals with maternal diabetes were 3.4 (2.3-4.9) and 2.7 (2.0-3.7), respectively; among individuals with paternal diabetes were 3.5 (2.3-5.2) and 1.7 (1.2-2.4), respectively; and among individuals with bilineal diabetes were 6.1 (2.9-13.0) and 5.2 (2.6-10.5), respectively. Although maternal and paternal diabetes conferred equivalent risk for offspring type 2 diabetes, offspring with maternal diabetes were slightly more likely to have abnormal glucose tolerance compared with those with paternal diabetes (OR 1.6, 95% CI 1.1-2.4). Offspring with maternal diabetes and an age of onset of \u003c50 years had marked increased risk for both type 2 diabetes (9.7, 4.3-22.0) and abnormal glucose tolerance (9.0, 4.2-19.7). We conclude that risk ratios for offspring type 2 diabetes are consistent with a simple additive risk model, where risk when both parents are affected equals the sum of risk when either parent is affected. For maternal diabetes to confer excess risk for mild but not overt glucose intolerance, offspring of diabetic fathers may transit abnormal to impaired glucose tolerance relatively quickly, or diabetic mothers may transmit risk for a mild slowly progressive form of abnormal glucose tolerance in addition to overt diabetes. Very high risk for abnormal glucose homeostasis among offspring with young age-of-onset maternal diabetes is consistent with hypotheses that perinatal exposures increase diabetes risk. Given equivalent risk ratios for type 2 diabetes, fathers may transmit unique paternal genetic factors of similar strength to maternal environmental factors." + }, + "questions": [ + { + "id": "b3fe0072-329d-447f-b64b-df1e90acd1df", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1871, + "text": "individuals with maternal diabetes" + }, + { + "answer_start": 1981, + "text": "paternal diabetes" + }, + { + "answer_start": 2061, + "text": "individuals with bilineal diabetes" + }, + { + "answer_start": 2410, + "text": "Offspring with maternal diabetes and an age of onset of \u003c50 years" + } + ] + } + ] +} \ No newline at end of file diff --git a/275c5f46-0e3e-4557-b9b6-084b1804f183.json b/275c5f46-0e3e-4557-b9b6-084b1804f183.json new file mode 100644 index 0000000000000000000000000000000000000000..191628579e4405455a1f206af66d788da9cc8b10 --- /dev/null +++ b/275c5f46-0e3e-4557-b9b6-084b1804f183.json @@ -0,0 +1,41 @@ +{ + "id": "275c5f46-0e3e-4557-b9b6-084b1804f183", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "22665546", + "text": "PURPOSE:\nColorectal carcinoma (CRC) has been described as a subsequent malignant neoplasm (SMN), although little is known about associated risk factors. We aimed to quantify the long-term risk of secondary CRC and identify treatment-related risk factors.\n\nPATIENTS AND METHODS:\nIn this nested case-control study, 19 cases of adenocarcinoma of the colon or rectum were identified from 13,048 oncology patients treated for childhood cancer at St Jude Children's Research Hospital. Group 1 controls (n = 148) were matched for age at primary malignancy and follow-up interval. Group 2 controls (n = 72) were matched on primary diagnosis in addition to group 1 criteria. Exact conditional logistic regression was performed to calculate odds ratios (ORs) for chemotherapy and radiation exposure.\n\nRESULTS:\nForty-year cumulative incidence of secondary CRC was 1.4%. Standardized incidence ratio was 10.9 (95% CI, 6.6 to 17.0) compared with that in the general US population. Secondary CRC was more likely in an irradiated segment of the colon (group 1 OR, 7.7; P = .001; group 2 OR, 15.4; P = .002). Risk increased by 70% with each 10-Gy increase in radiation dose. Increasing radiation volume increased risk (group 1 OR, 1.5; P \u003c .001; group 2 OR, 1.8; P \u003c .001). Alkylating agent exposure was associated with an 8.8-fold increased risk of secondary CRC (P = .03).\n\nCONCLUSION:\nIn matched analyses, radiation and alkylator exposure are associated with secondary CRC. This risk is proportional to dose and volume of radiation. Surveillance should be initiated at a young age among survivors receiving high-risk exposures." + }, + "questions": [ + { + "id": "56192c20-812d-4211-8b62-c58800d8957b", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1393, + "text": "radiation" + }, + { + "answer_start": 1407, + "text": "alkylator exposure" + } + ] + } + ] +} \ No newline at end of file diff --git a/278fcd4a-ef30-4708-86ac-5f5f2f2c0a5b.json b/278fcd4a-ef30-4708-86ac-5f5f2f2c0a5b.json new file mode 100644 index 0000000000000000000000000000000000000000..e29ed46b57e3e4f6af57c5c416038c2475112811 --- /dev/null +++ b/278fcd4a-ef30-4708-86ac-5f5f2f2c0a5b.json @@ -0,0 +1,45 @@ +{ + "id": "278fcd4a-ef30-4708-86ac-5f5f2f2c0a5b", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "31929014", + "text": "BACKGROUND:\nUlcerative colitis (UC) is a risk factor for colorectal cancer (CRC). However, available studies reflect older treatment and surveillance paradigms, and most have assessed risks for incident CRC without taking surveillance and lead-time bias into account, such as by assessing CRC incidence by tumour stage, or stage-adjusted mortality from CRC. We aimed to compare both overall and country-specific risks of CRC mortality and incident CRC among patients with UC.\n\nMETHODS:\nIn this population-based cohort study of 96 447 patients with UC in Denmark (n=32 919) and Sweden (n=63 528), patients were followed up for CRC incidence and CRC mortality between Jan 1, 1969, and Dec 31, 2017, and compared with matched reference individuals from the general population (n=949 207). Patients with UC were selected from national registers and included in the analysis if they had two or more records with a relevant International Classification of Disease in the patient register (in the country in question) or one such record plus a colorectal biopsy report with a morphology code suggestive of inflammatory bowel disease. For every patient with UC, we selected matched reference individuals from the total population registers of Denmark and Sweden, who were matched for sex, age, birth year, and place of residence. We used Cox regression to compute hazard ratios (HRs) for incident CRC, and for CRC mortality, taking tumour stage into account.\n\nFINDINGS:\nDuring follow-up, we observed 1336 incident CRCs in the UC cohort (1·29 per 1000 person-years) and 9544 incident CRCs in reference individuals (0·82 per 1000 person-years; HR 1·66, 95% CI 1·57-1·76). In the UC cohort, 639 patients died from CRC (0·55 per 1000 person-years), compared with 4451 reference individuals (0·38 per 1000 person-years; HR 1·59, 95% CI 1·46-1·72) during the same time period. The CRC stage distribution in people with UC was less advanced (p\u003c0·0001) than in matched reference individuals, but taking tumour stage into account, patients with UC and CRC remained at increased risk of CRC death (HR 1·54, 95% CI 1·33-1·78). The excess risks declined over calendar periods: during the last 5 years of follow-up (2013-17, Sweden only), the HR for incident CRC in people with UC was 1·38 (95% CI 1·20-1·60, or one additional case per 1058 patients with UC per 5 years) and the HR for death from CRC was 1·25 (95% CI 1·03-1·51, or one additional case per 3041 patients with UC per 5 years).\n\nINTERPRETATION:\nCompared with those without UC, individuals with UC are at increased risk of developing CRC, are diagnosed with less advanced CRC, and are at increased risk of dying from CRC, although these excess risks have declined substantially over time. There still seems to be room for improvement in international surveillance guidelines.\n\nFUNDING:\nThe Swedish Medical Society, Karolinska Institutet, Stockholm County Council, Swedish Research Council, Swedish Foundation for Strategic Research, Independent Research Fund Denmark, Forte Foundation, Swedish Cancer Foundation." + }, + "questions": [ + { + "id": "48e4fa82-838f-4230-9b79-b2a143252ac2", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 2245, + "text": "people with UC" + }, + { + "answer_start": 2520, + "text": "individuals with UC" + }, + { + "answer_start": 12, + "text": "Ulcerative colitis (UC)" + } + ] + } + ] +} \ No newline at end of file diff --git a/28657c0e-7e65-4db3-a070-4cc1ab60fe11.json b/28657c0e-7e65-4db3-a070-4cc1ab60fe11.json new file mode 100644 index 0000000000000000000000000000000000000000..ed04794a9257261e722c47f2a078cb74b5fb7b6f --- /dev/null +++ b/28657c0e-7e65-4db3-a070-4cc1ab60fe11.json @@ -0,0 +1,42 @@ +{ + "id": "28657c0e-7e65-4db3-a070-4cc1ab60fe11", + "disease": { + "id": "H00408", + "names": [ + "Type 1 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E10" + ], + "mesh": [ + "D003922" + ] + }, + "category": "Metabolic disease; Immune system disease; Endocrine disease" + }, + "article": { + "id": "23836309", + "text": "IMPORTANCE:\nThe incidence of type 1 diabetes mellitus (T1DM) is increasing worldwide, with the most rapid increase among children younger than 5 years of age.\n\nOBJECTIVE:\nTo examine the associations between perinatal and infant exposures, especially early infant diet, and the development of T1DM.\n\nDESIGN:\nThe Diabetes Autoimmunity Study in the Young (DAISY) is a longitudinal, observational study.\n\nSETTING:\nNewborn screening for human leukocyte antigen (HLA) was done at St. Joseph's Hospital in Denver, Colorado. First-degree relatives of individuals with T1DM were recruited from the Denver metropolitan area.\n\nPARTICIPANTS:\nA total of 1835 children at increased genetic risk for T1DM followed up from birth with complete prospective assessment of infant diet. Fifty-three children developed T1DM.\n\nEXPOSURES:\nEarly (\u003c4 months of age) and late (≥6 months of age) first exposure to solid foods compared with first exposures at 4 to 5 months of age (referent).\n\nMAIN OUTCOME AND MEASURE:\nRisk for T1DM diagnosed by a physician.\n\nRESULTS:\nBoth early and late first exposure to any solid food predicted development of T1DM (hazard ratio [HR], 1.91; 95% CI, 1.04-3.51, and HR, 3.02; 95% CI, 1.26-7.24, respectively), adjusting for the HLA-DR genotype, first-degree relative with T1DM, maternal education, and delivery type. Specifically, early exposure to fruit and late exposure to rice/oat predicted T1DM (HR, 2.23; 95% CI, 1.14-4.39, and HR, 2.88; 95% CI, 1.36-6.11, respectively), while breastfeeding at the time of introduction to wheat/barley conferred protection (HR, 0.47; 95% CI, 0.26-0.86). Complicated vaginal delivery was also a predictor of T1DM (HR, 1.93; 95% CI, 1.03-3.61).\n\nCONCLUSIONS AND RELEVANCE:\nThese results suggest the safest age to introduce solid foods in children at increased genetic risk for T1DM is between 4 and 5 months of age. Breastfeeding while introducing new foods may reduce T1DM risk." + }, + "questions": [ + { + "id": "c948e34c-c710-44b5-87af-a75521723eae", + "text": "What are the risk factors of Type 1 diabetes mellitus?", + "answers": [ + { + "answer_start": 1041, + "text": "Both early and late first exposure to any solid food predicted development of T1DM" + }, + { + "answer_start": 1338, + "text": "early exposure to fruit and late exposure to rice/oat predicted T1DM" + }, + { + "answer_start": 1601, + "text": "Complicated vaginal delivery was also a predictor of T1DM" + } + ] + } + ] +} \ No newline at end of file diff --git a/2869cc96-1a8e-4aa6-a14c-0cfe619bb817.json b/2869cc96-1a8e-4aa6-a14c-0cfe619bb817.json new file mode 100644 index 0000000000000000000000000000000000000000..3a2a0a6270358038a1bd2e95ef5d8300cb37fedb --- /dev/null +++ b/2869cc96-1a8e-4aa6-a14c-0cfe619bb817.json @@ -0,0 +1,52 @@ +{ + "id": "2869cc96-1a8e-4aa6-a14c-0cfe619bb817", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "26634245", + "text": "BACKGROUND:\nPulmonary function decline is a major contributor to morbidity and mortality among smokers. Post bronchodilator FEV1 and FEV1/FVC ratio are considered the standard assessment of airflow obstruction. We performed a genome-wide association study (GWAS) in 9919 current and former smokers in the COPDGene study (6659 non-Hispanic Whites [NHW] and 3260 African Americans [AA]) to identify associations with spirometric measures (post-bronchodilator FEV1 and FEV1/FVC). We also conducted meta-analysis of FEV1 and FEV1/FVC GWAS in the COPDGene, ECLIPSE, and GenKOLS cohorts (total n = 13,532).\n\nRESULTS:\nAmong NHW in the COPDGene cohort, both measures of pulmonary function were significantly associated with SNPs at the 15q25 locus [containing CHRNA3/5, AGPHD1, IREB2, CHRNB4] (lowest p-value = 2.17 × 10(-11)), and FEV1/FVC was associated with a genomic region on chromosome 4 [upstream of HHIP] (lowest p-value = 5.94 × 10(-10)); both regions have been previously associated with COPD. For the meta-analysis, in addition to confirming associations to the regions near CHRNA3/5 and HHIP, genome-wide significant associations were identified for FEV1 on chromosome 1 [TGFB2] (p-value = 8.99 × 10(-9)), 9 [DBH] (p-value = 9.69 × 10(-9)) and 19 [CYP2A6/7] (p-value = 3.49 × 10(-8)) and for FEV1/FVC on chromosome 1 [TGFB2] (p-value = 8.99 × 10(-9)), 4 [FAM13A] (p-value = 3.88 × 10(-12)), 11 [MMP3/12] (p-value = 3.29 × 10(-10)) and 14 [RIN3] (p-value = 5.64 × 10(-9)).\n\nCONCLUSIONS:\nIn a large genome-wide association study of lung function in smokers, we found genome-wide significant associations at several previously described loci with lung function or COPD. We additionally identified a novel genome-wide significant locus with FEV1 on chromosome 9 [DBH] in a meta-analysis of three study populations." + }, + "questions": [ + { + "id": "5b674752-e44f-459c-a205-202571b28071", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 716, + "text": "SNPs at the 15q25 locus [containing CHRNA3/5, AGPHD1, IREB2, CHRNB4]" + }, + { + "answer_start": 873, + "text": "chromosome 4 [upstream of HHIP]" + }, + { + "answer_start": 1078, + "text": "CHRNA3/5 and HHIP" + }, + { + "answer_start": 1162, + "text": "chromosome 1 [TGFB2]" + }, + { + "answer_start": 1308, + "text": "chromosome 1 [TGFB2]" + } + ] + } + ] +} \ No newline at end of file diff --git a/288b47dc-c7cd-43e0-b208-b92081523e88.json b/288b47dc-c7cd-43e0-b208-b92081523e88.json new file mode 100644 index 0000000000000000000000000000000000000000..7cf0e68be8a79365c77f405c315986b622221933 --- /dev/null +++ b/288b47dc-c7cd-43e0-b208-b92081523e88.json @@ -0,0 +1,34 @@ +{ + "id": "288b47dc-c7cd-43e0-b208-b92081523e88", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "18311140", + "text": "Our genome-wide association study of celiac disease previously identified risk variants in the IL2-IL21 region. To identify additional risk variants, we genotyped 1,020 of the most strongly associated non-HLA markers in an additional 1,643 cases and 3,406 controls. Through joint analysis including the genome-wide association study data (767 cases, 1,422 controls), we identified seven previously unknown risk regions (P \u003c 5 x 10(-7)). Six regions harbor genes controlling immune responses, including CCR3, IL12A, IL18RAP, RGS1, SH2B3 (nsSNP rs3184504) and TAGAP. Whole-blood IL18RAP mRNA expression correlated with IL18RAP genotype. Type 1 diabetes and celiac disease share HLA-DQ, IL2-IL21, CCR3 and SH2B3 risk regions. Thus, this extensive genome-wide association follow-up study has identified additional celiac disease risk variants in relevant biological pathways." + }, + "questions": [ + { + "id": "a2b34128-b54d-473e-b0b4-e608ad189be8", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 676, + "text": "HLA-DQ, IL2-IL21, CCR3 and SH2B3 risk regions" + } + ] + } + ] +} \ No newline at end of file diff --git a/28aac8ba-02d7-4042-93d7-8f95a55ea304.json b/28aac8ba-02d7-4042-93d7-8f95a55ea304.json new file mode 100644 index 0000000000000000000000000000000000000000..956556cf3c72c5fab6ea536e8fc8a419458e80da --- /dev/null +++ b/28aac8ba-02d7-4042-93d7-8f95a55ea304.json @@ -0,0 +1,49 @@ +{ + "id": "28aac8ba-02d7-4042-93d7-8f95a55ea304", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "7749056", + "text": "Some factors related to Westernization or industrialization increase risk of colon cancer. It is believed widely that this increase in risk is related to the direct effects of dietary fat and fiber in the colonic lumen. However, the fat and fiber hypotheses, at least as originally formulated, do not explain adequately many emerging findings from recent epidemiologic studies. An alternative hypothesis, that hyperinsulinemia promotes colon carcinogenesis, is presented here. Insulin is an important growth factor of colonic epithelial cells and is a mitogen of tumor cell growth in vitro. Epidemiologic evidence supporting the insulin/colon-cancer hypothesis is largely indirect and based on the similarity of factors which produce elevated insulin levels with those related to colon cancer risk. Specifically, obesity--particularly central obesity, physical inactivity, and possibly a low dietary polyunsaturated fat to saturated fat ratio--are major determinants of insulin resistance and hyperinsulinemia, and appear related to colon cancer risk. Moreover, a diet high in refined carbohydrates and low in water-soluble fiber, which is associated with an increased risk of colon cancer, causes rapid intestinal absorption of glucose into the blood leading to postprandial hyperinsulinemia. The combination of insulin resistance and high glycemic load produces particularly high insulin levels. Thus, hyperinsulinemia may explain why obesity, physical inactivity, and a diet low in fruits and vegetables and high in red meat and extensively processed foods, all common in the West, increase colon cancer risk." + }, + "questions": [ + { + "id": "c0d847cd-3b8e-4ec7-a250-2d258f1d5cfb", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1404, + "text": "hyperinsulinemia" + }, + { + "answer_start": 1437, + "text": "obesity" + }, + { + "answer_start": 1446, + "text": "physical inactivity" + }, + { + "answer_start": 1473, + "text": "diet low in fruits and vegetables and high in red meat and extensively processed foods" + } + ] + } + ] +} \ No newline at end of file diff --git a/28c646a7-2833-429f-89c1-611f2d1d6eaa.json b/28c646a7-2833-429f-89c1-611f2d1d6eaa.json new file mode 100644 index 0000000000000000000000000000000000000000..0cda7449faac12f1cffafe0e21aa778130cc2d4d --- /dev/null +++ b/28c646a7-2833-429f-89c1-611f2d1d6eaa.json @@ -0,0 +1,37 @@ +{ + "id": "28c646a7-2833-429f-89c1-611f2d1d6eaa", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "8514030", + "text": "BACKGROUND:\nOver 60 studies have addressed the hypothesis that the risk of colorectal cancer is increased following cholecystectomy; these studies have yielded inconsistent findings. The aim of the present study was to quantitatively summarize the results from the collective studies.\n\nMETHODS:\nA meta-analysis of the published studies addressing the relation between cholecystectomy and colorectal cancer was conducted.\n\nRESULTS:\nThe combined results from 33 case-control studies showed an association between cholecystectomy and risk of colorectal cancer (pooled relative risk [RR] = 1.34; 95% confidence interval [CI] = 1.14-1.57), particularly when limited to the proximal colon (RR = 1.88; 95% CI = 1.54-2.30). In most studies, the risk was stronger when the first 5-15 years following the surgery were excluded. The results from 6 cohort studies, with follow-up to approximately 15 years postcholecystectomy, were generally null (RR = 0.97; 95% CI = 0.82-1.14). A more limited body of evidence suggests that cholelithiasis is related to an elevated risk of proximal colon cancer.\n\nCONCLUSIONS:\nBecause the risks varied substantially by study design and because time since cholecystectomy or potentially confounding factors were often not considered, we could not firmly quantitate this risk. However, the findings are consistent with other evidence that suggests some characteristic of bile acid metabolism increases the risk of cancer of the proximal colon." + }, + "questions": [ + { + "id": "a7046007-9554-43a2-973f-b319d33dfb42", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 511, + "text": "cholecystectomy" + } + ] + } + ] +} \ No newline at end of file diff --git a/2a5bd282-cc00-459e-baa6-1253f88215e4.json b/2a5bd282-cc00-459e-baa6-1253f88215e4.json new file mode 100644 index 0000000000000000000000000000000000000000..aa28fe87f72b322b07c75529535b7acef65eace9 --- /dev/null +++ b/2a5bd282-cc00-459e-baa6-1253f88215e4.json @@ -0,0 +1,43 @@ +{ + "id": "2a5bd282-cc00-459e-baa6-1253f88215e4", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "20142267", + "text": "BACKGROUND:\nEpidemiological studies have suggested that female hormones might play a role in asthma and that menopausal hormone therapy (MHT or hormone replacement therapy (HRT)) might increase the risk of asthma in postmenopausal women. The only prospective study addressing this issue reports an increase in the risk of developing asthma which was similar for oestrogen alone and oestrogen/progestagen treatment.\n\nMETHODS:\nThe association between the use of different types of MHT and the risk of asthma onset in postmenopausal women was investigated prospectively from 1990 to 2002 by biennial questionnaires as part of the French E3N cohort study. Asthma onset was considered to be the time of medical diagnosis of asthma cases occurring during the follow-up of women who were asthma free at baseline. Cox proportional hazards models were used, adjusting for potential confounding factors.\n\nRESULTS:\nAmong 57 664 women free of asthma at menopause, 569 incident cases of asthma were identified during 495 448 years of follow-up. MHT was related to an increased risk of asthma onset (HR=1.20, 95% CI 0.98 to 1.46) among recent users. The increase in risk of asthma onset was only significant among women reporting the use of oestrogen alone (HR=1.54, 95% CI 1.13 to 2.09) particularly in never smokers (HR=1.80, 95% CI 1.15 to 2.80) and women reporting allergic disease prior to asthma onset (HR=1.86, 95% CI 1.18 to 2.93). A small increase in the risk of asthma onset associated with the use of oestrogen/progestagen was also observed in these subgroups.\n\nCONCLUSION:\nPostmenopausal use of oestrogen alone was associated with an increased rate of newly diagnosed asthma in menopausal women." + }, + "questions": [ + { + "id": "cad33623-21f9-45b6-a8b3-6887f0890734", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1571, + "text": "Postmenopausal use of oestrogen alone" + }, + { + "answer_start": 1491, + "text": "use of oestrogen/progestagen" + }, + { + "answer_start": 1200, + "text": "women reporting the use of oestrogen alone" + } + ] + } + ] +} \ No newline at end of file diff --git a/2b2634a5-32c2-47a3-9662-e69ed8daa81d.json b/2b2634a5-32c2-47a3-9662-e69ed8daa81d.json new file mode 100644 index 0000000000000000000000000000000000000000..c488c5520d5a5e83ede7b2b1816dcd8185e75948 --- /dev/null +++ b/2b2634a5-32c2-47a3-9662-e69ed8daa81d.json @@ -0,0 +1,36 @@ +{ + "id": "2b2634a5-32c2-47a3-9662-e69ed8daa81d", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "20870755", + "text": "RATIONALE:\nShort-term exposure to air pollution has been associated with exacerbation of chronic obstructive pulmonary disease (COPD), whereas the role of long-term exposures on the development of COPD is not yet fully understood.\n\nOBJECTIVES:\nWe assessed the effect of exposure to traffic-related air pollution over 35 years on the incidence of COPD in a prospective cohort study.\n\nMETHODS:\nWe followed 57,053 participants in the Danish Diet, Cancer, and Health cohort in the Hospital Discharge Register for their first hospital admission for COPD between 1993 and 2006. We estimated the annual mean levels of nitrogen dioxide (NO₂) and nitrogen oxides (NO(x)) at all residential addresses of the cohort participants since 1971 to an event or 2006 and used indicators of traffic near the residential address at recruitment. We assessed the association between exposure to air pollution and COPD incidence by Cox regression analyses for the full cohort, and for participants with and without comorbid conditions, including asthma, diabetes, or cardiovascular disease.\n\nMEASUREMENTS AND MAIN RESULTS:\nA first hospital admission for COPD was recorded for 1,786 (3.4%) of 52,799 eligible subjects between recruitment (1993-1997) and 2006. COPD incidence was associated with the 35-year mean NO₂ level (hazard ratio, 1.08; 95% confidence interval, 1.02-1.14, per interquartile range of 5.8 μg/m³), with stronger associations in subjects with diabetes (1.29; 1.05-1.50) and asthma (1.19; 1.03-1.38).\n\nCONCLUSIONS:\nLong-term exposure to traffic-related air pollution may contribute to the development of COPD with possibly enhanced susceptibility in people with diabetes and asthma." + }, + "questions": [ + { + "id": "508f65eb-e65d-4672-afad-4ea0c38720ea", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 1509, + "text": "Long-term exposure to traffic-related air pollution" + } + ] + } + ] +} \ No newline at end of file diff --git a/2b46e80a-eccd-4f4f-a5f3-e45c4e2d1551.json b/2b46e80a-eccd-4f4f-a5f3-e45c4e2d1551.json new file mode 100644 index 0000000000000000000000000000000000000000..f19bda71f59df40041f94f6b21a6d57053cb84a9 --- /dev/null +++ b/2b46e80a-eccd-4f4f-a5f3-e45c4e2d1551.json @@ -0,0 +1,38 @@ +{ + "id": "2b46e80a-eccd-4f4f-a5f3-e45c4e2d1551", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "21087481", + "text": "INTRODUCTION:\nBreast cancer is frequently a hormonally dependent cancer, and associations of circulating estrogens and androgens with subsequent breast cancer risk are well established in postmenopausal women. Associations of serum estrogens and androgens with breast cancer risk in premenopausal women are less well studied. The objective of this study was to determine whether estradiol and testosterone levels in serum collected before menopause are associated with subsequent breast cancer risk.\n\nMETHODS:\nWe conducted a prospective case-control study of 266 participants who were registered in the Columbia, Missouri, Serum Bank and not using exogenous hormones at the time of blood collection. Each of 98 in situ or invasive breast cancer cases with prediagnostic serum collected before menopause was matched to two controls by age, date, menstrual cycle day, and time of day of blood collection. Estradiol and testosterone concentrations were quantified by using specific radioimmunoassays, and sex hormone-binding globulin (SHBG) was quantified with a chemiluminescent immunoassay to allow calculation of the non-SHBG bound hormone fractions. Data were analyzed by using conditional logistic regression. All tests of statistical significance were two-sided.\n\nRESULTS:\nSerum testosterone was strongly and significantly associated with breast cancer risk. The relative odds (OR) for increasing quartiles of total testosterone were 1.0, 2.1 (95% confidence interval (CI) 0.9 to 4.8), 1.5 (95% CI, 0.6 to 3.4), and 3.3 (95% CI, 1.5 to 7.5, P(trend) = 0.006). Comparable ORs for the non-SHBG bound fraction of testosterone that is bioavailable were 1.0, 1.7 (95% CI, 0.7 to 4.2), 1.7 (95% CI, 0.7 to 4.0), and 4.2 (95% CI, 1.6 to 10.9, P(trend) = 0.002). Total and non-SHBG-bound estradiol were not associated with breast cancer, but extreme variation in levels across the menstrual cycle coupled with relatively small numbers, particularly for analyses stratified by cycle phase, limited the power to detect associations.\n\nCONCLUSIONS:\nResults suggest that premenopausal women with elevated serum testosterone levels are at an increased risk of breast cancer." + }, + "questions": [ + { + "id": "5d2ec68b-0fa5-44d0-95c5-e92bdb66c401", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1276, + "text": "Serum testosterone" + }, + { + "answer_start": 2086, + "text": "elevated serum testosterone levels" + } + ] + } + ] +} \ No newline at end of file diff --git a/2b60a44c-6ee0-4d15-abaa-0a8f76101be5.json b/2b60a44c-6ee0-4d15-abaa-0a8f76101be5.json new file mode 100644 index 0000000000000000000000000000000000000000..f353a73569d14ceab3ef38c4d78a1635175791e4 --- /dev/null +++ b/2b60a44c-6ee0-4d15-abaa-0a8f76101be5.json @@ -0,0 +1,39 @@ +{ + "id": "2b60a44c-6ee0-4d15-abaa-0a8f76101be5", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "21972241", + "text": "BACKGROUND:\nAs rheumatoid arthritis (RA) occurs more often in women than in men, it has been suggested that reproductive hormones may play an important role in the pathogenesis.\n\nMETHODS:\nBetween 1991 and 1996, 30 447 subjects (18 326 women) were included in a community-based health survey. Information on female hormonal changes and stress-related factors was obtained using a self-administered questionnaire. This population was linked to four different local and national RA registers. The medical records for patients with a diagnosis of RA were subjected to a structured review and all women with incident RA according to the 1987 American College of Rheumatology criteria after inclusion in the health survey were included in a nested case-control study. Matched controls (1:4) were selected from the health survey population.\n\nRESULTS:\nEarly age at menopause (≤45 years) was associated with the subsequent development of RA (OR 2.42, 95% CI 1.32 to 4.45). The effect of early menopause remained significant after adjusting for smoking, level of education and length of breastfeeding (OR 1.92, 95% CI 1.02 to 3.64)\n\nCONCLUSION:\nRA was predicted by an early age at menopause. This implicates an influence of hormonal changes during the fertile period on the development of RA in postmenopausal women." + }, + "questions": [ + { + "id": "160afdf5-cbbf-4bcd-8180-11401969a9b9", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 844, + "text": "Early age at menopause (≤45 years" + }, + { + "answer_start": 1158, + "text": "early age at menopause" + } + ] + } + ] +} \ No newline at end of file diff --git a/2ba3e950-edb6-46f7-b97a-c8e194596347.json b/2ba3e950-edb6-46f7-b97a-c8e194596347.json new file mode 100644 index 0000000000000000000000000000000000000000..22d727e9de7f946e4a0f9253e5519c197c375455 --- /dev/null +++ b/2ba3e950-edb6-46f7-b97a-c8e194596347.json @@ -0,0 +1,34 @@ +{ + "id": "2ba3e950-edb6-46f7-b97a-c8e194596347", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "4010740", + "text": "We investigated the use of analgesics containing phenacetin or acetaminophen in 173 young women with urinary bladder cancer and 173 matched controls. The cases, who were 20 to 49 years old at the time of diagnosis of cancer, were 6.5 times more likely to report regular use of analgesics containing phenacetin at least one year before diagnosis than were their matched controls (odds ratio, 6.5; 95 per cent confidence interval, 1.5 to 59.2). Among the 15 women (13 cases and 2 controls) reporting regular use of phenacetin-containing drugs, 8 of the cases and 1 of the controls reported daily use for over one year (P = 0.04). Excessive use of analgesics containing acetaminophen was not reported. The increased risk of bladder cancer in young women who regularly used phenacetin-containing products remained present after adjustments for all other identified risk factors." + }, + "questions": [ + { + "id": "967cd4bb-f59a-405a-ae7d-783d28c4b7e9", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 739, + "text": "young women who regularly used phenacetin-containing products" + } + ] + } + ] +} \ No newline at end of file diff --git a/2be347d4-4dd0-4efa-8356-64af3f8f12cd.json b/2be347d4-4dd0-4efa-8356-64af3f8f12cd.json new file mode 100644 index 0000000000000000000000000000000000000000..5d26f625676b75bad2029d6cd8dfa1409674a9d5 --- /dev/null +++ b/2be347d4-4dd0-4efa-8356-64af3f8f12cd.json @@ -0,0 +1,39 @@ +{ + "id": "2be347d4-4dd0-4efa-8356-64af3f8f12cd", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "21036953", + "text": "The present study explores the effect of age at menarche on the incidence of asthma during early adulthood. The analysis was based on Canadian girls followed up from 8-11 to 18-21 years of age during the first 6 cycles (1994-2005) of the National Longitudinal Survey of Children and Youth. Early menarche was defined as 1 standard deviation less than the average age at menarche. Asthma occurrence after menarche was measured as asthma that was diagnosed by a health care professional. The authors used logistic regression to investigate the association between early menarche and incidence of asthma, adjusting for possible confounders. A total of 1,176 girls weighted to represent 352,345 Canadian girls were analyzed. The incidence of asthma after menarche was 11.2% (95% confidence interval: 8.3, 14.0). The onset of early menarche (\u003c11.56 years of age) predicted postmenarcheal incidence of asthma; girls who matured early had more than twice the risk of developing asthma during early adulthood than did girls who matured at an average age (odds ratio, 2.34, 95% confidence interval: 1.19, 4.59). The present study provides partial insight into the worldwide rapid increase in asthma rates that coincides with the declining trends in menarcheal timing. Further studies within different contexts are warranted to assess the generalizability of these Canadian findings." + }, + "questions": [ + { + "id": "7109c404-9058-4bb0-a612-a13e87974e60", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 808, + "text": "The onset of early menarche (\u003c11.56 years of age)" + }, + { + "answer_start": 904, + "text": "girls who matured early" + } + ] + } + ] +} \ No newline at end of file diff --git a/2c2961d8-de82-4697-b9ce-bebb4e31f269.json b/2c2961d8-de82-4697-b9ce-bebb4e31f269.json new file mode 100644 index 0000000000000000000000000000000000000000..bacf333e9dbcffd0959c673c86c7e4734910cd75 --- /dev/null +++ b/2c2961d8-de82-4697-b9ce-bebb4e31f269.json @@ -0,0 +1,34 @@ +{ + "id": "2c2961d8-de82-4697-b9ce-bebb4e31f269", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "12827008", + "text": "BACKGROUND:\nThe prevalence of celiac disease (CD) in children with diabetes mellitus type 1 (DM) is significantly higher than in the nondiabetic population. Most patients with DM and associated CD do not experience typical gastrointestinal symptoms of CD. There is no agreement on the necessity of screening and management of silent CD for patients with DM or on the time scale for screening. Only few data on follow-up evaluation of children with DM and CD-related antibodies are available.\n\nMETHODS:\nOne hundred fifty-seven patients with DM (mean age, 14.8 years; range, 4-21 years; male, 83) were screened with endomysial antibodies (EMA) between 1993 and 2001. A follow-up period of at least 3 years, with at least 2 EMA measurements, was possible. Group 1 comprised 37 patients whose first measurement was at the onset of DM. Group 2 comprised 120 patients whose first measurement was during the course of the disease. In patients with positive EMA, small bowel biopsy was performed. Thyroid peroxidase (TPO), thyroglobulin (TgA), glutamate decarboxylase (GAD), antiinsulin (IAA), and islet cell antibodies (IA2) were measured in all patients.\n\nRESULTS:\nEMA was positive in 16 patients, in 5 at onset of DM and in 11 during the course of DM (mean duration, 33.6 months; range, 11-105 months). Biopsy results showed normal mucosa in seven patients, increased intraepithelial lymphocyte counts in one, and flat mucosa in eight. There was no significant difference between EMA-positive and EMA-negative patients regarding height, weight, HbA1c level, frequency of hypoglycemia or hyperglycemia, TPO, TgA, GAD, IAA, or IA2.\n\nCONCLUSION:\nThis study emphasizes the high prevalence of CD in patients with DM. Although several patients already had positive EMA titers at the onset of DM, seroconversion may also occur during the course of the disease. Screening for CD with EMA or tissue transglutaminase should be included in the initial investigation of DM, but should also be repeated over time to detect late seroconversion." + }, + "questions": [ + { + "id": "bc753516-7873-47ad-84b0-be10f1f95053", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 53, + "text": "children with diabetes mellitus type 1 (DM)" + } + ] + } + ] +} \ No newline at end of file diff --git a/2ce8b6f5-8f36-43f4-8c0b-aeafb44e17d6.json b/2ce8b6f5-8f36-43f4-8c0b-aeafb44e17d6.json new file mode 100644 index 0000000000000000000000000000000000000000..77415dc9797d9f0f12284b890388d11d64febbb1 --- /dev/null +++ b/2ce8b6f5-8f36-43f4-8c0b-aeafb44e17d6.json @@ -0,0 +1,42 @@ +{ + "id": "2ce8b6f5-8f36-43f4-8c0b-aeafb44e17d6", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "17671226", + "text": "Cigarette smoking is a major risk factor for bladder cancer and a prominent point source of 4-aminobiphenyl (4-ABP), a recognized human bladder carcinogen. 4-ABP-hemoglobin (Hb) adducts are established biomarkers of 4-ABP exposure in humans. The role of environmental tobacco smoke (ETS) in the etiology of bladder cancer is largely unknown. As part of a large population-based bladder cancer study in Los Angeles County, California, lifetime exposure to ETS was ascertained for 148 cases and 292 control subjects who had never used any tobacco products over their lifetime. 4-ABP-Hb adducts were quantitatively measured on 230 control subjects. Female lifelong nonsmokers living with two or more smokers during childhood were significantly related to risk of bladder cancer [odds ratio (OR), 3.08; 95% confidence interval (95% CI), 1.16-8.22]. During adulthood, approximately 2-fold risks were seen among women living with a spouse/domestic partner who smoked for \u003e or =10 years or having a coworker who smoked in an indoor environment for \u003e or =10 years. When all sources of ETS exposure were combined, a statistically significant, dose-dependent association (P for trend = 0.03) was noted in women, with the OR for the highest category of ETS exposure being 5.48 (95% CI, 1.06-28.36). Levels of 4-ABP-Hb adducts varied by ETS exposure status among female control subjects. Mean level was lowest in women never exposed to ETS (16.4 pg/g Hb) and highest in those with current ETS exposure (23.6 pg/g Hb). ETS exposure was associated with neither bladder cancer risk nor 4-ABP-Hb adduct levels in male lifelong nonsmokers. In conclusion, ETS is a risk factor for bladder cancer in women who were lifelong nonusers of any tobacco products." + }, + "questions": [ + { + "id": "c026d435-5fa3-4abd-9436-21f7f0e41a3b", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 646, + "text": "Female lifelong nonsmokers living with two or more smokers during childhood" + }, + { + "answer_start": 906, + "text": "women living with a spouse/domestic partner who smoked for \u003e or =10 years or having a coworker who smoked in an indoor environment for \u003e or =10 years" + }, + { + "answer_start": 254, + "text": "environmental tobacco smoke (ETS" + } + ] + } + ] +} \ No newline at end of file diff --git a/2cf49b09-fb68-4e3d-8493-402bd1d64cf5.json b/2cf49b09-fb68-4e3d-8493-402bd1d64cf5.json new file mode 100644 index 0000000000000000000000000000000000000000..bb6cae8547733f21039b044dcbf121f928836858 --- /dev/null +++ b/2cf49b09-fb68-4e3d-8493-402bd1d64cf5.json @@ -0,0 +1,34 @@ +{ + "id": "2cf49b09-fb68-4e3d-8493-402bd1d64cf5", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "11036120", + "text": "BACKGROUND:\nChronic inflammation is believed to increase the risk of coronary events by making atherosclerotic plaques in coronary vessels prone to rupture. We examined blood constituents potentially affected by inflammation as predictors of risk in men with hypercholesterolemia who were enrolled in the West of Scotland Coronary Prevention Study, a trial that evaluated the value of pravastatin in the prevention of coronary events.\n\nMETHODS:\nA total of 580 men who had had a coronary event (nonfatal myocardial infarction, death from coronary heart disease, or a revascularization procedure) were each matched for age and smoking status with 2 control subjects (total, 1160) from the same cohort who had not had a coronary event. Lipoprotein-associated phospholipase A2, C-reactive protein, and fibrinogen levels, and the white-cell count were measured at base line, along with other traditional risk factors. The association of these variables with the risk of coronary events was tested in regression models and by dividing the range of values according to quintiles.\n\nRESULTS:\nLevels of C-reactive protein, the white-cell count, and fibrinogen levels were strong predictors of the risk of coronary events; the risk in the highest quintile of the study cohort for each variable was approximately twice that in the lowest quintile. However, the association of these variables with risk was markedly attenuated when age, systolic blood pressure, and lipoprotein levels were included in multivariate models. Levels of lipoprotein-associated phospholipase A2 (platelet-activating factor acetylhydrolase), the expression of which is regulated by mediators of inflammation, had a strong, positive association with risk that was not confounded by other factors. It was associated with almost a doubling of the risk in the highest quintile as compared with the lowest quintile.\n\nCONCLUSIONS:\nInflammatory markers are predictors of the risk of coronary events, but their predictive ability is attenuated by associations with other coronary risk factors. Elevated levels of lipoprotein-associated phospholipase A2 appear to be a strong risk factor for coronary heart disease, a finding that has implications for atherogenesis and the assessment of risk." + }, + "questions": [ + { + "id": "6de0c3a3-4460-486f-9c78-9bff77596cd2", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 2050, + "text": "Elevated levels of lipoprotein-associated phospholipase A2" + } + ] + } + ] +} \ No newline at end of file diff --git a/2db2f7c3-c212-4a14-8cae-3274792b8fc2.json b/2db2f7c3-c212-4a14-8cae-3274792b8fc2.json new file mode 100644 index 0000000000000000000000000000000000000000..1c8a979263bcbe688c43e26d56f9dff6b5187eeb --- /dev/null +++ b/2db2f7c3-c212-4a14-8cae-3274792b8fc2.json @@ -0,0 +1,38 @@ +{ + "id": "2db2f7c3-c212-4a14-8cae-3274792b8fc2", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "11696721", + "text": "PURPOSE:\nWe analyzed the risk of bladder cancer in offspring according to parental and sibling cancer using the national Swedish Family Cancer Database.\n\nMATERIALS AND METHODS:\nCancer data were obtained from the Swedish Cancer Registry for 1958 to 1996, including 2,105 cases of bladder cancer in offspring. The standardized incidence ratio was used to measure cancer risk in offspring according to familial cancer status.\n\nRESULTS:\nThe incidence ratio of bladder cancer increased in Sweden from 1958 to 1996 and it was 3 to 4-fold higher in males than in females. We identified 65 families in which the parents and offspring had bladder cancer with a familial risk of 1.35 (95% confidence interval [CI] 0.97 to 1.79) in sons and 2.29 (95% CI 1.46 to 3.29) in daughters. Discordant cancer sites associated with bladder cancer in the 2 generations were the kidney and thyroid with a standardized incidence ratio of 1.58 (95% CI 1.18 to 2.05) and 1.89 (95% CI 1.00 to 3.05), respectively. Sibling risk was higher compared with offspring risk with a standardized incidence ratio of 2.96 (95% CI 1.41 to 5.08) and in males there was a statistically significant ratio of sibling-to-offspring risk of 2.66 (95% CI 1.29 to 5.45). Patient age at onset modified the familial risk. The highest familial risk of 7.26 (95% CI 2.61 to 14.24) was observed in the brothers of bladder cancer probands diagnosed before age 45 years.\n\nCONCLUSIONS:\nThe relatively high ratio of sibling-to-offspring risk as well as observed gender specific effects in bladder cancer may reflect an X linked susceptibility gene." + }, + "questions": [ + { + "id": "d0291bbb-e4d2-4341-b8be-c98ee0b8eb10", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 1166, + "text": "sibling-to-offspring" + }, + { + "answer_start": 1349, + "text": "brothers of bladder cancer probands diagnosed before age 45 years" + } + ] + } + ] +} \ No newline at end of file diff --git a/2dd6257c-a6d3-4094-98e5-c144825571b3.json b/2dd6257c-a6d3-4094-98e5-c144825571b3.json new file mode 100644 index 0000000000000000000000000000000000000000..7d65bd7303c558161f0e0a92c9eb33cee41b49c0 --- /dev/null +++ b/2dd6257c-a6d3-4094-98e5-c144825571b3.json @@ -0,0 +1,34 @@ +{ + "id": "2dd6257c-a6d3-4094-98e5-c144825571b3", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "16697804", + "text": "PURPOSE:\nWe reviewed the clinical course of patients in whom urothelial carcinoma developed following radiation therapy for prostate cancer.\n\nMATERIALS AND METHODS:\nA retrospective review of all patients between 1990 and 2005 with the diagnosis of bladder and prostate cancer was performed. Of 125 total patients new onset urothelial carcinoma developed in 11 after undergoing external beam radiation therapy for prostate cancer.\n\nRESULTS:\nWhole pelvis external beam radiation therapy with a proton boost to the prostate was the radiation modality in 7 of the 11 patients (64%), while the remaining 4 patients received standard external beam radiation only. Urothelial carcinoma was detected a mean of 3.07 years after completion of radiation therapy in the proton group, compared to a mean latency period of 5.75 years in the standard radiation group (p = 0.09). Average patient age at diagnosis was 72 years (range 64 to 84). All patients presented with gross hematuria and had cystoscopic findings of coexisting radiation cystitis. Of the 11 patients 5 (45%) presented with grade 3 carcinoma and eventually 7 (64%) required radical cystectomy. Urothelial tumors with sarcomatoid features (carcinosarcoma and spindle cell sarcomatoid) developed in 2 patients (18%). Of the 11 patients 10 (91%) were nonsmokers at the time of urothelial carcinoma diagnosis.\n\nCONCLUSIONS:\nUrothelial carcinoma in patients with previous radiation therapy for prostate cancer is often high grade, and the majority of patients have cancer progression requiring cystectomy. A high incidence of urothelial carcinoma with sarcomatoid features was seen in these patients." + }, + "questions": [ + { + "id": "d6349d42-21fc-44a1-8153-cfb31c294fdd", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 1397, + "text": "patients with previous radiation therapy for prostate cancer" + } + ] + } + ] +} \ No newline at end of file diff --git a/2e56eb11-2f59-4d76-a67b-c5822cf610b3.json b/2e56eb11-2f59-4d76-a67b-c5822cf610b3.json new file mode 100644 index 0000000000000000000000000000000000000000..88661ed364bc11e32508ffef4f92a5920a5fc36f --- /dev/null +++ b/2e56eb11-2f59-4d76-a67b-c5822cf610b3.json @@ -0,0 +1,34 @@ +{ + "id": "2e56eb11-2f59-4d76-a67b-c5822cf610b3", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "17031696", + "text": "BACKGROUND:\nCigarette smoking causes about 30% of all cancer mortality in developed countries. Although smoking is decreasing in developed countries, it is increasing in some developing countries.\n\nDISCUSSION:\nCigarette smoke contains over 60 well established carcinogens. There are strong links between some of these carcinogens and various types of smoking-induced cancers. Mechanisms by which cigarette smoke carcinogens cause cancer are well established and are discussed here.\n\nCONCLUSIONS:\nA great deal is known about cigarette smoke carcinogens and the mechanisms by which they cause cancer. It is hoped that this will provide new insights for the prevention and cure of tobacco-induced cancer." + }, + "questions": [ + { + "id": "9f4205aa-d2a9-4d6a-8fbd-7710b65bdaf4", + "text": "What are the risk factors of Bladder Cancer?", + "answers": [ + { + "answer_start": 12, + "text": "Cigarette smoking" + } + ] + } + ] +} \ No newline at end of file diff --git a/2e6ebaec-a3c5-406e-b277-a36fba8afb85.json b/2e6ebaec-a3c5-406e-b277-a36fba8afb85.json new file mode 100644 index 0000000000000000000000000000000000000000..64354d970379193fae233c8cdb9d91b5ba0358b2 --- /dev/null +++ b/2e6ebaec-a3c5-406e-b277-a36fba8afb85.json @@ -0,0 +1,35 @@ +{ + "id": "2e6ebaec-a3c5-406e-b277-a36fba8afb85", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "23941287", + "text": "BACKGROUND:\nChildhood asthma and obesity prevalence have increased in recent years suggesting a potential association. However, the direction of any association is poorly understood and the potential causal-relationship is unknown.\n\nMETHODS:\nWe examined the association between overweight/obesity, defined by body mass index (BMI) \u003c18 years of age, and subsequent physician-diagnosed incident asthma at least one year after BMI assessment. We sought to explore potential effect modification by sex. PubMed and Embase were searched using keywords and restricted to subjects aged 0-18 years. There were no date or language restrictions. From each study we extracted: authors, publication date, location, overweight/obesity definitions, asthma definitions, number of participants, recruitment duration, description of cohort, follow-up time, adjusted effect estimates (with 95% CI) and estimates of subgroup analysis.\n\nRESULTS:\nSix prospective cohort studies which focused on children \u003c18 years of age met criteria for inclusion. The combined risk ratio (RR) of overweight was associated with asthma (RR = 1.35; 95% CI = 1.15, 1.58). In boys, the combined RR of overweight on asthma was significant (RR = 1.41; 95% CI = 1.05, 1.88). For girls, when BMI was defined by Z-score, the combined RR of overweight on asthma was also significant (RR = 1.19; 95% CI = 1.06, 1.34). The combined risk ratio (RR) of obesity was associated with asthma in both boys and girls (RR = 1.50; 95% CI = 1.22, 1.83), in boys only (RR = 1.40; 95% CI = 1.01, 1.93) and in girls only (RR = 1.53; 95% CI = 1.09, 2.14).\n\nCONCLUSIONS:\nOverweight and, especially, obese children are at increased risk of subsequent physician diagnosed asthma in comparison to normal weight children. Except for sex, no studies reported any other potential effect modifiers. The observed sex effects were inconsistent." + }, + "questions": [ + { + "id": "b93f1d8d-2523-47b4-b9a9-219a252d65b0", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1401, + "text": "obesity" + } + ] + } + ] +} \ No newline at end of file diff --git a/2e9d03df-492c-4cf7-9a2b-ccde1a8637a5.json b/2e9d03df-492c-4cf7-9a2b-ccde1a8637a5.json new file mode 100644 index 0000000000000000000000000000000000000000..637bdee194a8becdcd005a2fdbeb1faa401ed68b --- /dev/null +++ b/2e9d03df-492c-4cf7-9a2b-ccde1a8637a5.json @@ -0,0 +1,41 @@ +{ + "id": "2e9d03df-492c-4cf7-9a2b-ccde1a8637a5", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "26919270", + "text": "BACKGROUND:\nA rigorous assessment of the risk of colorectal cancer (CRC) among prostate cancer (PC) survivors that controls for important confounding factors and competing risks is necessary to determine the risk of CRC in this population and to inform screening guidelines.\n\nMETHODS:\nWith data from Manitoba, Canada, subjects diagnosed with PC as their first cancer between 1987 and 2009 were age-matched with up to 5 men with no history of invasive cancer on the PC diagnosis date. Subjects were followed to the date of diagnosis of CRC or another cancer, death, emigration, or the study endpoint (December 31, 2009). Competing risk proportional hazards models were used to compare the CRC incidence between those with PC and those without PC with the following model covariates: history of lower gastrointestinal endoscopy, frequency of health care visits, diabetes, and socioeconomic status. Mutually exclusive competing outcomes included CRC, another primary cancer, and death.\n\nRESULTS:\nFor a total of 559,081 person-years, 14,164 men with PC and 69,051 men without PC were followed. Men diagnosed with PC had an increased risk of a subsequent diagnosis of CRC (all CRC: hazard ratio [HR], 1.14; 95% confidence interval [CI], 1.02-1.27; rectal cancer: HR, 1.36; 95% CI, 1.09-1.71). The treatment of PC with radiation was associated with an increased risk for rectal cancer (HR, 2.06; 95% CI, 1.42-2.99) in comparison with PC cases not treated with radiation.\n\nCONCLUSIONS:\nThe risk of CRC is increased after a diagnosis of PC and is highest for rectal cancer among those treated with radiation. CRC screening should be considered soon after the diagnosis of PC, especially for men planning for radiotherapy." + }, + "questions": [ + { + "id": "f7ef66da-fea3-4327-a9fb-7288dc6a1eb0", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1516, + "text": "diagnosis of PC" + }, + { + "answer_start": 1090, + "text": "Men diagnosed with PC" + } + ] + } + ] +} \ No newline at end of file diff --git a/2eac0135-4fcd-4347-bd5a-94074925d8d7.json b/2eac0135-4fcd-4347-bd5a-94074925d8d7.json new file mode 100644 index 0000000000000000000000000000000000000000..031799f224fc2af39a3ae3b050c5725be73ebe30 --- /dev/null +++ b/2eac0135-4fcd-4347-bd5a-94074925d8d7.json @@ -0,0 +1,50 @@ +{ + "id": "2eac0135-4fcd-4347-bd5a-94074925d8d7", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "11556298", + "text": "BACKGROUND:\nPrevious studies have examined individual dietary and lifestyle factors in relation to type 2 diabetes, but the combined effects of these factors are largely unknown.\n\nMETHODS:\nWe followed 84,941 female nurses from 1980 to 1996; these women were free of diagnosed cardiovascular disease, diabetes, and cancer at base line. Information about their diet and lifestyle was updated periodically. A low-risk group was defined according to a combination of five variables: a bodymass index (the weight in kilograms divided by the square of the height in meters) of less than 25; a diet high in cereal fiber and polyunsaturated fat and low in trans fat and glycemic load (which reflects the effect of diet on the blood glucose level); engagement in moderate-to-vigorous physical activity for at least half an hour per day; no current smoking; and the consumption of an average of at least half a drink of an alcoholic beverage per day.\n\nRESULTS:\nDuring 16 years of follow-up, we documented 3300 new cases of type 2 diabetes. Overweight or obesity was the single most important predictor of diabetes. Lack of exercise, a poor diet, current smoking, and abstinence from alcohol use were all associated with a significantly increased risk of diabetes, even after adjustment for the body-mass index. As compared with the rest of the cohort, women in the low-risk group (3.4 percent of the women) had a relative risk of diabetes of 0.09 (95 percent confidence interval, 0.05 to 0.17). A total of 91 percent of the cases of diabetes in this cohort (95 percent confidence interval, 83 to 95) could be attributed to habits and forms of behavior that did not conform to the low-risk pattern.\n\nCONCLUSIONS:\nOur findings support the hypothesis that the vast majority of cases of type 2 diabetes could be prevented by the adoption of a healthier lifestyle." + }, + "questions": [ + { + "id": "0203af7e-205b-47ba-be32-ce85a27f6929", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1030, + "text": "Overweight or obesity" + }, + { + "answer_start": 1105, + "text": "Lack of exercise" + }, + { + "answer_start": 1125, + "text": "poor diet" + }, + { + "answer_start": 1136, + "text": "current smoking" + }, + { + "answer_start": 1157, + "text": "abstinence from alcohol" + } + ] + } + ] +} \ No newline at end of file diff --git a/2f0335d7-051d-40ea-8f9d-e6424efe1c01.json b/2f0335d7-051d-40ea-8f9d-e6424efe1c01.json new file mode 100644 index 0000000000000000000000000000000000000000..c1606fe2f3accc1257b6de969f68649da0b8892a --- /dev/null +++ b/2f0335d7-051d-40ea-8f9d-e6424efe1c01.json @@ -0,0 +1,39 @@ +{ + "id": "2f0335d7-051d-40ea-8f9d-e6424efe1c01", + "disease": { + "id": "H00056", + "names": [ + "Alzheimer disease", + "Dementia due to Alzheimer disease" + ], + "dbLinks": { + "icd10": [ + "G30" + ], + "mesh": [ + "D000544" + ] + }, + "category": "Neurodegenerative disease" + }, + "article": { + "id": "16682673", + "text": "OBJECTIVE:\nTo examine the associations between postmortem Alzheimer disease (AD) neuropathology and autopsy-verified cardiovascular disease.\n\nMETHODS:\nThe authors examined 99 subjects (mean age at death = 87.6; SD = 8.7) from the Mount Sinai School of Medicine Department of Psychiatry Brain Bank who were devoid of cerebrovascular disease-associated lesions or of non-AD-related neuropathology. Density of neuritic plaques (NPs) and neurofibrillary tangles (NFTs) as well as coronary artery and aortic atherosclerosis, left ventricular wall thickness, and heart weight were measured. Partial correlations were used to assess the associations of the four cardiovascular variables with NPs and NFTs in the hippocampus, entorhinal cortex, and multiple regions of the cerebral cortex after controlling for age at death, sex, dementia severity, body mass index, and ApoE genotype. These analyses were also repeated separately for ApoE4 carriers and noncarriers.\n\nRESULTS:\nThe extent of coronary artery disease and to a lesser extent atherosclerosis were significantly associated with the density of cardinal neuropathologic lesions of AD in this autopsy sample (significant correlations between 0.22 and 0.29). These associations were more pronounced for the ApoE4 allele carriers (n = 42; significant correlations between 0.34 and 0.47).\n\nCONCLUSIONS:\nThe degree of coronary artery disease is independently associated with the cardinal neuropathological lesions of Alzheimer disease. These associations are primarily attributable to individuals with the ApoE4 allele." + }, + "questions": [ + { + "id": "3db980f6-41c7-4881-b05c-7cfe5410e079", + "text": "What are the risk factors of Alzheimer disease?", + "answers": [ + { + "answer_start": 1353, + "text": "degree of coronary artery disease" + }, + { + "answer_start": 1029, + "text": "atherosclerosis" + } + ] + } + ] +} \ No newline at end of file diff --git a/2f0d90bb-2499-405f-8a8a-7a910d2629f3.json b/2f0d90bb-2499-405f-8a8a-7a910d2629f3.json new file mode 100644 index 0000000000000000000000000000000000000000..b371d0c93c7ea60b8a6c932d2451e9b263be0273 --- /dev/null +++ b/2f0d90bb-2499-405f-8a8a-7a910d2629f3.json @@ -0,0 +1,34 @@ +{ + "id": "2f0d90bb-2499-405f-8a8a-7a910d2629f3", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "19454285", + "text": "BACKGROUND \u0026 AIMS:\nCeliac disease (CD) is a common chronic disorder of the small intestine, resulting from aberrant cellular responses to gluten peptides, and often remains undiagnosed. It is a complex genetic disorder, although 95% of the patients carry the risk heterodimer human leukocyte antigen (HLA)-DQ2. Genome-wide association studies on CD have identified 9 non-HLA loci that also contribute to CD risk, most of which are shared with other immune-related diseases. Our aim is to predict the genetic risk for CD using HLA and non-HLA risk alleles.\n\nMETHODS:\nWe selected 10 independent polymorphisms in 2,308 cases and 4,585 controls from Dutch, UK, and Irish populations and categorized the individuals into 3 risk groups, based on their HLA-DQ2 genotype. We used the summed number of non-HLA risk alleles per individual to analyze their cumulative effect on CD risk, adjusting for gender and population group in logistic regression analysis. We validated our findings in 436 Italian cases and 532 controls.\n\nRESULTS:\nCD cases carried more non-HLA risk alleles than controls: individuals carrying \u003e or = 13 risk alleles had a higher CD risk (odds ratio, 6.2; 95% confidence interval, 4.1-9.3) compared with those carrying 0-5 risk alleles. Combining HLA and non-HLA risk genotypes in one model increases sensitivity by 6.2% compared with using only HLA for identification of high-risk individuals with slight decrease in specificity.\n\nCONCLUSIONS:\nWe can use non-HLA risk factors for CD to improve identification of high-risk individuals. Our risk model is a first step toward better diagnosis and prognosis in high-risk families and population-based screening." + }, + "questions": [ + { + "id": "8c942f4f-3f27-42fe-b230-413ee2bac210", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 1084, + "text": "individuals carrying \u003e or = 13 risk alleles" + } + ] + } + ] +} \ No newline at end of file diff --git a/2f1ca650-ba8d-4cc7-add0-031b5a234112.json b/2f1ca650-ba8d-4cc7-add0-031b5a234112.json new file mode 100644 index 0000000000000000000000000000000000000000..cbe8bf2cc6999dfbe7bc7b8da3532356c1b365fd --- /dev/null +++ b/2f1ca650-ba8d-4cc7-add0-031b5a234112.json @@ -0,0 +1,43 @@ +{ + "id": "2f1ca650-ba8d-4cc7-add0-031b5a234112", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "19251785", + "text": "Few studies have investigated the relationship between vehicle exhaust and the new onset of asthma among adults. The aim of the present prospective cohort study was to investigate the relationship between the cumulative incidence of asthma and onset of asthma among adults and vehicle exhaust concentrations at home. Participants from three Swedish cities included in the Respiratory Health in Northern Europe cohort constituted the study population. Exposure at each participant's home was calculated using dispersion models. We also used \u003c50 m distance to nearest major road as a more simple indicator of exposure. The adjusted model included 3,609 participants, of which 107 were classified as onset cases and 55 as true incident cases of asthma. There was a positive association between asthma onset (odds ratio (OR) per 10 microg x m(-3) 1.46, 95% confidence interval (CI) 1.07-1.99) and incident asthma (OR per 10 microg x m(-3) 1.54, 95% CI 1.00-2.36) and the levels of nitrogen dioxide (NO(2)), which remained statistically significant after adjusting for potential confounders. The relationship between asthma and NO(2) was not significantly modified by sex, hay fever or wheeze. The risk of developing asthma was also significantly related to living close to a major road. The current study suggests that elevated levels of vehicle exhaust outside the home increase the risk of onset and incident asthma among adults." + }, + "questions": [ + { + "id": "05bf1047-97aa-4db8-9084-61f42f68411f", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1253, + "text": "living close to a major road" + }, + { + "answer_start": 1315, + "text": "elevated levels of vehicle exhaust outside the home" + }, + { + "answer_start": 967, + "text": "levels of nitrogen dioxide (NO(2))" + } + ] + } + ] +} \ No newline at end of file diff --git a/2f8ad816-cfed-49a8-969b-41af27164684.json b/2f8ad816-cfed-49a8-969b-41af27164684.json new file mode 100644 index 0000000000000000000000000000000000000000..1fb8e19edea0c329f6d1ee3b18138618d8b2a3c7 --- /dev/null +++ b/2f8ad816-cfed-49a8-969b-41af27164684.json @@ -0,0 +1,47 @@ +{ + "id": "2f8ad816-cfed-49a8-969b-41af27164684", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "16478846", + "text": "BACKGROUND:\nAsthma development and prognosis have been studied extensively in at-risk populations, but knowledge of the natural history of asthma in the general population is limited.\n\nOBJECTIVE:\nTo describe the incidence and remission of asthma and its predictors, data from a 12-year follow-up study of a random population sample (n = 291; age range, 7 to 17 years) at enrollment, were analyzed.\n\nMETHODS:\nThe sample was examined in 1986 and in 1998. A case history, including data on asthma, allergic diseases, and lifestyle factors, was obtained by questionnaire and interview. Airway hyperresponsiveness (AHR) to histamine, lung function, and skin-prick test reactivity to a standard panel of 10 aeroallergens were measured.\n\nRESULTS:\nThe point prevalence of asthma increased from 4.1% at the first survey to 11.7% at follow-up, at which point 19.6% of the sample had ever experienced asthma symptoms. Of the subjects with ever-asthma, 40% had remitted at follow-up. Asthma developed in 45 subjects (16.1%) during the follow-up period, which was predicted by the following factors: wheezing in childhood (odds ratio [OR], 3.61; 95% confidence interval [CI], 1.34 to 9.75), AHR (OR, 4.94; 95% CI, 2.42 to 10.08), allergic sensitization to house dust mites (OR, 3.23; 95% CI, 1.00 to 10.40), and dermatitis (OR, 2.94; 95% CI, 1.22 to 7.11). The simultaneous presence of more than one of these risk factors was associated with a high probability of developing asthma at follow-up (61.5%). In subjects without any risk factors, such as AHR, allergic sensitization, rhinitis, dermatitis or wheezing in childhood; paternal/maternal allergy, or asthma, asthma developed in only 4% during follow-up.\n\nCONCLUSION:\nThe presence of AHR and concomitant atopic manifestations in childhood increase the risk of developing asthma in adulthood, and should be recognized as markers of prognostic significance, whereas the absence of these manifestations predicts a very low risk of future asthma." + }, + "questions": [ + { + "id": "bc6c0581-ee4b-45c8-9906-519df2b7c7bc", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1087, + "text": "wheezing in childhood" + }, + { + "answer_start": 1217, + "text": "allergic sensitization to house dust mites" + }, + { + "answer_start": 1178, + "text": "AHR" + }, + { + "answer_start": 1299, + "text": "dermatitis" + } + ] + } + ] +} \ No newline at end of file diff --git a/2faf0317-57c1-4704-9f24-04c23ea7736a.json b/2faf0317-57c1-4704-9f24-04c23ea7736a.json new file mode 100644 index 0000000000000000000000000000000000000000..86a9d0428664a7ce07c9c9995828b40f9b7c7bd7 --- /dev/null +++ b/2faf0317-57c1-4704-9f24-04c23ea7736a.json @@ -0,0 +1,38 @@ +{ + "id": "2faf0317-57c1-4704-9f24-04c23ea7736a", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "21128002", + "text": "BACKGROUND:\nObesity is one of the most important modifiable risk factors for the prevention of type 2 diabetes. The aim of this study was to examine the prevalence of diabetes with increasing severity of obesity and the distribution of HbA1c levels in diabetics participating in the latest National Health and Nutrition Examination Survey (NHANES).\n\nMETHODS:\nData from a representative sample of adults with diabetes participating in the NHANES between 1999 and 2006 were reviewed. The prevalence of diabetes and levels of fasting glucose, insulin, c-peptide, and HbA1c were examined across different weight classes with normal weight, overweight, and obesity classes 1, 2, and 3 were defined as body mass index (BMI) of \u003c25.0, 25.0-29.9, 30.0-34.9, 35.0-39.9, and equal to 40.0, respectively. The distribution of HbA1c levels among adults with diabetes was also examined.\n\nRESULTS:\nThere were 2,894 adults with diabetes (13.6%) among the 21,205 surveyed participants. Among the adults with diabetes, the mean age was 59 years, the mean fasting glucose was 155 ± 2 mg/dl, and the mean HbA1c was 7.2%; 80.3% of diabetics were considered overweight (BMI ≥ 25) and 49.1% of diabetics were considered obese (BMI ≥ 30). The prevalence of adults with diabetes increased with increasing weight classes, from 8% for normal weight individuals to 43% for individuals with obesity class 3; the distribution of HbA1c levels were considered as good (\u003c7.0%) in 60%, fair (7.0-8.0%) in 17%, and poor (\u003e8.0%) in 23%. The mean fasting glucose and HbA1c levels were highest for diabetics with BMI \u003c25.0, suggesting a state of higher severity of disease. Mean insulin and c-peptide levels were highest for diabetics with BMI = 35.0, suggesting a state of insulin resistance.\n\nCONCLUSIONS:\nIn a nationally representative sample of US adults, the prevalence of diabetes increases with increasing weight classes. Nearly one fourth of adults with diabetes have poor glycemic control and nearly half of adult diabetics are considered obese suggesting that weight loss is an important intervention in an effort to reduce the impact of diabetes on the health care system." + }, + "questions": [ + { + "id": "52497059-eb94-456e-be36-201d879705e4", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1863, + "text": " increasing weight classes" + }, + { + "answer_start": 1269, + "text": "increasing weight classes" + } + ] + } + ] +} \ No newline at end of file diff --git a/2fd8decb-d48f-4a5e-b442-7af0a6feab47.json b/2fd8decb-d48f-4a5e-b442-7af0a6feab47.json new file mode 100644 index 0000000000000000000000000000000000000000..bb0cb84697975dfa5fa827818f30921648269581 --- /dev/null +++ b/2fd8decb-d48f-4a5e-b442-7af0a6feab47.json @@ -0,0 +1,46 @@ +{ + "id": "2fd8decb-d48f-4a5e-b442-7af0a6feab47", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "29228305", + "text": "BACKGROUND:\nFamily history of bladder cancer confers an increased risk for concordant and discordant cancers in relatives. However, previous studies investigating this relationship lack any correction for smoking status of family members. We conducted a population-based study of cancer risks in relatives of bladder cancer patients and matched controls with exclusion of variant subtypes to improve the understanding of familial cancer clustering.\n\nMETHODS:\nCase subjects with urothelial carcinoma were identified using the Utah Cancer Registry and matched 1:5 to cancer-free controls from the Utah Population Database. Cox regression was used to determine the risk of cancer in first-degree relatives, second-degree relatives, first cousins, and spouses. A total of 229 251 relatives of case subjects and 1 197 552 relatives of matched control subjects were analyzed. To correct for smoking status, we performed a secondary analysis excluding families with elevated rates of smoking-related cancers. All statistical tests were two-sided.\n\nRESULTS:\nFirst- and second-degree relatives of case subjects had an increased risk for any cancer diagnosis (hazard ratio [HR] = 1.06, 95% confidence interval [CI] = 1.03 to 1.09, P \u003c .001; HR = 1.04, 95% CI = 1.02 to 1.07, P = .001) and urothelial cancer (HR = 1.73, 95% CI = 1.50 to 1.99, P \u003c .001; HR = 1.35, 95% CI = 1.21 to 1.51, P \u003c .001). Site-specific analysis found increased risk for bladder (HR = 1.69, 95% CI = 1.47 to 1.95, P \u003c .001), kidney (HR = 1.30, 95% CI = 1.08 to 1.57, P = .006), cervical (HR = 1.25, 95% CI = 1.06 to 1.49, P = .01), and lung cancer (HR = 1.34, 95% CI = 1.19 to 1.51, P \u003c .001) in first-degree relatives. Second-degree relatives had increased risk for bladder (HR = 1.35, 95% CI = 1.2 to 1.5, P \u003c .001) and thyroid cancer (HR = 1.18, 95% CI = 1.03 to 1.35, P = .02). Spouses showed an increased risk for laryngeal (HR = 2.68, 95% CI = 1.02 to 7.05, P = .04) and cervical cancer (HR = 1.57, 95% CI = 1.13 to 2.17, P = .007). These results did not substantively change after correction for suspected smoking behaviors.\n\nCONCLUSION:\nOur results suggest familial urothelial cancer clustering independent of smoking, with increased risk in relatives for both concordant and discordant cancers, suggesting shared genetic or environmental roots. Identifying families with statistically significant risks for non-smoking-related urothelial cancer would be extremely informative for genetic linkage studies." + }, + "questions": [ + { + "id": "aceea4cf-749b-4580-9ade-deda3f78e6d6", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 1050, + "text": "First- and second-degree relatives of case subjects" + }, + { + "answer_start": 1684, + "text": "Second-degree relatives" + }, + { + "answer_start": 2214, + "text": "relatives for both concordant and discordant cancers" + }, + { + "answer_start": 2129, + "text": "familial urothelial cancer" + } + ] + } + ] +} \ No newline at end of file diff --git a/306d7fe3-2b81-4e8e-88e4-05e4f611eadd.json b/306d7fe3-2b81-4e8e-88e4-05e4f611eadd.json new file mode 100644 index 0000000000000000000000000000000000000000..32ebccc7ef92e525fe8a8ab6759c32f1f8d857d6 --- /dev/null +++ b/306d7fe3-2b81-4e8e-88e4-05e4f611eadd.json @@ -0,0 +1,32 @@ +{ + "id": "306d7fe3-2b81-4e8e-88e4-05e4f611eadd", + "disease": { + "id": "M2023_04_26_16_49_01", + "names": [ + "Metabolic syndrome" + ], + "dbLinks": { + "mesh": [ + "C18.452.394.968.500.570", + "C18.452.625" + ] + }, + "description": "Metabolic syndrome is a complex constellation of metabolic derangements that increase the risk of atherosclerotic cardiovascular disease, type 2 diabetes, and all-cause mortality. The key features of metabolic syndrome include central obesity, insulin resistance, dyslipidemia, and hypertension. These abnormalities are believed to arise from a combination of genetic predisposition and environmental factors, such as sedentary behavior, poor dietary habits, and chronic stress. Diagnosis of metabolic syndrome requires meeting three or more established criteria, based on standardized guidelines. Management of metabolic syndrome involves a comprehensive approach, including lifestyle modifications such as weight loss, physical activity, and dietary changes, as well as pharmacotherapy to address underlying risk factors such as hypertension, dyslipidemia, and hyperglycemia. Early intervention and aggressive management of metabolic syndrome are critical to preventing or delaying the onset of complications and improving long-term health outcomes." + }, + "article": { + "id": "10335688", + "text": "BACKGROUND:\nThe degree of clustering for common metabolic coronary disease risk factors is not well known, the antecedents of clustering are not well studied, and the impact of such clusters on coronary risk has not been assessed systematically.\n\nMETHODS:\nProspective community sample of 2406 men and 2569 women aged 18 to 74 years at baseline. The 6 metabolically linked risk factors considered were the lowest sex-specific quintile of high-density lipoprotein cholesterol and the highest quintiles of body mass index, systolic blood pressure, triglycerides, glucose, and serum total cholesterol.\n\nRESULTS:\nAt baseline the risk factor sum, represented as integer values, ranged from 0 to 6, and clusters of 3 or more risk factors occurred at twice the rate predicted by chance. After adjustment for age and obesity level, a 2.25-kg (5-lb) weight increase over 16 years was associated with an increased risk factor sum in men (+20%; P=.002) and women (+37%; P\u003c.001), and a 2.25-kg weight loss was associated with a decreased risk factor sum in men (-48%; P\u003c.001) and women (-40%; P\u003c.001). Clusters of 3 or more risk factors were associated with a 2.39 (95% confidence interval, 1.56-3.36) and 5.90 (95% confidence interval, 2.54-13.73) times greater risk of coronary heart disease in men and women, respectively (both P\u003c.001).\n\nCONCLUSIONS:\nAtherogenic risk factor clustering is common in both sexes, worsens with weight gain, and is associated with greatly increased risk of coronary disease risk in both sexes." + }, + "questions": [ + { + "id": "63826d1a-9014-460f-a4d1-72e8260b7c58", + "text": "What is a risk factor for Metabolic Syndrome?", + "answers": [ + { + "answer_start": 823, + "text": "a 2.25-kg (5-lb) weight increase over 16 years" + } + ] + } + ] +} \ No newline at end of file diff --git a/30c536ed-df9f-4ee3-888f-6083ab72317a.json b/30c536ed-df9f-4ee3-888f-6083ab72317a.json new file mode 100644 index 0000000000000000000000000000000000000000..ec354bad0beec07b8901fa98197a052514b131e6 --- /dev/null +++ b/30c536ed-df9f-4ee3-888f-6083ab72317a.json @@ -0,0 +1,39 @@ +{ + "id": "30c536ed-df9f-4ee3-888f-6083ab72317a", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "11312420", + "text": "BACKGROUND:\nOral methoxsalen (psoralen) and ultraviolet A radiation (PUVA) is a highly effective therapy for psoriasis and many other skin conditions. It is carcinogenic. Previously we reported an increased risk of melanoma that first emerged 15 years after first treatment.\n\nOBJECTIVE:\nOur purpose is to present additional data concerning the associations of previous exposure to PUVA, the passage of time, and the risk of malignant melanoma.\n\nMETHODS:\nWe have prospectively studied a cohort of 1380 patients first treated with PUVA in 1975 and 1976. We have documented the occurrence of melanoma and in this report compare the observed and expected incidence of melanoma in this cohort, particularly melanomas developing since our earlier report (ie, after March 1996).\n\nRESULTS:\nSince 1975, 23 patients have developed 26 invasive or in situ cutaneous melanomas. In an average of 2.25 years since our last report, we detected 7 additional invasive melanomas (incidence rate ratio, 8.4; 95% confidence interval, 3.4-17.3).\n\nCONCLUSION:\nBeginning 15 years after first exposure to PUVA, an increased risk of melanoma is observed in our cohort of PUVA-treated patients. This risk is greater in patients exposed to high doses of PUVA, appears to be increasing with the passage of time, and should be considered in determining the risks and benefits of this therapy." + }, + "questions": [ + { + "id": "20caa562-d7f8-4c67-8afd-164be20fc1ea", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 1068, + "text": "exposure to PUVA" + }, + { + "answer_start": 44, + "text": "ultraviolet A radiation (PUVA)" + } + ] + } + ] +} \ No newline at end of file diff --git a/30c54a23-fd71-49be-b9d5-dfcba147c871.json b/30c54a23-fd71-49be-b9d5-dfcba147c871.json new file mode 100644 index 0000000000000000000000000000000000000000..73ffe4de6f1f76fcb5dcd8f16fc66ad8011fd9a9 --- /dev/null +++ b/30c54a23-fd71-49be-b9d5-dfcba147c871.json @@ -0,0 +1,43 @@ +{ + "id": "30c54a23-fd71-49be-b9d5-dfcba147c871", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "24429203", + "text": "BACKGROUND:\nIndoor air pollution from a range of household cooking fuels has been implicated in the development and exacerbation of respiratory diseases. In both rich and poor countries, the effects of cooking fuels on asthma and allergies in childhood are unclear. We investigated the association between asthma and the use of a range of cooking fuels around the world.\n\nMETHODS:\nFor phase three of the International Study of Asthma and Allergies in Childhood (ISAAC), written questionnaires were self-completed at school by secondary school students aged 13-14 years, 244,734 (78%) of whom were then shown a video questionnaire on wheezing symptoms. Parents of children aged 6-7 years completed the written questionnaire at home. We investigated the association between types of cooking fuels and symptoms of asthma using logistic regression. Adjustments were made for sex, region of the world, language, gross national income, maternal education, parental smoking, and six other subject-specific covariates. The ISAAC study is now closed, but researchers can continue to use the instruments for further research.\n\nFINDINGS:\nData were collected between 1999 and 2004. 512,707 primary and secondary school children from 108 centres in 47 countries were included in the analysis. The use of an open fire for cooking was associated with an increased risk of symptoms of asthma and reported asthma in both children aged 6-7 years (odds ratio [OR] for wheeze in the past year, 1·78, 95% CI 1·51-2·10) and those aged 13-14 years (OR 1·20, 95% CI 1·06-1·37). In the final multivariate analyses, ORs for wheeze in the past year and the use of solely an open fire for cooking were 2·17 (95% CI 1·64-2·87) for children aged 6-7 years and 1·35 (1·11-1·64) for children aged 13-14 years. Odds ratios for wheeze in the past year and the use of open fire in combination with other fuels for cooking were 1·51 (1·25-1·81 for children aged 6-7 years and 1·35 (1·15-1·58) for those aged 13-14 years. In both age groups, we detected no evidence of an association between the use of gas as a cooking fuel and either asthma symptoms or asthma diagnosis.\n\nINTERPRETATION:\nThe use of open fires for cooking is associated with an increased risk of symptoms of asthma and of asthma diagnosis in children. Because a large percentage of the world population uses open fires for cooking, this method of cooking might be an important modifiable risk factor if the association is proven to be causal.\n\nFUNDING:\nBUPA Foundation, the Auckland Medical Research Foundation, the Health Research Council of New Zealand, the Asthma and Respiratory Foundation of New Zealand, the Child Health Research Foundation, the Hawke's Bay Medical Research Foundation, the Waikato Medical Research Foundation, Glaxo Wellcome New Zealand, the NZ Lottery Board, Astra Zeneca New Zealand, Hong Kong Research Grant Council, Glaxo Wellcome International Medical Affairs." + }, + "questions": [ + { + "id": "5efd6ae5-836c-41d4-83c1-7acc62c737d9", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1294, + "text": "open fire for cooking" + }, + { + "answer_start": 1630, + "text": "use of solely an open fire for cooking" + }, + { + "answer_start": 2157, + "text": "use of open fires for cooking" + } + ] + } + ] +} \ No newline at end of file diff --git a/311cb4f0-7996-4c39-9433-4f87acfbaadc.json b/311cb4f0-7996-4c39-9433-4f87acfbaadc.json new file mode 100644 index 0000000000000000000000000000000000000000..ae61ee32a21f46915ce080724d5e697b59898a67 --- /dev/null +++ b/311cb4f0-7996-4c39-9433-4f87acfbaadc.json @@ -0,0 +1,32 @@ +{ + "id": "311cb4f0-7996-4c39-9433-4f87acfbaadc", + "disease": { + "id": "M2023_04_26_16_49_01", + "names": [ + "Metabolic syndrome" + ], + "dbLinks": { + "mesh": [ + "C18.452.394.968.500.570", + "C18.452.625" + ] + }, + "description": "Metabolic syndrome is a complex constellation of metabolic derangements that increase the risk of atherosclerotic cardiovascular disease, type 2 diabetes, and all-cause mortality. The key features of metabolic syndrome include central obesity, insulin resistance, dyslipidemia, and hypertension. These abnormalities are believed to arise from a combination of genetic predisposition and environmental factors, such as sedentary behavior, poor dietary habits, and chronic stress. Diagnosis of metabolic syndrome requires meeting three or more established criteria, based on standardized guidelines. Management of metabolic syndrome involves a comprehensive approach, including lifestyle modifications such as weight loss, physical activity, and dietary changes, as well as pharmacotherapy to address underlying risk factors such as hypertension, dyslipidemia, and hyperglycemia. Early intervention and aggressive management of metabolic syndrome are critical to preventing or delaying the onset of complications and improving long-term health outcomes." + }, + "article": { + "id": "16009797", + "text": "BACKGROUND:\nFew studies have reported the relationship between cardiorespiratory fitness and metabolic syndrome incidence, particularly in women.\n\nMETHODS AND RESULTS:\nWe prospectively studied 9007 men (mean+/-SD age, 44+/-9 years; body mass index, 25+/-3 kg/m2) and 1491 women (age, 44+/-9 years; body mass index, 22+/-2 kg/m2) who were free of metabolic syndrome and for whom measures of waist girth, resting blood pressure, fasting lipids, and glucose were taken during baseline and follow-up examinations. Baseline cardiorespiratory fitness was quantified as duration of a maximal treadmill test. Metabolic syndrome was defined with NCEP ATP-III criteria. During a mean follow-up of 5.7 years, 1346 men and 56 women developed metabolic syndrome. Age-adjusted incidence rates were significantly lower (linear trend, P\u003c0.001) across incremental thirds of fitness in men and women. After further adjustment for potential confounders, multivariable hazard ratios for incident metabolic syndrome among men in the low, middle, and upper thirds of fitness, were 1.0 (referent), 0.74 (95% CI, 0.65 to 0.84), and 0.47 (95% CI, 0.40 to 0.54) (linear trend P\u003c0.001); in women, they were 1.0 (referent), 0.80 (95% CI, 0.44 to 1.46), and 0.37 (95% CI, 0.18 to 0.80) (linear trend P=0.01), respectively. Similar patterns of significant inverse associations between fitness and metabolic syndrome incidence were seen when men were stratified on categories of body mass index, age, and number of baseline metabolic risk factors, but patterns were variable in women.\n\nCONCLUSIONS:\nLow cardiorespiratory fitness is a strong and independent predictor of incident metabolic syndrome in women and men. Clinicians should consider the potential benefits of greater cardiorespiratory fitness in the primary prevention of metabolic syndrome, particularly among patients who have already begun to cluster metabolic syndrome components." + }, + "questions": [ + { + "id": "1777f0c0-35e2-4a6a-97e5-435542e575f5", + "text": "What is a risk factor for Metabolic Syndrome?", + "answers": [ + { + "answer_start": 1568, + "text": "Low cardiorespiratory fitness" + } + ] + } + ] +} \ No newline at end of file diff --git a/318341b1-3860-4a2a-b30a-aa029b72140a.json b/318341b1-3860-4a2a-b30a-aa029b72140a.json new file mode 100644 index 0000000000000000000000000000000000000000..7d97163a7b1e4ec855ceae6bb0fce52432c4e0c8 --- /dev/null +++ b/318341b1-3860-4a2a-b30a-aa029b72140a.json @@ -0,0 +1,39 @@ +{ + "id": "318341b1-3860-4a2a-b30a-aa029b72140a", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "18805333", + "text": "BACKGROUND:\nA close relation between asthma and allergic rhinitis has been reported by several epidemiological and clinical studies. However, the nature of this relation remains unclear. We used the follow-up data from the European Community Respiratory Health Survey to investigate the onset of asthma in patients with allergic and non-allergic rhinitis during an 8.8-year period.\n\nMETHODS:\nWe did a longitudinal population-based study, which included 29 centres (14 countries) mostly in western Europe. Frequency of asthma was studied in 6461 participants, aged 20-44 years, without asthma at baseline. Incident asthma was defined as reporting ever having had asthma confirmed by a physician between the two surveys. Atopy was defined as a positive skin-prick test to mites, cat, Alternaria, Cladosporium, grass, birch, Parietaria, olive, or ragweed. Participants were classified into four groups at baseline: controls (no atopy, no rhinitis; n=3163), atopy only (atopy, no rhinitis; n=704), non-allergic rhinitis (rhinitis, no atopy; n=1377), and allergic rhinitis (atopy+rhinitis; n=1217). Cox proportional hazards models were used to study asthma onset in the four groups.\n\nFINDINGS:\nThe 8.8-year cumulative incidence of asthma was 2.2% (140 events), and was different in the four groups (1.1% (36), 1.9% (13), 3.1% (42), and 4.0% (49), respectively; p\u003c0.0001). After controlling for country, sex, baseline age, body-mass index, forced expiratory volume in 1 s (FEV(1)), log total IgE, family history of asthma, and smoking, the adjusted relative risk for asthma was 1.63 (95% CI 0.82-3.24) for atopy only, 2.71 (1.64-4.46) for non-allergic rhinitis, and 3.53 (2.11-5.91) for allergic rhinitis. Only allergic rhinitis with sensitisation to mite was associated with increased risk of asthma independently of other allergens (2.79 [1.57-4.96]).\n\nINTERPRETATION:\nRhinitis, even in the absence of atopy, is a powerful predictor of adult-onset asthma." + }, + "questions": [ + { + "id": "dff4b815-9e14-49df-bf37-407752fff1cf", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1865, + "text": "Rhinitis" + }, + { + "answer_start": 1705, + "text": "allergic rhinitis with sensitisation to mite" + } + ] + } + ] +} \ No newline at end of file diff --git a/3183598b-5bfc-461b-b159-c481b0c06441.json b/3183598b-5bfc-461b-b159-c481b0c06441.json new file mode 100644 index 0000000000000000000000000000000000000000..b115685ecde22a9cc49db5f928a1c5101ffd5993 --- /dev/null +++ b/3183598b-5bfc-461b-b159-c481b0c06441.json @@ -0,0 +1,34 @@ +{ + "id": "3183598b-5bfc-461b-b159-c481b0c06441", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "14757619", + "text": "BACKGROUND:\nBoth diabetes mellitus and alcohol consumption are prevalent in the United States, yet physicians are poorly informed about how alcohol use affects risk for or management of diabetes.\n\nPURPOSE:\nTo conduct a systematic review assessing the effect of alcohol use on the incidence, management, and complications of diabetes mellitus in adults.\n\nDATA SOURCES:\nEnglish-language studies in persons 19 years of age or older that were identified by searching the MEDLINE database from 1966 to the third week of August 2003 and the reference lists of key articles.\n\nSTUDY SELECTION:\nTwo independent assessors reviewed 974 retrieved citations to identify all experimental, cohort, or case-control studies that assessed the effect of alcohol use on diabetes risk, control, self-management, adverse drug events, or complications.\n\nDATA EXTRACTION:\nTwo independent reviewers extracted data and evaluated study quality on the basis of established criteria.\n\nDATA SYNTHESIS:\nThirty-two studies that met inclusion criteria were reviewed. Compared with no alcohol use, moderate consumption (one to 3 drinks/d) is associated with a 33% to 56% lower incidence of diabetes and a 34% to 55% lower incidence of diabetes-related coronary heart disease. Compared with moderate consumption, heavy consumption (\u003e3 drinks/d) may be associated with up to a 43% increased incidence of diabetes. Moderate alcohol consumption does not acutely impair glycemic control in persons with diabetes.\n\nCONCLUSIONS:\nModerate alcohol consumption is associated with a decreased incidence of diabetes mellitus and a decreased incidence of heart disease in persons with diabetes. Further studies are needed to assess the long-term effects of alcohol consumption on glycemic control and noncardiac complications in persons with diabetes." + }, + "questions": [ + { + "id": "83463cdf-c0ba-4838-a06b-496b5f3ae62d", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1278, + "text": "heavy consumption (\u003e3 drinks/d)" + } + ] + } + ] +} \ No newline at end of file diff --git a/32343685-5d7c-4e50-b44e-d21293d54690.json b/32343685-5d7c-4e50-b44e-d21293d54690.json new file mode 100644 index 0000000000000000000000000000000000000000..fb27af6f56e2836068381a18d2b735679722383c --- /dev/null +++ b/32343685-5d7c-4e50-b44e-d21293d54690.json @@ -0,0 +1,50 @@ +{ + "id": "32343685-5d7c-4e50-b44e-d21293d54690", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "7707439", + "text": "BACKGROUND:\nCyclophosphamide is an established bladder carcinogen, but few studies have examined the relationship between dose and effect. The largest analysis to date included only seven cases of bladder cancer. No investigation has estimated the risk of kidney cancer.\n\nPURPOSE:\nThe purpose of this study was to quantify the risk of bladder and kidney cancer following cyclophosphamide therapy.\n\nMETHODS:\nWithin a cohort of 6171 two-year survivors of non-Hodgkin's lymphoma (NHL), 48 patients with secondary cancer of the urinary tract were identified and matched to 136 control subjects with NHL who did not develop a second malignancy. Detailed information on chemotherapeutic drugs and cumulative dose received was collected for all subjects. Radiation dose to the target organ was estimated from individual radiotherapy records. Evaluations of the risk of second cancer as a result of treatment with cyclophosphamide alone, radiation alone, or both therapies were made relative to those patients who were exposed to neither treatment modality.\n\nRESULTS:\nA significant 4.5-fold risk of bladder cancer (95% confidence interval [CI] = 1.5-13.6) followed therapy with cyclophosphamide, and risk was dependent upon cumulative dose. Among patients who received a total amount of cyclophosphamide of less than 20 g, a nonsignificant 2.4-fold risk of bladder cancer was apparent. Significantly elevated sixfold (95% CI = 1.3-29) and 14.5-fold (95% CI = 2.3-94) risks of bladder malignancy followed cumulative doses of 20-49 g and 50 g or more, respectively (P value for trend = .004). Radiotherapy given without cyclophosphamide was associated with a nonsignificant increased risk of bladder malignancy. Excess bladder cancer risk following treatment with both radiotherapy and cyclophosphamide was as expected if individual risks were summed. Neither radiotherapy nor cyclophosphamide was associated with excesses of kidney cancer.\n\nCONCLUSIONS:\nCyclophosphamide-related bladder cancer is dose dependent. For patients given cumulative doses between 20 and 49 g, the absolute risk of bladder cancer is on the order of three excess cancers per 100 NHL patients after 15 years of follow-up. At cumulative doses of 50 g or more, the excess risk increases to approximately seven excess bladder cancers per 100 NHL patients.\n\nIMPLICATIONS:\nThe strong dose-response relationship and high absolute risk of bladder cancer underscore the importance of limiting the cumulative dose of cyclophosphamide to what is required to achieve therapeutic end points. The risk of secondary bladder malignancy and other late sequelae of therapy must be carefully weighted against the curative gains provided by cyclophosphamide. Moreover, long-term side effects of therapy that might be acceptable in cancer treatment may need to be re-evaluated for patients with non-neoplastic disorders." + }, + "questions": [ + { + "id": "dd209156-db44-4400-b2c2-3bc6ac8dccc2", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 1157, + "text": "therapy with cyclophosphamide" + }, + { + "answer_start": 1496, + "text": "cumulative doses of 20-49 g and 50 g or more" + }, + { + "answer_start": 1754, + "text": "both radiotherapy and cyclophosphamide" + }, + { + "answer_start": 1945, + "text": "Cyclophosphamide-related" + }, + { + "answer_start": 2454, + "text": "cumulative dose of cyclophosphamide" + } + ] + } + ] +} \ No newline at end of file diff --git a/3258afb2-7b45-492b-9314-f395e6037c17.json b/3258afb2-7b45-492b-9314-f395e6037c17.json new file mode 100644 index 0000000000000000000000000000000000000000..d1e1e08c899c5f0405eb245b6baa00dab72a7ea0 --- /dev/null +++ b/3258afb2-7b45-492b-9314-f395e6037c17.json @@ -0,0 +1,39 @@ +{ + "id": "3258afb2-7b45-492b-9314-f395e6037c17", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "3988369", + "text": "The histories of exposure to sun through occupational, recreational and vacation activities of 595 patients with newly incident cutaneous melanoma excluding lentigo maligna and acral lentiginous melanoma, were compared to those of comparison subjects drawn randomly from the same population and matched for age, sex and province of residence in Western Canada. Significant increases in risk were seen with increasing amount of sun exposure through outdoor activities associated with recreation and vacations; activities likely to involve more intense sun exposure were associated with greater increases in risk. While a moderate amount of occupational exposure was associated with increased risk, greater occupational exposure resulted in no further increase; in men a decrease in risk was seen. These findings were independent of the effects of hair and skin colour, freckles, ethnic origin and socio-economic status. The results suggest that short-term exposure to unusually intense sunlight increases the risk of melanoma, while long-term constant exposure has no effect or may decrease risk. No simple relationship was seen between melanoma risk and total sunlight exposure. This study introduces new methods of assessing different types of sun exposure from retrospective data." + }, + "questions": [ + { + "id": "837c687f-3dba-4e2f-8fb4-8e2480f45c84", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 406, + "text": "increasing amount of sun exposure through outdoor activities associated with recreation and vacations" + }, + { + "answer_start": 509, + "text": "activities likely to involve more intense sun exposure" + } + ] + } + ] +} \ No newline at end of file diff --git a/327312a2-77d4-439d-a2af-a7d8f476bfd8.json b/327312a2-77d4-439d-a2af-a7d8f476bfd8.json new file mode 100644 index 0000000000000000000000000000000000000000..a366c91fe71787df448f531149bbed7431f94f56 --- /dev/null +++ b/327312a2-77d4-439d-a2af-a7d8f476bfd8.json @@ -0,0 +1,38 @@ +{ + "id": "327312a2-77d4-439d-a2af-a7d8f476bfd8", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "29274927", + "text": "AIM:\nRed and processed meat may be risk factors for breast cancer due to their iron content, administration of oestrogens to cattle or mutagens created during cooking. We studied the associations in UK Biobank and then included the results in a meta-analysis of published cohort studies.\n\nMETHODS:\nUK Biobank, a general population cohort study, recruited participants aged 40-69 years. Incident breast cancer was ascertained via linkage to routine hospital admission, cancer registry and death certificate data. Univariate and multivariable Cox proportional hazard models were used to explore the associations between red and processed meat consumption and breast cancer. Previously published cohort studies were identified from a systematic review using PubMed and Ovid and a meta-analysis conducted using a random effects model.\n\nRESULTS:\nOver a median of 7 years follow-up, 4819 of the 262,195 women developed breast cancer. The risk was increased in the highest tertile (\u003e9 g/day) of processed meat consumption (adjusted hazard ratio [HR] 1.21, 95% confidence interval [CI] 1.08-1.35, p = 0.001). Collation with 10 previous cohort studies provided data on 40,257 incident breast cancers in 1.65 million women. On meta-analysis, processed meat consumption was associated with overall (relative risk [RR] 1.06, 95% CI 1.01-1.11) and post-menopausal (RR 1.09, 95% CI 1.03-1.15), but not pre-menopausal (RR 0.99, 95% CI 0.88-1.10), breast cancer. In UK Biobank and the meta-analysis, red meat consumption was not associated with breast cancer (adjusted HR 0.99 95% CI 0.88-1.12 and RR 1.03, 95% CI 0.99-1.08, respectively).\n\nCONCLUSIONS:\nConsumption of processed meat, but not red meat, may increase the risk of breast cancer." + }, + "questions": [ + { + "id": "229c80a8-76d9-47f6-8d75-dd5b903f5675", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1638, + "text": "Consumption of processed meat" + }, + { + "answer_start": 958, + "text": "highest tertile (\u003e9 g/day) of processed meat consumption" + } + ] + } + ] +} \ No newline at end of file diff --git a/328c3085-5578-4cc9-a051-896f25bdc948.json b/328c3085-5578-4cc9-a051-896f25bdc948.json new file mode 100644 index 0000000000000000000000000000000000000000..319a6baa7085fc3ff039856dc769b29653ae0100 --- /dev/null +++ b/328c3085-5578-4cc9-a051-896f25bdc948.json @@ -0,0 +1,34 @@ +{ + "id": "328c3085-5578-4cc9-a051-896f25bdc948", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "16506213", + "text": "An increase in breast cancer incidence has been reported in areas of Belarus and Ukraine contaminated by the Chernobyl accident and has become an issue of public concern. The authors carried out an ecological epidemiological study to describe the spatial and temporal trends in breast cancer incidence in the most contaminated regions of Belarus and Ukraine, and to evaluate whether increases seen since 1986 correlate to radiation exposure from the Chernobyl accident. The authors investigated the trends through age-cohort-period-region analyses of district-specific incidence rates of breast cancer for Gomel and Mogilev regions of Belarus and Chernigiv, Kyiv and Zhytomir regions of Ukraine. Dose-response analyses were based on Poisson regression, using average district-specific whole body doses accumulated since the accident from external exposure and ingestion of long-lived radionuclides. The study demonstrated increases in breast cancer incidence in all areas following the Chernobyl accident, reflecting improvements in cancer diagnosis and registration. In addition, a significant 2-fold increase in risk was observed, during the period 1997-2001, in the most contaminated districts (average cumulative dose of 40.0 mSv or more) compared with the least contaminated districts (relative risk [RR] in Belarus 2.24, 95% confidence interval [CI] 1.51-3.32 and in Ukraine 1.78, 95% CI=1.08-2.93). The increase, though based on a relatively small number of cases, appeared approximately 10 years after the accident, was highest among women who were younger at the time of exposure and was observed for both localised and metastatic diseases. It is unlikely that this excess could be entirely due to the increased diagnostic activity in these areas." + }, + "questions": [ + { + "id": "db93cfe2-da6f-4cc5-9b34-0ec457edb9af", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 966, + "text": "areas following the Chernobyl accident" + } + ] + } + ] +} \ No newline at end of file diff --git a/32e7810c-5614-4209-8d4d-310a719de6e9.json b/32e7810c-5614-4209-8d4d-310a719de6e9.json new file mode 100644 index 0000000000000000000000000000000000000000..fbb622297b9d6dd63c6ef17bb9ceaaf3bccda500 --- /dev/null +++ b/32e7810c-5614-4209-8d4d-310a719de6e9.json @@ -0,0 +1,39 @@ +{ + "id": "32e7810c-5614-4209-8d4d-310a719de6e9", + "disease": { + "id": "H00056", + "names": [ + "Alzheimer disease", + "Dementia due to Alzheimer disease" + ], + "dbLinks": { + "icd10": [ + "G30" + ], + "mesh": [ + "D000544" + ] + }, + "category": "Neurodegenerative disease" + }, + "article": { + "id": "22197095", + "text": "BACKGROUND:\nEnvironmental tobacco smoke (ETS) is known to be harmful; however, its association with dementia remains controversial and with Alzheimer's disease (AD) is unknown.\n\nMETHODS:\nUsing a standard interview method, the author carried out a multicenter cross-sectional study of dementia in China by examining 2692 never-smoking people aged ≥60 years. Relative risks (RRs) of AD and all dementia, as diagnosed by psychiatrists, in relation to ETS were calculated in a multivariate regression model.\n\nRESULTS:\nThe adjusted RR for all dementia was 1.78 (95% confidence interval [CI]: 1.18-2.68). The increased risk was mainly from exposure to ETS at home (1.87, 95% CI: 1.19-2.93), and it was associated with exposure duration. The adjusted RR for AD was 2.28 (95% CI: 1.82-2.84); the matched figure for ETS exposure at home, at work, and at other places was 2.15 (95% CI: 1.69-2.74), 2.04 (95% CI: 1.72-2.42), and 1.80 (95% CI: 0.96-3.38), respectively. The association of the increased risk with a total cumulative exposure dose was at borderline significance.\n\nCONCLUSIONS:\nThe risk of dementia and AD increased with ETS exposure. Banning smoking in public areas may help reduce a dementia epidemic worldwide." + }, + "questions": [ + { + "id": "a0ded3b1-dbde-4361-b9df-27b00dbd9143", + "text": "What are the risk factors of Alzheimer disease?", + "answers": [ + { + "answer_start": 1123, + "text": "ETS exposure" + }, + { + "answer_start": 634, + "text": "exposure to ETS at home" + } + ] + } + ] +} \ No newline at end of file diff --git a/33a83123-748a-4aae-b7aa-d68b2d3bbc6b.json b/33a83123-748a-4aae-b7aa-d68b2d3bbc6b.json new file mode 100644 index 0000000000000000000000000000000000000000..ffe3ef35e94f94b272d8076d787ad69a1e65e3e1 --- /dev/null +++ b/33a83123-748a-4aae-b7aa-d68b2d3bbc6b.json @@ -0,0 +1,44 @@ +{ + "id": "33a83123-748a-4aae-b7aa-d68b2d3bbc6b", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "22492989", + "text": "RATIONALE:\nThere is limited evidence from population-based studies demonstrating incidence of spirometric-defined chronic obstructive pulmonary disease (COPD) in association with occupational exposures.\n\nOBJECTIVES:\nWe evaluated the association between occupational exposures and incidence of COPD in the Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults (SAPALDIA).\n\nMEASUREMENTS AND MAIN RESULTS:\nPrebronchodilator ratio of forced expiratory volume in 1 second over forced vital capacity (FEV(1)/FVC) was measured in 4,267 nonasthmatic SAPALDIA participants ages 18-62 at baseline in 1991 and at follow-up in 2001-2003. COPD was defined by the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criterion (FEV(1)/FVC \u003c 0.70) and Quanjer reference equation (FEV(1)/FVC \u003c lower limit of normal [LLN]), and categorized by severity (≥ 80% and \u003c80% predicted FEV(1) for stage I and stage II+, respectively). Using a job-exposure matrix, self-reported occupations at baseline were assigned exposures to biological dusts, mineral dusts, gases/fumes, and vapors, gases, dusts, or fumes (VGDF) (high, low, or unexposed as reference). Adjusted incident rate ratios (IRRs) of stage I and stage II+ COPD were estimated in mixed Poisson regression models. Statistically significant (P \u003c 0.05) IRRs of stage II+ GOLD and LLN-COPD, indicating risks between two- and fivefold, were observed for all occupational exposures at high levels. Occupational exposure-associated risk of stage II+ COPD was observed mainly in males and ages ≥ 40 years, and remained elevated when restricted to nonsmokers.\n\nCONCLUSIONS:\nIn a Swiss working adult population, occupational exposures to biological dusts, mineral dusts, gases/fumes, and VGDF were associated with incidence of COPD of at least moderate severity." + }, + "questions": [ + { + "id": "9d3fb414-5c9b-459f-a4fb-f8c8d0130f00", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 1420, + "text": "occupational exposures at high levels" + }, + { + "answer_start": 983, + "text": "occupations at baseline were assigned exposures to biological dusts, mineral dusts, gases/fumes, and vapors, gases, dusts, or fumes (VGDF) (high, low, or unexposed as reference)" + }, + { + "answer_start": 1669, + "text": "occupational exposures to biological dusts, mineral dusts, gases/fumes, and VGDF" + } + ] + } + ] +} \ No newline at end of file diff --git a/33f34065-9175-4575-8b2e-3ec4c04d6f92.json b/33f34065-9175-4575-8b2e-3ec4c04d6f92.json new file mode 100644 index 0000000000000000000000000000000000000000..bb29147db900ea36be0bac1f7abc18f92ccaf010 --- /dev/null +++ b/33f34065-9175-4575-8b2e-3ec4c04d6f92.json @@ -0,0 +1,38 @@ +{ + "id": "33f34065-9175-4575-8b2e-3ec4c04d6f92", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "8602705", + "text": "OBJECTIVE:\nTo describe the incidence of, clinical manifestations of, and risk factors for cyclophosphamide-induced urinary bladder toxicity in patients treated for nonmalignant disease.\n\nDESIGN:\nRetrospective analysis of patients followed at the National Institutes of Allergy and Infectious Diseases from 1967 to 1993.\n\nSETTING:\nThe Warren G. Magnuson Clinical Center of the National Institutes of Health (NIH).\n\nPATIENTS:\n145 patients who received cyclophosphamide for the treatment of Wegener granulomatosis and were followed for 0.5 to 27 years (median, 8.5 years), for a total of 1333 patient-years.\n\nMEASUREMENTS:\nClinical characteristics, cystoscopic findings, results of cytologic examination of urine, surgical pathology, and total dose and duration of cyclophosphamide therapy were recorded and analyzed using a computer-based information retrieval system.\n\nRESULTS:\nNonglomerular hematuria occurred in 73 of 145 patients treated with cyclophosphamide (50%). Sixty of the 73 patients with nonglomerular hematuria (82%) had cystoscopy at the NIH. Forty-two of the 60 patients (70%) who had cystoscopy had macroscopic changes consistent with cyclophosphamide-induced bladder injury. Seven patients (5%) developed transitional-cell carcinoma of the urinary bladder. In 6 of these 7 patients, the total cumulative cyclophosphamide dose exceeded 100 g, and the cumulative duration of cyclophosphamide therapy exceeded 2.7 years. Before they were given a diagnosis of bladder cancer, all 7 patients had had one or more episodes of microscopic or gross nonglomerular hematuria. In contrast, none of the 72 patients who had never had nonglomerular hematuria developed bladder cancer. Cox proportional hazards regression analysis showed that only microscopic nonglomerular hematuria was a significant risk factor for the development of bladder cancer (P \u003c 0.01).\n\nCONCLUSION:\nLong-term oral cyclophosphamide therapy is associated with substantial urotoxicity, including the development of transitional-cell carcinoma of the urinary bladder. In this cohort of patients, the estimated incidence of bladder cancer after the first exposure to cyclophosphamide was 5% at 10 years and 16% at 15 years. Nonglomerular hematuria was a frequent manifestation of cyclophosphamide-induced cystitis, and it identified a subgroup of patients at high risk for the development of bladder cancer." + }, + "questions": [ + { + "id": "37aa25f6-8cd5-4a3b-aa54-af6a0f1fe70f", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 1877, + "text": "Long-term oral cyclophosphamide therapy" + }, + { + "answer_start": 1748, + "text": "microscopic nonglomerular hematuria" + } + ] + } + ] +} \ No newline at end of file diff --git a/34387754-5119-4c93-b664-af3b09ce6fab.json b/34387754-5119-4c93-b664-af3b09ce6fab.json new file mode 100644 index 0000000000000000000000000000000000000000..32b57a21a408b3c52ea64c62ae2ed147fb176543 --- /dev/null +++ b/34387754-5119-4c93-b664-af3b09ce6fab.json @@ -0,0 +1,60 @@ +{ + "id": "34387754-5119-4c93-b664-af3b09ce6fab", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "24383474", + "text": "RATIONALE:\nPulmonary emphysema overlaps partially with spirometrically defined chronic obstructive pulmonary disease and is heritable, with moderately high familial clustering.\n\nOBJECTIVES:\nTo complete a genome-wide association study (GWAS) for the percentage of emphysema-like lung on computed tomography in the Multi-Ethnic Study of Atherosclerosis (MESA) Lung/SNP Health Association Resource (SHARe) Study, a large, population-based cohort in the United States.\n\nMETHODS:\nWe determined percent emphysema and upper-lower lobe ratio in emphysema defined by lung regions less than -950 HU on cardiac scans. Genetic analyses were reported combined across four race/ethnic groups: non-Hispanic white (n = 2,587), African American (n = 2,510), Hispanic (n = 2,113), and Chinese (n = 704) and stratified by race and ethnicity.\n\nMEASUREMENTS AND MAIN RESULTS:\nAmong 7,914 participants, we identified regions at genome-wide significance for percent emphysema in or near SNRPF (rs7957346; P = 2.2 × 10(-8)) and PPT2 (rs10947233; P = 3.2 × 10(-8)), both of which replicated in an additional 6,023 individuals of European ancestry. Both single-nucleotide polymorphisms were previously implicated as genes influencing lung function, and analyses including lung function revealed independent associations for percent emphysema. Among Hispanics, we identified a genetic locus for upper-lower lobe ratio near the α-mannosidase-related gene MAN2B1 (rs10411619; P = 1.1 × 10(-9); minor allele frequency [MAF], 4.4%). Among Chinese, we identified single-nucleotide polymorphisms associated with upper-lower lobe ratio near DHX15 (rs7698250; P = 1.8 × 10(-10); MAF, 2.7%) and MGAT5B (rs7221059; P = 2.7 × 10(-8); MAF, 2.6%), which acts on α-linked mannose. Among African Americans, a locus near a third α-mannosidase-related gene, MAN1C1 (rs12130495; P = 9.9 × 10(-6); MAF, 13.3%) was associated with percent emphysema.\n\nCONCLUSIONS:\nOur results suggest that some genes previously identified as influencing lung function are independently associated with emphysema rather than lung function, and that genes related to α-mannosidase may influence risk of emphysema." + }, + "questions": [ + { + "id": "3620136d-a9d7-47bf-8a79-9d0dc3c97fa9", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 964, + "text": "SNRPF" + }, + { + "answer_start": 1004, + "text": "PPT2" + }, + { + "answer_start": 1400, + "text": "α-mannosidase-related gene MAN2B1" + }, + { + "answer_start": 1465, + "text": "minor allele frequency [MAF]" + }, + { + "answer_start": 1531, + "text": "single-nucleotide polymorphisms associated with upper-lower lobe ratio near DHX15" + }, + { + "answer_start": 1659, + "text": "MGAT5B" + }, + { + "answer_start": 1765, + "text": "a locus near a third α-mannosidase-related gene, MAN1C1" + } + ] + } + ] +} \ No newline at end of file diff --git a/35ad6964-f3bd-4c11-a895-171835e8564f.json b/35ad6964-f3bd-4c11-a895-171835e8564f.json new file mode 100644 index 0000000000000000000000000000000000000000..db7c6456e11160b3220120e45dfc68d2cb452359 --- /dev/null +++ b/35ad6964-f3bd-4c11-a895-171835e8564f.json @@ -0,0 +1,35 @@ +{ + "id": "35ad6964-f3bd-4c11-a895-171835e8564f", + "disease": { + "id": "H00056", + "names": [ + "Alzheimer disease", + "Dementia due to Alzheimer disease" + ], + "dbLinks": { + "icd10": [ + "G30" + ], + "mesh": [ + "D000544" + ] + }, + "category": "Neurodegenerative disease" + }, + "article": { + "id": "9549720", + "text": "The epsilon 4 allele of the apolipoprotein E (apoE) is associated with Alzheimer's disease (AD) and also with elevated serum total cholesterol and low-density lipoprotein levels. However, the interrelationships between apoE genotype, plasma cholesterol levels and AD risk have been studied very little. We examined the possible role of serum total cholesterol in the pathogenesis of AD in a population-based sample of 444 men, aged 70-89 years, who were survivors of the Finnish cohorts of the Seven Countries Study. Previous high serum cholesterol level (mean level \u003e or = 6.5 mmol/l) was a significant predictor of the prevalence of AD (odds ratio = 3.1; 95% confidence interval = 1.2, 8.5) after controlling for age and the presence of apoE epsilon 4 allele. In men who subsequently developed AD the cholesterol level decreased before the clinical manifestations of AD. We conclude that high serum total cholesterol may be an independent risk factor for AD and some of the effect of the apoE epsilon 4 allele on risk of AD might be mediated through high serum cholesterol." + }, + "questions": [ + { + "id": "7b427308-4f85-4760-917d-a34f7a3af520", + "text": "What are the risk factors of Alzheimer disease?", + "answers": [ + { + "answer_start": 890, + "text": "high serum total cholesterol" + } + ] + } + ] +} \ No newline at end of file diff --git a/35b5581f-1db9-4bff-8b6d-ecc918bb89ac.json b/35b5581f-1db9-4bff-8b6d-ecc918bb89ac.json new file mode 100644 index 0000000000000000000000000000000000000000..762a3d008234c3e659226fcf5699c7f6cc5efa5d --- /dev/null +++ b/35b5581f-1db9-4bff-8b6d-ecc918bb89ac.json @@ -0,0 +1,40 @@ +{ + "id": "35b5581f-1db9-4bff-8b6d-ecc918bb89ac", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "7599868", + "text": "It has been hypothesized that nonspecific airway hyperresponsiveness is a risk factor for accelerated pulmonary-function decline during aging and the development of chronic airflow obstruction. We tested this hypothesis in a prospective, longitudinal study of 912 middle-aged and older men (median age, 60 yr; range, 41 to 86 yr) participating in the Normative Aging Study (NAS). Subjects underwent methacholine challenge testing and spirometry at the time of a regularly scheduled NAS examination, and follow-up spirometry was performed after a median interval of 3.3 yr. Allergy skin testing with a panel of four aeroallergens (mixed grasses, mixed trees, ragweed, and house dust) was also performed at the initial examination. Methacholine responsiveness was expressed as the dose-response slope (DRS) (i.e., the slope of a line connecting the origin with the last point of the methacholine dose-response plot) in units of percent decline FEV1/mumol methacholine. The relationship of the methacholine DRS to the subsequent rate of annual decline in lung function (FEV1, FVC, and FEV1/FVC) was examined using multiple linear-regression models with the rates of pulmonary-function decline as the outcome variables. After adjusting for age, height, smoking status, and initial level of lung function, the log10 DRS was a significant predictor of the rate of decline of FEV1 (regression coefficient beta = 12.8, p = 0.03) and FEV1/FVC x 100 (beta = 0.506, p = 0.0001), and a borderline significant predictor of FVC (beta = 15.3, p = 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)" + }, + "questions": [ + { + "id": "e578fe85-cb2d-4439-a6f7-5fa802b136d3", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 1311, + "text": "DRS" + }, + { + "answer_start": 779, + "text": "dose-response slope (DRS) (i.e., the slope of a line connecting the origin with the last point of the methacholine dose-response plot)" + } + ] + } + ] +} \ No newline at end of file diff --git a/360972a2-a549-4a50-9851-d7e8855bf469.json b/360972a2-a549-4a50-9851-d7e8855bf469.json new file mode 100644 index 0000000000000000000000000000000000000000..393a8c96b705a7d5c8a010e3b86c4000d7dcc189 --- /dev/null +++ b/360972a2-a549-4a50-9851-d7e8855bf469.json @@ -0,0 +1,38 @@ +{ + "id": "360972a2-a549-4a50-9851-d7e8855bf469", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "9075814", + "text": "Risk factors associated with the progression from impaired glucose tolerance (IGT) to NIDDM were examined in data from six prospective studies. IGT and NIDDM were defined in all studies by World Health Organization (WHO) criteria, and baseline risk factors were measured at the time of first recognition of IGT. The studies varied in size from 177 to 693 participants with IGT, and included men and women followed from 2 to 27 years after the recognition of IGT. Across the six studies, the incidence rate of NIDDM was 57.2/1,000 person-years and ranged from 35.8/1,000 to 87.3/1,000 person-years. Although baseline measures of fasting and 2-h postchallenge glucose levels were both positively associated with NIDDM incidence, incidence rates were sharply higher for those in the top quartile of fasting plasma glucose levels, but increased linearly with increasing 2-h postchallenge glucose quartiles. Incidence rates were higher among the Hispanic, Mexican-American, Pima, and Nauruan populations than among Caucasians. The effect of baseline age on NIDDM incidence rates differed among the studies; the rates did not increase or rose only slightly with increasing baseline age in three of the studies and formed an inverted U in three studies. In all studies, estimates of obesity (including BMI, waist-to-hip ratio, and waist circumference) were positively associated with NIDDM incidence. BMI was associated with NIDDM incidence independently of fasting and 2-h post challenge glucose levels in the combined analysis of all six studies and in three cohorts separately, but not in the three studies with the highest NIDDM incidence rates. Sex and family history of diabetes were generally not related to NIDDM progression. This analysis indicates that persons with IGT are at high risk and that further refinement of risk can be made by other simple measurements. The ability to identify persons at high risk of NIDDM should facilitate clinical trials in diabetes prevention." + }, + "questions": [ + { + "id": "ce385284-aa46-4c47-bdbc-e18e76f51fd5", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1263, + "text": "estimates of obesity (including BMI, waist-to-hip ratio, and waist circumference)" + }, + { + "answer_start": 1394, + "text": "BMI" + } + ] + } + ] +} \ No newline at end of file diff --git a/361e8deb-7626-401c-b927-aba62a88bb28.json b/361e8deb-7626-401c-b927-aba62a88bb28.json new file mode 100644 index 0000000000000000000000000000000000000000..2fa2e65e2920e4bc14b518048387dc5d79b53293 --- /dev/null +++ b/361e8deb-7626-401c-b927-aba62a88bb28.json @@ -0,0 +1,49 @@ +{ + "id": "361e8deb-7626-401c-b927-aba62a88bb28", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "21912438", + "text": "OBJECTIVES:\nDiabetes mellitus (DM) has been associated with an increased risk of colorectal cancer (CRC). The American College of Gastroenterology Guidelines for Colorectal Cancer Screening 2008 recommend that clinicians be aware of an increased CRC risk in patients with smoking and obesity, but do not highlight the increase in CRC risk in patients with DM. To provide an updated quantitative assessment of the association of DM with colon cancer (CC) and rectal cancer (RC), we conducted a meta-analysis of case-control and cohort studies. We also evaluated whether the association varied by sex, and assessed potential confounders including obesity, smoking, and exercise.\n\nMETHODS:\nWe identified studies by searching the EMBASE and MEDLINE databases (from inception through 31 December 2009) and by searching bibliographies of relevant articles. Summary relative risks (RRs) with 95% confidence intervals (CIs) were calculated with fixed- and random-effects models. Several subgroup analyses were performed to explore potential study heterogeneity and bias.\n\nRESULTS:\nDM was associated with an increased risk of CC (summary RR 1.38, 95% CI 1.26-1.51; n=14 studies) and RC (summary RR 1.20, 95% CI 1.09-1.31; n=12 studies). The association remained when we limited the meta-analysis to studies that either controlled for smoking and obesity, or for smoking, obesity, and physical exercise. DM was associated with an increased risk of CC for both men (summary RR 1.43, 95% CI 1.30-1.57; n=11 studies) and women (summary RR 1.35, 95% CI 1.14-1.53; n=10 studies). For RC, there was a significant association between DM and cancer risk for men (summary RR 1.22, 95% CI 1.07-1.40; n=8 studies), but not for women (summary RR 1.09, 95% CI=0.99-1.19; n=8 studies).\n\nCONCLUSIONS:\nThese data suggest that DM is an independent risk factor for colon and rectal cancer. Although these findings are based on observational epidemiological studies that have inherent limitations due to diagnostic bias and confounding, subgroup analyses confirmed the consistency of our findings across study type and population. This information can inform risk models and specialty society CRC screening guidelines." + }, + "questions": [ + { + "id": "09598b98-7887-4e87-9231-20a95a050ca2", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1073, + "text": "DM" + }, + { + "answer_start": 12, + "text": "Diabetes mellitus (DM)" + }, + { + "answer_start": 1394, + "text": "DM" + }, + { + "answer_start": 1800, + "text": "DM" + } + ] + } + ] +} \ No newline at end of file diff --git a/3627acf5-3b33-4628-bda9-95803e2531ca.json b/3627acf5-3b33-4628-bda9-95803e2531ca.json new file mode 100644 index 0000000000000000000000000000000000000000..31a8946b27d5f7173bea21bf191016ef12bfb284 --- /dev/null +++ b/3627acf5-3b33-4628-bda9-95803e2531ca.json @@ -0,0 +1,39 @@ +{ + "id": "3627acf5-3b33-4628-bda9-95803e2531ca", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "27050141", + "text": "IMPORTANCE:\nDespite the unquestioned relationship of UV radiation (UVR) exposure and melanoma development, UVR-independent development of melanoma has only recently been described in mice. These findings in mice highlight the importance of the genetic background of the host and could be relevant for preventive measures in humans.\n\nOBJECTIVE:\nTo study the role of the melanocortin-1 receptor (MC1R) and melanoma risk independently from UVR in a clinical setting.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nHospital-based case-control study, including genetic testing, questionnaires, and physical data (Molecular Markers of Melanoma Study data set) including 991 melanoma patients (cases) and 800 controls.\n\nMAIN OUTCOMES AND MEASURES:\nAssociation of MC1R variants and melanoma risk independent from sun exposure variables.\n\nRESULTS:\nThe 1791 participants included 991 with a diagnosis of melanoma and 800 control patients (mean [SD] age, 59.2 [15.6] years; 50.5% male). Compared with wild-type carriers, carriers of MC1R variants were at higher melanoma risk after statistically adjusting for previous UVR exposure (represented by prior sunburns and signs of actinic skin damage identified by dermatologists), age, and sex compared with wild-type carriers (≥2 variants, OR, 2.13 [95% CI, 1.66-2.75], P \u003c .001; P for trend \u003c.001). After adjustment for sex, age, sunburns in the past, and signs of actinic skin damage, the associations remained significant (OR, 1.65 [95% CI, 1.02-2.67] for R/R, OR, 2.63 [95% CI, 1.82-3.81] for R/r; OR, 1.83 [95% CI, 1.36-2.48] for R/0; and OR, 1.50 [95% CI, 1.01-2.21] for r/r, with P values ranging from \u003c.001 to .04 when adjusted for facial actinic skin damage; OR, 2.36 [95% CI, 1.62-3.43] for R/r; and OR, 1.47 [95% CI, 1.08-1.99] for R/0 with P values ranging from \u003c.001 to .01 when adjusted for dorsal actinic skin damage; and OR, 2.54 [95% CI, 1.76-3.67] for R/r, OR, 1.75 [95% CI, 1.30-2.36] for R/0; and OR, 1.50 [95% CI, 1.02-2.20] for r/r with P values ranging from \u003c.001 to .04 when adjusted for actinic skin damage on the hands).\n\nCONCLUSIONS AND RELEVANCE:\nCarriers of MC1R variants were at increased melanoma risk independent of their sun exposure. Further studies are required to elucidate the causes of melanoma development in these individuals." + }, + "questions": [ + { + "id": "9d6e2bcb-16e9-46a6-875d-dbd1689d5e76", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 999, + "text": "carriers of MC1R variants" + }, + { + "answer_start": 2100, + "text": "Carriers of MC1R variants" + } + ] + } + ] +} \ No newline at end of file diff --git a/369e22b1-c164-4e0c-9d91-21fcb77791a0.json b/369e22b1-c164-4e0c-9d91-21fcb77791a0.json new file mode 100644 index 0000000000000000000000000000000000000000..ae91e94d125eca32ec716559ad2e20974fe08a8d --- /dev/null +++ b/369e22b1-c164-4e0c-9d91-21fcb77791a0.json @@ -0,0 +1,50 @@ +{ + "id": "369e22b1-c164-4e0c-9d91-21fcb77791a0", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "19910503", + "text": "OBJECTIVE:\nTo assess the relationship between habitual sleep disturbances and the incidence of type 2 diabetes and to obtain an estimate of the risk.\n\nRESEARCH DESIGN AND METHODS:\nWe conducted a systematic search of publications using MEDLINE (1955-April 2009), EMBASE, and the Cochrane Library and manual searches without language restrictions. We included studies if they were prospective with follow-up \u003e3 years and had an assessment of sleep disturbances at baseline and incidence of type 2 diabetes. We recorded several characteristics for each study. We extracted quantity and quality of sleep, how they were assessed, and incident cases defined with different validated methods. We extracted relative risks (RRs) and 95% CI and pooled them using random-effects models. We performed sensitivity analysis and assessed heterogeneity and publication bias.\n\nRESULTS:\nWe included 10 studies (13 independent cohort samples; 107,756 male and female participants, follow-up range 4.2-32 years, and 3,586 incident cases of type 2 diabetes). In pooled analyses, quantity and quality of sleep predicted the risk of development of type 2 diabetes. For short duration of sleep (\u003c or =5-6 h/night), the RR was 1.28 (95% CI 1.03-1.60, P = 0.024, heterogeneity P = 0.015); for long duration of sleep (\u003e8-9 h/night), the RR was 1.48 (1.13-1.96, P = 0.005); for difficulty in initiating sleep, the RR was 1.57 (1.25-1.97, P \u003c 0.0001); and for difficulty in maintaining sleep, the RR was 1.84 (1.39-2.43, P \u003c 0.0001).\n\nCONCLUSIONS:\nQuantity and quality of sleep consistently and significantly predict the risk of the development of type 2 diabetes. The mechanisms underlying this relation may differ between short and long sleepers." + }, + "questions": [ + { + "id": "7429d735-84d3-4abe-a8a5-a789a1e9e179", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1146, + "text": "short duration of sleep (\u003c or =5-6 h/night)" + }, + { + "answer_start": 1267, + "text": "long duration of sleep (\u003e8-9 h/night)" + }, + { + "answer_start": 1350, + "text": "difficulty in initiating sleep" + }, + { + "answer_start": 1431, + "text": "difficulty in maintaining sleep" + }, + { + "answer_start": 1519, + "text": "Quantity and quality of sleep" + } + ] + } + ] +} \ No newline at end of file diff --git a/387162f1-e7e4-476f-89c2-c5d0e00ef15e.json b/387162f1-e7e4-476f-89c2-c5d0e00ef15e.json new file mode 100644 index 0000000000000000000000000000000000000000..ea5b133f47c4122e7183c41e53ec8a8b2db37d7e --- /dev/null +++ b/387162f1-e7e4-476f-89c2-c5d0e00ef15e.json @@ -0,0 +1,35 @@ +{ + "id": "387162f1-e7e4-476f-89c2-c5d0e00ef15e", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "15583688", + "text": "Among 14,088 patients, with a primary diagnosis of Parkinson's disease during the period 1977-98 identified from the National Register of Patients, 1282 cancers were subsequently recorded in the Danish Cancer Registry, compared with 1464 expected, with a standardised incidence ratio (SIR) of 0.88 (95% confidence interval (CI), 0.8-0.9). Significantly reduced risks were found for smoking-related cancers, for example, cancers of the lung (SIR, 0.38), larynx (0.47) and urinary bladder (0.52), although moderate reductions in risk were also seen for several nonsmoking-related cancers. In contrast, increased risks were seen for malignant melanoma (SIR, 1.95; 95% CI, 1.4-2.6), nonmelanocytic skin cancer (1.25; 1.1-1.4) and breast cancer (1.24; 1.0-1.5). The observed cancer pattern supports the hypothesis that constituents of tobacco smoke inhibit or delay the development of Parkinson's disease, but a low smoking prevalence appears to be only part of the explanation for the decreased cancer incidence. The increased relative risks of melanoma and nonmelanoma skin cancer are not likely to be artefactual, but further investigations of potential mechanisms are warranted." + }, + "questions": [ + { + "id": "d190cda7-ea7a-4195-9df3-6fb3e21b0565", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 51, + "text": "Parkinson's disease" + } + ] + } + ] +} \ No newline at end of file diff --git a/38760717-d9f4-4d14-86b3-712640540f7f.json b/38760717-d9f4-4d14-86b3-712640540f7f.json new file mode 100644 index 0000000000000000000000000000000000000000..8a11e76cabd41f2bf45a4f5605c9f6007e264967 --- /dev/null +++ b/38760717-d9f4-4d14-86b3-712640540f7f.json @@ -0,0 +1,37 @@ +{ + "id": "38760717-d9f4-4d14-86b3-712640540f7f", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "24292448", + "text": "BACKGROUND:\nThe BRCA1 and BRCA2 genes confer increased susceptibility to breast and ovarian cancer and to a spectrum of other cancers. There is controversy regarding the risk of colorectal cancer conferred by germline mutations in these two genes.\n\nMETHODS:\nWe followed 7015 women with a BRCA mutation for new cases of colorectal cancer. Incidence rates in carriers were compared with population-specific incidence rates, and standardised incidence ratios (SIRs) were estimated. The expected numbers of cancers were computed by multiplying person-years at risk by the appropriate age-, sex- and country-specific incidence rates from the five countries.\n\nRESULTS:\nTwenty-one incident colorectal cancer cases were observed among all mutation carriers, compared with 23.6 cases expected. The SIR for BRCA1 carriers was 0.92 (95% confidence interval (CI), 0.54-1.40, P=0.7) and for BRCA2 carriers was 0.82 (95% CI, 0.30-1.81, P=0.7). The SIR for colon cancer was 3.81 (95% CI 1.77-7.23) for women below the age of 50 years (both genes combined) and was 0.60 (95% CI 0.33-1.00) for women aged 50 years and above.\n\nCONCLUSION:\nThe risk of colorectal cancer is increased in female carriers of BRCA1 mutations below the age of 50 years but not in women with BRCA2 mutations or in older women." + }, + "questions": [ + { + "id": "bfb709dd-5dfa-4bc4-9dbf-f70d67d0f32c", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1167, + "text": "female carriers of BRCA1 mutations below the age of 50 years" + } + ] + } + ] +} \ No newline at end of file diff --git a/38bbd75f-7a28-4b27-b0ab-8582c1391085.json b/38bbd75f-7a28-4b27-b0ab-8582c1391085.json new file mode 100644 index 0000000000000000000000000000000000000000..7a10d332df513e2e3fea7d182b513a927ac63835 --- /dev/null +++ b/38bbd75f-7a28-4b27-b0ab-8582c1391085.json @@ -0,0 +1,38 @@ +{ + "id": "38bbd75f-7a28-4b27-b0ab-8582c1391085", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "12681453", + "text": "PURPOSE:\nRecent reports suggest that decreased functional capacity in patients with heart failure may be associated with abnormalities in glucose metabolism. We followed patients with coronary artery disease who participated in the Bezafibrate Infarction Prevention study to determine the incidence of diabetes by baseline functional status during a 7.7-year follow-up.\n\nMETHODS:\nThe sample comprised 2616 nondiabetic patients aged 45 to 74 years with a fasting blood glucose level \u003c7 mmol/L (126 mg/dL). They were divided into three groups by New York Heart Association (NYHA) criteria: class I (n = 1986 patients), class II (n = 518), and class III (n = 112). The detection of a fasting blood glucose level \u003e or =7 mmol/L during follow-up was defined as the criterion for the development of diabetes.\n\nRESULTS:\nThe study groups had similar demographic and clinical characteristics, except that patients with symptomatic heart failure (NYHA class II or III) were more likely to have angina. During follow-up, diabetes developed in 259 patients (13%) in NYHA class I, 76 (15%) in class II, and 22 (20%) in class III (P for trend = 0.05). At the last visit, patients in NYHA class III were twice as likely (17% [n = 19]) to have fasting blood glucose levels \u003e or =7 mmol/L as those in NYHA class I (7.8% [n = 154]) or class II (8.7% [n = 45]) (P = 0.005). In a multivariate analysis, NYHA class III was associated with a 1.7-fold (95% confidence interval [CI]: 1.1 to 2.6) increase in the rate of development of diabetes, but NYHA class II was not (hazard ratio = 1.0; 95% CI: 0.8 to 1.3).\n\nCONCLUSION:\nAmong patients with coronary artery disease, advanced heart failure (NYHA class III) is associated with a significantly increased risk of developing diabetes during a 6- to 9-year follow-up." + }, + "questions": [ + { + "id": "7601efaa-bec6-420f-ac49-0b60edb6e423", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1647, + "text": "advanced heart failure (NYHA class III)" + }, + { + "answer_start": 1383, + "text": "NYHA class III" + } + ] + } + ] +} \ No newline at end of file diff --git a/38c84030-084a-4ae3-9c60-b84f1b2c7f17.json b/38c84030-084a-4ae3-9c60-b84f1b2c7f17.json new file mode 100644 index 0000000000000000000000000000000000000000..d20285756e8c91d6c77cf1fa05ad6de048c3d44b --- /dev/null +++ b/38c84030-084a-4ae3-9c60-b84f1b2c7f17.json @@ -0,0 +1,43 @@ +{ + "id": "38c84030-084a-4ae3-9c60-b84f1b2c7f17", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "25495759", + "text": "The impact of early childhood traffic-related air pollution (TRAP) exposure on development of asthma and allergies remains unclear. Birth cohort studies are the best available study design to answer this question, but the evidence from such studies has not been synthesized to date. We conducted a systematic review and meta-analyses of published birth cohort studies to understand the association between early childhood TRAP exposure, and subsequent asthma, allergies and sensitization. Increased longitudinal childhood exposure to PM2.5 and black carbon was associated with increasing risk of subsequent asthma in childhood (PM2.5 : OR 1.14, 95%CI 1.00 to 1.30 per 2 μg/m(3) and black carbon: OR 1.20, 95%CI 1.05 to 1.38 per 1 × 10(-5) m(-1) ). Also, early childhood exposure to TRAP was associated with development of asthma across childhood up to 12 years of age. The magnitude of these associations increased with age, and the pattern was prominent for PM2.5 . Increasing exposure to PM2.5 was associated with sensitization to both aero- and food allergens. There was some evidence that TRAP was associated with eczema and hay fever. In summary, exposure to TRAP was related to asthma and allergic diseases. However, the substantial variability across studies warrants long-term birth cohort studies with regular repeated follow-ups to confirm these findings." + }, + "questions": [ + { + "id": "0baa9f11-87d5-43fb-860d-1c77876e849b", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 512, + "text": "childhood exposure to PM2.5 and black carbon" + }, + { + "answer_start": 754, + "text": "early childhood exposure to TRAP " + }, + { + "answer_start": 1152, + "text": "exposure to TRAP" + } + ] + } + ] +} \ No newline at end of file diff --git a/38ee30d2-adba-405c-8ea8-18ff0498c287.json b/38ee30d2-adba-405c-8ea8-18ff0498c287.json new file mode 100644 index 0000000000000000000000000000000000000000..9f58e6452aeff67c226a158d30dd5a6360814f26 --- /dev/null +++ b/38ee30d2-adba-405c-8ea8-18ff0498c287.json @@ -0,0 +1,41 @@ +{ + "id": "38ee30d2-adba-405c-8ea8-18ff0498c287", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "20883538", + "text": "This study was to evaluate the frequency of colorectal neoplasia in renal transplant recipients and to investigate the association with Epstein-Barr virus (EBV) and cytomegalovirus (CMV) infection. We compared the frequency of colorectal neoplasia among renal transplant recipients with that of the healthy subjects. Specimens of colorectal neoplasia were examined for EBV and CMV using in situ hybridization and immunohistochemistry, respectively. Of 796 renal transplantation cohorts, 315 were enrolled. The frequency of colorectal neoplasia among the patients was 22.9%. Compared with the healthy subjects, the odds ratio (OR) for advanced adenoma was 3.32 (95% CI, 1.81-6.10). The frequency of cancer among the patients was 1.9% (OR, 12.0; 95% CI, 1.45-99.7). A long interval between transplantation and colonoscopy was a significant factor in the development of advanced colorectal neoplasia. EBV positivity was detected in 30.6% of colorectal neoplasia specimens from renal transplant recipients, which was higher than that for the controls (p = 0.002). CMV was not detected in any lesions of patients or controls. In conclusion, renal transplant recipients have a significantly increased risk of advanced colorectal neoplasia. EBV was more frequently found in specimens of advanced colorectal neoplasm obtained from the renal transplant recipients." + }, + "questions": [ + { + "id": "5acc1521-f874-45cb-931d-79491a6bdd3a", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1136, + "text": "renal transplant recipients" + }, + { + "answer_start": 764, + "text": "A long interval between transplantation and colonoscopy" + } + ] + } + ] +} \ No newline at end of file diff --git a/38f10a47-ead7-4536-af82-da481b9d41ee.json b/38f10a47-ead7-4536-af82-da481b9d41ee.json new file mode 100644 index 0000000000000000000000000000000000000000..7e93b6639148ab8ca049395df81c717429e95b82 --- /dev/null +++ b/38f10a47-ead7-4536-af82-da481b9d41ee.json @@ -0,0 +1,50 @@ +{ + "id": "38f10a47-ead7-4536-af82-da481b9d41ee", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "24590452", + "text": "Recent cohort studies suggest that increased breast cancer risks were associated with longer smoking duration, higher pack-years and a dose-response relationship with increasing pack-years of smoking between menarche and first full-term pregnancy (FFTP). Studies with comprehensive quantitative life-time measures of passive smoking suggest an association between passive smoking dose and breast cancer risk. We conducted a study within the European Prospective Investigation into Cancer and Nutrition to examine the association between passive and active smoking and risk of invasive breast cancer and possible effect modification by known breast cancer risk factors. Among the 322,988 women eligible for the study, 9,822 developed breast cancer (183,608 women with passive smoking information including 6,264 cases). When compared to women who never smoked and were not being exposed to passive smoking at home or work at the time of study registration, current, former and currently exposed passive smokers were at increased risk of breast cancer (hazard ratios (HR) [95% confidence interval (CI)] 1.16 [1.05-1.28], 1.14 [1.04-1.25] and 1.10 [1.01-1.20], respectively). Analyses exploring associations in different periods of life showed the most important increase in risk with pack-years from menarche to FFTP (1.73 [1.29-2.32] for every increase of 20 pack-years) while pack-years smoked after menopause were associated with a significant decrease in breast cancer risk (HR = 0.53, 95% CI: 0.34-0.82 for every increase of 20 pack-years). Our results provide an important replication, in the largest cohort to date, that smoking (passively or actively) increases breast cancer risk and that smoking between menarche and FFTP is particularly deleterious." + }, + "questions": [ + { + "id": "e2c6a484-e271-4dbb-8934-65a6f6167320", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 956, + "text": "current, former and currently exposed passive smokers" + }, + { + "answer_start": 1282, + "text": "pack-years from menarche to FFTP" + }, + { + "answer_start": 227, + "text": "full-term pregnancy (FFTP)" + }, + { + "answer_start": 111, + "text": "higher pack-years and a dose-response relationship with increasing pack-years of smoking between menarche and first full-term pregnancy (FFTP)" + }, + { + "answer_start": 1696, + "text": "smoking between menarche and FFTP" + } + ] + } + ] +} \ No newline at end of file diff --git a/38f67829-ccd7-4c07-8581-1aea94da4b01.json b/38f67829-ccd7-4c07-8581-1aea94da4b01.json new file mode 100644 index 0000000000000000000000000000000000000000..4dcc5db7d40d15eb96e4c6576e212385fb2eb84c --- /dev/null +++ b/38f67829-ccd7-4c07-8581-1aea94da4b01.json @@ -0,0 +1,35 @@ +{ + "id": "38f67829-ccd7-4c07-8581-1aea94da4b01", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "25359350", + "text": "Are maternal vitamin D and E intakes during pregnancy associated with asthma in 10-year-old children? In a longitudinal study of 1924 children born to women recruited during pregnancy, maternal vitamin D intake during pregnancy was assessed by the Food Frequency Questionnaire (FFQ) and vitamin E by FFQ and plasma α-tocopherol; respiratory questionnaires were completed for the 10-year-old children. Their treatment for asthma was also ascertained using administrative data. Longitudinal analyses included data collected at 1, 2, 5 and 10 years. Symptom data were available for 934 (49%) children and use of asthma medication for 1748 (91%). In the children maternal vitamin D intake during pregnancy was negatively associated with doctor-diagnosed asthma at 10 years of age (OR per intake quintile 0.86, 95% CI 0.74-0.99) and over the first 10 years (hazard ratio 0.90, 95% CI 0.81-1.00). Maternal plasma α-tocopherol at 11 weeks gestation was negatively associated with children receiving asthma treatment (OR per standard deviation increase 0.52, 95% CI 0.31-0.87). Maternal vitamin E intake was negatively associated with doctor-diagnosed asthma (OR 0.89, 95% CI 0.81-0.99) in the first 10 years. Low maternal vitamin D and E intakes during pregnancy are associated with increased risk of children developing asthma in the first 10 years of life. These associations may have significant public health implications." + }, + "questions": [ + { + "id": "f67c630e-bee0-4015-94d5-863bc7f1df36", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1202, + "text": "Low maternal vitamin D and E intakes during pregnancy" + } + ] + } + ] +} \ No newline at end of file diff --git a/395714e9-d336-4843-8dae-217a1387e13b.json b/395714e9-d336-4843-8dae-217a1387e13b.json new file mode 100644 index 0000000000000000000000000000000000000000..0085298c07646f1528ab3de247a4b17fcea511b5 --- /dev/null +++ b/395714e9-d336-4843-8dae-217a1387e13b.json @@ -0,0 +1,39 @@ +{ + "id": "395714e9-d336-4843-8dae-217a1387e13b", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "26825289", + "text": "OBJECTIVE:\nTo assess our prospective mother-child cohort and the national registry data to analyze the risk of asthma by delivery mode and whether cesarean delivery before or after membrane rupture affects this risk differently.\n\nSTUDY DESIGN:\nThe Copenhagen Prospective Studies on Asthma in Childhood2000 is a high-risk birth cohort of 411 Danish children. Asthma was diagnosed prospectively by physicians at the research site, and associations with cesarean delivery were investigated using Cox proportional hazard models. From the Danish national prospective registry we included data from 1997-2010. Childhood asthma was defined from recurrent use of inhaled corticosteroids filled at pharmacies. Cesarean delivery was classified as either before or after rupture of membranes, and the risk of asthma was compared with vaginal delivery. Results were adjusted stepwise for age and calendar year, sex, birth weight, gestational age, multiple births, parity, and maternal factors (age, smoking/antibiotics during pregnancy, employment status, and asthma).\n\nRESULTS:\nIn the Copenhagen Prospective Studies on Asthma in Childhood2000 cohort, the adjusted hazard ratio for asthma was increased by cesarean delivery relative to vaginal birth 2.18 (1.27-3.73). Registry data replicated these findings. Cesarean delivery performed before rupture of membranes carried significantly higher risk of asthma, (incidence rate ratio to vaginal delivery 1.20 [1.16-1.23]) than cesarean delivery after rupture of membranes (incidence rate ratio to vaginal delivery 1.12 [1.09-1.16]).\n\nCONCLUSIONS:\nWe confirmed cesarean delivery to be a risk factor for childhood asthma. This effect was more pronounced for cesarean delivery performed before rupture of membranes." + }, + "questions": [ + { + "id": "c320b9a1-4405-498b-b9d9-caa71f111899", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1596, + "text": "cesarean delivery" + }, + { + "answer_start": 1692, + "text": "cesarean delivery performed before rupture of membranes" + } + ] + } + ] +} \ No newline at end of file diff --git a/39cab779-3e78-4fb3-aaec-b2a95579bf74.json b/39cab779-3e78-4fb3-aaec-b2a95579bf74.json new file mode 100644 index 0000000000000000000000000000000000000000..4bf6afda7646fe82b01af3fcd6a54bbdf0353f06 --- /dev/null +++ b/39cab779-3e78-4fb3-aaec-b2a95579bf74.json @@ -0,0 +1,34 @@ +{ + "id": "39cab779-3e78-4fb3-aaec-b2a95579bf74", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "10889174", + "text": "Our knowledge of celiac disease pathogenesis has recently made rapid progress. The disorder is now considered the result of a complex interplay of intrinsic (genetic) and variable extrinsic (environmental) factors that explain the wide spectrum of clinical manifestations ranging from asymptomatic to severe malabsorption. Gluten peptides are efficiently presented by celiac disease-specific HLA-DQ2- and HLA-DQ8-positive antigen-presenting cells, and thus drive the immune response, predominantly in the connective tissue of the lamina propria. Tissue transglutaminase, which has been identified as the highly specific endomysial autoantigen, is released from cells during inflammation. It may potentiate antigen presentation by HLA-DQ2 and HLA-DQ8 by deamidating or cross-linking gluten peptides. The result is lamina propria T-cell activation and mucosal transformation by activated intestinal fibroblasts. In the future, manipulation of the gut-associated lymphoid tissue may allow reduced sensitivity or even generate oral tolerance to gluten. Long-standing untreated celiac disease, even if clinically silent, predisposes for other autoimmune diseases. Therefore, population screening for immunoglobulin A antibodies to tissue transglutaminase seems justified." + }, + "questions": [ + { + "id": "a1e9cbea-6119-401d-bbd1-f8f7d72e71bf", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 392, + "text": "HLA-DQ2- and HLA-DQ8-positive antigen-presenting cells" + } + ] + } + ] +} \ No newline at end of file diff --git a/3a2fcf91-7a0f-43aa-9e73-5507026af360.json b/3a2fcf91-7a0f-43aa-9e73-5507026af360.json new file mode 100644 index 0000000000000000000000000000000000000000..ccf0864a5c8fa9dcefe45d2fefc38d59ec141cb4 --- /dev/null +++ b/3a2fcf91-7a0f-43aa-9e73-5507026af360.json @@ -0,0 +1,39 @@ +{ + "id": "3a2fcf91-7a0f-43aa-9e73-5507026af360", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "7952544", + "text": "The association between passive exposure to tobacco smoke and respiratory symptoms was examined in a sample of 4,197 never-smoking adults. They constituted the never-smoking subsample of a random sample of 9,651 adults (age, 18 to 60 yr) in eight areas in Switzerland. Information on passive smoking exposure and standardized questions on respiratory symptoms were obtained via a questionnaire administered by trained examiners. After controlling for age, sex, body mass index (BMI), study area, atopy, and parental and sibling history, passive smoking exposure was associated with an elevated risk of wheezing apart from colds (odds ratio [OR] = 1.94, 95% CI = 1.39 to 2.70), an elevated risk of bronchitis symptoms (OR = 1.59, 95% CI = 1.17 to 2.15), an elevated risk of symptoms of chronic bronchitis (OR = 1.65, 95% CI = 1.28 to 2.16), an elevated risk of dyspnea (OR = 1.45, 95% CI = 1.20 to 1.76), and an elevated risk of physician diagnosed asthma (OR = 1.39, 95% CI = 1.04 to 1.86). It was not associated with any increased risk of allergic rhinitis including hayfever. Adding a variable for low educational level, excluding subjects whose mother ever smoked or subjects with end-expiratory CO levels \u003e or = 7 ppm, and controlling for paternal smoking during childhood or occupational exposure had little impact on the association. The association of passive smoking exposure with dyspnea, wheeze, and asthma showed evidence of a dose-dependent increase with hours per day of exposure, whereas association with symptoms of bronchitis was stronger with years of exposure.(ABSTRACT TRUNCATED AT 250 WORDS)" + }, + "questions": [ + { + "id": "ec91b356-7ef9-44e5-8272-40fb61265f3d", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 537, + "text": "passive smoking exposure" + }, + { + "answer_start": 1359, + "text": "passive smoking exposure" + } + ] + } + ] +} \ No newline at end of file diff --git a/3ab00786-1e44-4a94-bcf2-8a350a5c70aa.json b/3ab00786-1e44-4a94-bcf2-8a350a5c70aa.json new file mode 100644 index 0000000000000000000000000000000000000000..bf5d6d383495b915097f34543faa93316445fa24 --- /dev/null +++ b/3ab00786-1e44-4a94-bcf2-8a350a5c70aa.json @@ -0,0 +1,39 @@ +{ + "id": "3ab00786-1e44-4a94-bcf2-8a350a5c70aa", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "25779102", + "text": "OBJECTIVE:\nTo test the a priori hypothesis that acute and chronic work exposures to the World Trade Center (WTC) site on or after September 11, 2001 were associated with risk of new-onset systemic autoimmune diseases.\n\nMETHODS:\nA nested case-control study was performed in WTC rescue/recovery workers who had received a rheumatologist-confirmed systemic autoimmune disease diagnosis between September 12, 2001 and September 11, 2013 (n = 59), each of whom was individually matched to 4 randomly selected controls (n = 236) on the basis of year of hire (±1 year), sex, race, and work assignment (firefighter or emergency medical service). Acute exposure was defined according to the earliest time of arrival (morning of 9/11 versus later) at the WTC site, and chronic exposure was defined as duration (number of months) of WTC site-related work. Rheumatologists were blinded with regard to each subject's exposure status. The conditional odds ratios (CORs) with 95% confidence intervals (95% CIs) for incident autoimmune disease were derived from exact conditional logistic regression models.\n\nRESULTS:\nRheumatoid arthritis was the most common autoimmune diagnosis (37% of subjects), followed by spondyloarthritis (22%), inflammatory myositis (14%), systemic lupus erythematosus (12%), systemic sclerosis (5%), Sjögren's syndrome (5%), antiphospholipid syndrome (3%), and granulomatosis with polyangiitis (Wegener's) (2%). The COR for incident autoimmune disease increased by 13% (COR 1.13, 95% CI 1.02-1.26) for each additional month worked at the WTC site. These odds were independent of the association between high acute exposure (working during the morning of 9/11) and disease outcome, which conveyed an elevated, but not statistically significant, risk (COR 1.85, 95% CI 0.86-3.89).\n\nCONCLUSION:\nProlonged work at the WTC site, independent of acute exposure, was an important predictor of post-9/11 systemic autoimmune diseases. The WTC Health Program should expand surveillance efforts for those with extended exposures, as early detection can facilitate early treatment, which has been shown to minimize organ damage and improve quality of life." + }, + "questions": [ + { + "id": "90a2f442-cc67-480a-a73d-6e5ad3341717", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 1802, + "text": "Prolonged work at the WTC" + }, + { + "answer_start": 88, + "text": "World Trade Center (WTC)" + } + ] + } + ] +} \ No newline at end of file diff --git a/3c2be877-4fa6-4722-8acc-bb38d8803196.json b/3c2be877-4fa6-4722-8acc-bb38d8803196.json new file mode 100644 index 0000000000000000000000000000000000000000..430087ffa09e20ba92e432473f0811369c6ba44f --- /dev/null +++ b/3c2be877-4fa6-4722-8acc-bb38d8803196.json @@ -0,0 +1,39 @@ +{ + "id": "3c2be877-4fa6-4722-8acc-bb38d8803196", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "22430451", + "text": "OBJECTIVES:\nExposure to passive smoke is a common and avoidable risk factor for wheeze and asthma in children. Substantial growth in the prospective cohort study evidence base provides an opportunity to generate new and more detailed estimates of the magnitude of the effect. A systematic review and meta-analysis was conducted to provide estimates of the prospective effect of smoking by parents or household members on the risk of wheeze and asthma at different stages of childhood.\n\nMETHODS:\nWe systematically searched Medline, Embase, and conference abstracts to identify cohort studies of the incidence of asthma or wheeze in relation to exposure to prenatal or postnatal maternal, paternal, or household smoking in subjects aged up to 18 years old. Pooled odds ratios (ORs) with 95% confidence intervals (CIs) were estimated by using random effects model.\n\nRESULTS:\nWe identified 79 prospective studies. Exposure to pre- or postnatal passive smoke exposure was associated with a 30% to 70% increased risk of incident wheezing (strongest effect from postnatal maternal smoking on wheeze in children aged ≤2 years, OR = 1.70, 95% CI = 1.24-2.35, 4 studies) and a 21% to 85% increase in incident asthma (strongest effect from prenatal maternal smoking on asthma in children aged ≤2 years, OR = 1.85, 95% CI = 1.35-2.53, 5 studies).\n\nCONCLUSIONS:\nBuilding upon previous findings, exposure to passive smoking increases the incidence of wheeze and asthma in children and young people by at least 20%. Preventing parental smoking is crucially important to the prevention of asthma." + }, + "questions": [ + { + "id": "83a89cf0-6974-4a65-b152-bd8be044f12f", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 910, + "text": "Exposure to pre- or postnatal passive smoke exposure" + }, + { + "answer_start": 1382, + "text": "exposure to passive smoking" + } + ] + } + ] +} \ No newline at end of file diff --git a/3c4dd817-9b25-4e15-a87f-c36738543f61.json b/3c4dd817-9b25-4e15-a87f-c36738543f61.json new file mode 100644 index 0000000000000000000000000000000000000000..9865afa4720d027332e59fd8321c2eeadbb7f4d5 --- /dev/null +++ b/3c4dd817-9b25-4e15-a87f-c36738543f61.json @@ -0,0 +1,68 @@ +{ + "id": "3c4dd817-9b25-4e15-a87f-c36738543f61", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "19251797", + "text": "Little is known about chronic obstructive pulmonary disease (COPD) in Chinese nonsmokers. The present study aimed to investigate the profiles of COPD among nonsmokers based on the Chinese Epidemiological Survey of COPD (CESCOPD). In the CESCOPD, 20,245 subjects aged 40 yrs or older were interviewed with questionnaires and spirometry tests. Subjects with a post-bronchodilator forced expiratory volume in one second (FEV(1))/forced vital capacity (FVC) ratio of \u003c0.70 were identified as having COPD. Data of 12,471 nonsmokers and 1,024 smoking COPD patients were analysed in the current study. The overall prevalence of COPD among nonsmokers was 5.2% (95% confidence interval 4.8-5.6). Being male, of advanced age, lower body mass index (BMI) and lower educational level, having exposure to environmental tobacco smoke, coal and/or biomass smoke, poor ventilation in the kitchen, a family history of respiratory disease and recurrent childhood cough were all independently associated with a higher risk of having COPD among nonsmokers. Nonsmokers with respiratory symptoms without airflow limitation showed a somewhat different pattern of risk factors. Nonsmokers with COPD were less likely to present with chronic productive coughs and lower BMI, while more likely to have received a physician diagnosis of asthma and respiratory diseases in childhood, than smokers with COPD. Chronic obstructive pulmonary disease is prevalent among Chinese nonsmokers, and nonsmoking chronic obstructive pulmonary disease may have different profiles from smoking chronic obstructive pulmonary disease." + }, + "questions": [ + { + "id": "66763e81-e071-4b17-8e69-b68c95f61317", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 687, + "text": "Being male" + }, + { + "answer_start": 702, + "text": "advanced age" + }, + { + "answer_start": 716, + "text": "lower body mass index (BMI)" + }, + { + "answer_start": 748, + "text": "lower educational level" + }, + { + "answer_start": 773, + "text": "having exposure to environmental tobacco smoke" + }, + { + "answer_start": 821, + "text": "coal and/or biomass smoke" + }, + { + "answer_start": 848, + "text": "poor ventilation in the kitchen" + }, + { + "answer_start": 883, + "text": "family history of respiratory disease" + }, + { + "answer_start": 925, + "text": "recurrent childhood cough" + } + ] + } + ] +} \ No newline at end of file diff --git a/3cf15445-1d57-497f-ab25-dead9fae75b3.json b/3cf15445-1d57-497f-ab25-dead9fae75b3.json new file mode 100644 index 0000000000000000000000000000000000000000..eb7f08d25ab62187b13441d87b47b6c5735b318c --- /dev/null +++ b/3cf15445-1d57-497f-ab25-dead9fae75b3.json @@ -0,0 +1,45 @@ +{ + "id": "3cf15445-1d57-497f-ab25-dead9fae75b3", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "2215606", + "text": "BACKGROUND:\nThe risk of colorectal cancer is increased among patients with ulcerative colitis. The magnitude of this increase in risk and the effects of the length of follow-up, the extent of disease at diagnosis, and age at diagnosis vary substantially in different studies.\n\nMETHODS:\nTo provide accurate estimates of the risk of colorectal cancer among patients with ulcerative colitis, we studied a population-based cohort of 3117 patients given a diagnosis of ulcerative colitis from 1922 through 1983 who were followed up through 1984.\n\nRESULTS:\nNinety-two cases of colorectal cancer occurred in 91 patients. As compared with the expected incidence, the incidence of colorectal cancer in the cohort was increased (standardized incidence ratio [ratio of observed to expected cases] = 5.7; 95 percent confidence interval, 4.6 to 7.0). Less extensive disease at diagnosis was associated with a lower risk; for patients with ulcerative proctitis, the standardized incidence ratio was 1.7 (95 percent confidence interval, 0.8 to 3.2); for those with left-sided colitis, 2.8 (95 percent confidence interval, 1.6 to 4.4); and for those with pancolitis (extensive colitis, or inflammation of the entire colon), 14.8 (95 percent confidence interval, 11.4 to 18.9). Age at diagnosis and the extent of disease at diagnosis were strong and independent risk factors for colorectal cancer. For each increase in age group at diagnosis (less than 15 years, 15 to 29 years, 30 to 39 years, 40 to 49 years, 50 to 59 years, and greater than or equal to 60 years), the relative risk of colorectal cancer, adjusted for the extent of disease at diagnosis, decreased by about half (adjusted standardized incidence ratio = 0.51; 95 percent confidence interval, 0.46 to 0.56). The absolute risk of colorectal cancer 35 years after diagnosis was 30 percent for patients with pancolitis at diagnosis and 40 percent for those given this diagnosis at less than 15 years of age.\n\nCONCLUSIONS:\nClose surveillance and perhaps even prophylactic proctocolectomy should be recommended for patients given a diagnosis of pancolitis, especially those who are less than 15 years of age at diagnosis." + }, + "questions": [ + { + "id": "a6787c7e-aafe-4175-8954-f418e88ac6b6", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 912, + "text": "patients with ulcerative proctitis" + }, + { + "answer_start": 1050, + "text": "left-sided colitis" + }, + { + "answer_start": 1139, + "text": "pancolitis (extensive colitis, or inflammation of the entire colon)" + } + ] + } + ] +} \ No newline at end of file diff --git a/3d5d67d8-c09b-4fdf-9610-8639b8e7b698.json b/3d5d67d8-c09b-4fdf-9610-8639b8e7b698.json new file mode 100644 index 0000000000000000000000000000000000000000..9e5a3f21fbea596c96da1c7372dbba6c5592fb32 --- /dev/null +++ b/3d5d67d8-c09b-4fdf-9610-8639b8e7b698.json @@ -0,0 +1,34 @@ +{ + "id": "3d5d67d8-c09b-4fdf-9610-8639b8e7b698", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "10969260", + "text": "OBJECTIVES:\nThe transglutaminase (TG) antibody test is accurate in identifying celiac disease in symptomatic children. We sought to determine the positive predictive value of this test in asymptomatic children at genetic risk for celiac disease.\n\nSTUDY DESIGN:\nAsymptomatic children with a genetic risk for celiac disease were studied to investigate the relationships between TG antibody titer, small bowel histology, growth, and clinical features. Small bowel biopsy histology was graded by using the system of Marsh.\n\nRESULTS:\nOf 30 children with a positive TG antibody test result, 21 (70%) had definite (Marsh score 2 or 3) and 4 (13%) had possible (Marsh score 1) biopsy evidence of celiac disease. TG antibody titer correlated with Marsh score (r = 0.569, P \u003c.01). There was an inverse correlation between Marsh score and height z score (r = -0.361, P =. 05).\n\nCONCLUSIONS:\nIn this group of asymptomatic children screened because of a genetic risk, TG antibodies have a positive predictive value of 70% to 83% for biopsy evidence of celiac disease and may identify children before clinical features of celiac disease develop." + }, + "questions": [ + { + "id": "6d6e0657-a7c5-4275-b37b-be074565b78c", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 551, + "text": "positive TG antibody test result" + } + ] + } + ] +} \ No newline at end of file diff --git a/3dd67f27-4065-4c19-bbfe-b41565a73b15.json b/3dd67f27-4065-4c19-bbfe-b41565a73b15.json new file mode 100644 index 0000000000000000000000000000000000000000..792bb77cdf083e90bf71d81b46e9199af1efe473 --- /dev/null +++ b/3dd67f27-4065-4c19-bbfe-b41565a73b15.json @@ -0,0 +1,34 @@ +{ + "id": "3dd67f27-4065-4c19-bbfe-b41565a73b15", + "disease": { + "id": "H00408", + "names": [ + "Type 1 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E10" + ], + "mesh": [ + "D003922" + ] + }, + "category": "Metabolic disease; Immune system disease; Endocrine disease" + }, + "article": { + "id": "7789630", + "text": "Coxsackievirus B infections have been associated with clinical manifestation of insulin-dependent diabetes mellitus (IDDM) in several studies, but their initiating role in the slowly progressing beta-cell damage is not known. This is the first prospective study designed to assess the role of coxsackie B and other enterovirus infections in the induction and acceleration of this process. Three separate series were studied: 1) an intrauterine exposure series comprising 96 pregnant mothers whose children subsequently manifested IDDM and 96 control mothers whose children remained nondiabetic; 2) a cohort of 22 initially unaffected siblings of diabetic children who were followed until they developed clinical IDDM (mean observation time, 29 months) and 110 control siblings who remained nondiabetic; 3) a case-control series comprising 90 children with newly diagnosed IDDM and 90 control subjects. Enterovirus infections were identified on the basis of significant increases in serum IgG, IgM, or IgA class antibodies against a panel of enterovirus antigens (capture radioimmunoassay). Enterovirus antibodies were significantly elevated in pregnant mothers whose children subsequently manifested IDDM, particularly in cases in which IDDM appeared at a very young age, before the age of 3 years (P \u003c 0.005). Serologically verified enterovirus infections were almost two times more frequent in siblings who developed clinical IDDM than in siblings who remained nondiabetic (mean, 1.0 vs. 0.6 infections/follow-up year; P \u003c 0.001). This difference was seen both close to the diagnosis of IDDM and several years before diagnosis.(ABSTRACT TRUNCATED AT 250 WORDS)" + }, + "questions": [ + { + "id": "cf10e273-46ca-4900-9742-1c555bfad8a6", + "text": "What are the risk factors of Type 1 diabetes mellitus?", + "answers": [ + { + "answer_start": 1311, + "text": "Serologically verified enterovirus infections" + } + ] + } + ] +} \ No newline at end of file diff --git a/3de593d7-30bb-4c41-a286-d97e43b735be.json b/3de593d7-30bb-4c41-a286-d97e43b735be.json new file mode 100644 index 0000000000000000000000000000000000000000..054aa38d4525f7232d5cd72e7b4bdf038af10c3a --- /dev/null +++ b/3de593d7-30bb-4c41-a286-d97e43b735be.json @@ -0,0 +1,37 @@ +{ + "id": "3de593d7-30bb-4c41-a286-d97e43b735be", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "20215514", + "text": "Although the relation between red and processed meat intake and colorectal cancer has been reported in several epidemiologic studies, very few investigated the potential mechanisms. This study examined multiple potential mechanisms in a large U.S. prospective cohort with a detailed questionnaire on meat type and meat cooking methods linked to databases for estimating intake of mutagens formed in meats cooked at high temperatures (heterocyclic amines, polycyclic aromatic hydrocarbons), heme iron, nitrate, and nitrite. During 7 years of follow-up, 2,719 colorectal cancer cases were ascertained from a cohort of 300,948 men and women. The hazard ratios (HR) and 95% confidence intervals (95% CI) comparing the fifth to the first quintile for both red (HR, 1.24; 95% CI, 1.09-1.42; P(trend) \u003c 0.001) and processed meat (HR, 1.16; 95% CI, 1.01-1.32; P(trend) = 0.017) intakes indicated an elevated risk for colorectal cancer. The potential mechanisms for this relation include heme iron (HR, 1.13; 95% CI, 0.99-1.29; P(trend) = 0.022), nitrate from processed meats (HR, 1.16; 95% CI, 1.02-1.32; P(trend) = 0.001), and heterocyclic amine intake [HR, 1.19; 95% CI, 1.05-1.34; P(trend) \u003c 0.001 for 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline (MeIQx) and HR, 1.17; 95% CI, 1.05-1.29; P(trend) \u003c0.001 for 2-amino-3,4,8-trimethylimidazo[4,5-f]quinoxaline (DiMeIQx)]. In general, the elevated risks were higher for rectal cancer than for colon cancer, with the exception of MeIQx and DiMeIQx, which were only associated with colon cancer. In conclusion, we found a positive association for red and processed meat intake and colorectal cancer; heme iron, nitrate/nitrite, and heterocyclic amines from meat may explain these associations." + }, + "questions": [ + { + "id": "44548437-4607-42e3-9651-11c5d725ce91", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1587, + "text": "red and processed meat" + } + ] + } + ] +} \ No newline at end of file diff --git a/3ee09b10-aec9-4116-b1ca-4a151c93df81.json b/3ee09b10-aec9-4116-b1ca-4a151c93df81.json new file mode 100644 index 0000000000000000000000000000000000000000..6ac4e81b0cc09a2f207d41bf28d46e4fbb237c84 --- /dev/null +++ b/3ee09b10-aec9-4116-b1ca-4a151c93df81.json @@ -0,0 +1,34 @@ +{ + "id": "3ee09b10-aec9-4116-b1ca-4a151c93df81", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "20548022", + "text": "We previously investigated bladder cancer risk in a cohort of dyestuff workers who were heavily exposed to aromatic amines from 1922 through 1972. We updated the follow-up by 14 years (through 2003) for 590 exposed workers to include more than 30 years of follow-up since last exposure to aromatic amines. Expected numbers of deaths from bladder cancer and other causes were computed by use of national mortality rates from 1951 to 1980 and regional mortality rates subsequently. There were 394 deaths, compared with 262.7 expected (standardized mortality ratio = 1.50, 95% confidence interval = 1.36 to 1.66). Overall, 56 deaths from bladder cancer were observed, compared with 3.4 expected (standardized mortality ratio = 16.5, 95% confidence interval = 12.4 to 21.4). The standardized mortality ratio for bladder cancer increased with younger age at first exposure and increasing duration of exposure. Although the standardized mortality ratio for bladder cancer steadily decreased with time since exposure stopped, the absolute risk remained approximately constant at 3.5 deaths per 1000 man-years up to 29 years after exposure stopped. Excess risk was apparent 30 years or more after last exposure." + }, + "questions": [ + { + "id": "6704ba7f-3be0-431c-8004-c9d4e211d195", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 88, + "text": "heavily exposed to aromatic amines" + } + ] + } + ] +} \ No newline at end of file diff --git a/3f9b2f82-8fb5-451f-86bf-b20d19f997ea.json b/3f9b2f82-8fb5-451f-86bf-b20d19f997ea.json new file mode 100644 index 0000000000000000000000000000000000000000..0749872bb1c2cf60fa2a99ccc2e64bcc4073462e --- /dev/null +++ b/3f9b2f82-8fb5-451f-86bf-b20d19f997ea.json @@ -0,0 +1,34 @@ +{ + "id": "3f9b2f82-8fb5-451f-86bf-b20d19f997ea", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "2646537", + "text": "We studied the relation of serum insulin levels to plasma lipid levels and blood pressure in two groups drawn from among 247 healthy, normotensive nonobese subjects with normal glucose tolerance. One group of 32 subjects was defined as having hyperinsulinemia (serum insulin, greater than 2 SD above the mean) and then compared with 32 normoinsulinemic subjects (serum insulin within 1 SD of the mean) matched for age (mean, 39 years), sex (22 men and 10 women), and body-mass index (24.7). The two groups had similar patterns of smoking, drinking, and physical exercise. Plasma glucose levels after an oral glucose challenge were significantly higher (P less than 0.05) in the hyperinsulinemic group. In addition, the mean (+/- SEM) fasting plasma triglyceride levels in subjects with hyperinsulinemia were significantly higher (1.73 +/- 0.2 vs. 1.24 +/- 0.1 mmol per liter) and the plasma high-density lipoprotein cholesterol concentrations were lower (1.21 +/- 0.06 vs. 1.43 +/- 0.06 mmol per liter) than in subjects with normoinsulinemia. Both systolic (126 vs. 119 mm Hg; P less than 0.05) and diastolic (85 vs. 78 mm Hg; P less than 0.01) blood pressures were significantly elevated in the group with hyperinsulinemia. We conclude that healthy persons with hyperinsulinemia and normal glucose tolerance have an increase in risk factors for coronary artery disease, as compared with a well-matched group of healthy subjects with normal insulin levels." + }, + "questions": [ + { + "id": "dde54e84-f771-452c-bf16-df5786e18e7a", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1242, + "text": "healthy persons with hyperinsulinemia and normal glucose tolerance" + } + ] + } + ] +} \ No newline at end of file diff --git a/3fd2d1d8-e0d8-4bb9-a722-885f870e46bc.json b/3fd2d1d8-e0d8-4bb9-a722-885f870e46bc.json new file mode 100644 index 0000000000000000000000000000000000000000..1dc77534c1c6903bca15c4c6ee23d91299ba403a --- /dev/null +++ b/3fd2d1d8-e0d8-4bb9-a722-885f870e46bc.json @@ -0,0 +1,41 @@ +{ + "id": "3fd2d1d8-e0d8-4bb9-a722-885f870e46bc", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "24743840", + "text": "Dietary factors, including meat, fruits, vegetables and fiber, are associated with colorectal cancer; however, there is limited information as to whether these dietary factors interact with genetic variants to modify risk of colorectal cancer. We tested interactions between these dietary factors and approximately 2.7 million genetic variants for colorectal cancer risk among 9,287 cases and 9,117 controls from ten studies. We used logistic regression to investigate multiplicative gene-diet interactions, as well as our recently developed Cocktail method that involves a screening step based on marginal associations and gene-diet correlations and a testing step for multiplicative interactions, while correcting for multiple testing using weighted hypothesis testing. Per quartile increment in the intake of red and processed meat were associated with statistically significant increased risks of colorectal cancer and vegetable, fruit and fiber intake with lower risks. From the case-control analysis, we detected a significant interaction between rs4143094 (10p14/near GATA3) and processed meat consumption (OR = 1.17; p = 8.7E-09), which was consistently observed across studies (p heterogeneity = 0.78). The risk of colorectal cancer associated with processed meat was increased among individuals with the rs4143094-TG and -TT genotypes (OR = 1.20 and OR = 1.39, respectively) and null among those with the GG genotype (OR = 1.03). Our results identify a novel gene-diet interaction with processed meat for colorectal cancer, highlighting that diet may modify the effect of genetic variants on disease risk, which may have important implications for prevention." + }, + "questions": [ + { + "id": "cce171a9-082c-47c4-b6b2-c380db76babf", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1086, + "text": "processed meat consumption" + }, + { + "answer_start": 1212, + "text": "The risk of colorectal cancer associated with processed meat was increased among individuals with the rs4143094-TG and -TT genotypes" + } + ] + } + ] +} \ No newline at end of file diff --git a/3ff77903-5f28-45d2-971a-fb3b5d9c247c.json b/3ff77903-5f28-45d2-971a-fb3b5d9c247c.json new file mode 100644 index 0000000000000000000000000000000000000000..6855a228be3f79e3150f1d82df0115e9bdbc7daa --- /dev/null +++ b/3ff77903-5f28-45d2-971a-fb3b5d9c247c.json @@ -0,0 +1,41 @@ +{ + "id": "3ff77903-5f28-45d2-971a-fb3b5d9c247c", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "20145170", + "text": "PURPOSE:\nLynch syndrome family members with inherited germline mutations in DNA mismatch repair (MMR) genes have a high risk of colorectal cancer (CRC), and cases typically have tumors that exhibit a high level of microsatellite instability (MSI). There is some evidence that smoking is a risk factor for CRCs with high MSI; however, the association of smoking with CRC among those with Lynch syndrome is unknown.\n\nEXPERIMENTAL DESIGN:\nA multicentered retrospective cohort of 752 carriers of pathogenic MMR gene mutations was analyzed, using a weighted Cox regression analysis, adjusting for sex, ascertainment source, the specific mutated gene, year of birth, and familial clustering.\n\nRESULTS:\nCompared with never smokers, current smokers had a significantly increased CRC risk [adjusted hazard ratio (HR), 1.62; 95% confidence interval (95% CI), 1.01-2.57] and former smokers who had quit smoking for 2 or more years were at decreased risk (HR, 0.53; 95% CI, 0.35-0.82). CRC risk did not vary according to age at starting. However, light smoking (\u003c10 cigarettes per day) and shorter duration of smoking (\u003c10 years) were associated with decreased CRC risk (HR, 0.51; 95% CI, 0.29-0.91 and HR, 0.52; 95% CI, 0.30-0.89, respectively). For former smokers, CRC risk decreased with years since quitting (P trend \u003c0.01).\n\nCONCLUSIONS:\nPeople with Lynch syndrome may be at increased risk of CRC if they smoke regularly. Although our data suggest that former smokers, short-term smokers, and light smokers are at decreased CRC risk, these findings need further confirmation, preferably using prospective designs." + }, + "questions": [ + { + "id": "d008ffed-f04a-44c4-ab53-3758c305787f", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 725, + "text": "current smokers" + }, + { + "answer_start": 1331, + "text": "People with Lynch syndrome" + } + ] + } + ] +} \ No newline at end of file diff --git a/402d1bcc-89e8-46e5-8776-203600ad8e8c.json b/402d1bcc-89e8-46e5-8776-203600ad8e8c.json new file mode 100644 index 0000000000000000000000000000000000000000..f1cf7917193536df9c1b7b965d39436c87f6bf3a --- /dev/null +++ b/402d1bcc-89e8-46e5-8776-203600ad8e8c.json @@ -0,0 +1,34 @@ +{ + "id": "402d1bcc-89e8-46e5-8776-203600ad8e8c", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "29555305", + "text": "OBJECTIVE:\nTo determine whether family history of coronary heart disease (FH) definitions differ in their association with atherosclerotic cardiovascular disease (ASCVD) events.\n\nPATIENTS AND METHODS:\nParticipants who provided FH data from July 17, 2000, through February 24, 2004, were identified. Definitions of FH were any, premature, and Familial Risk Assessment (FRA). Outcomes included coronary heart disease (CHD), stroke, peripheral artery disease, angina, and congestive heart failure. Multivariable-adjusted Cox models examined the association of FH definitions with events. C statistics and the net reclassification index examined the incremental prognostic contribution of each definition.\n\nRESULTS:\nIn 6200 participants, the proportions of any FH and premature FH were 36% and 16%, respectively, and of weak, moderate, and strong familial risk were 20%, 16%, and 20%, respectively. Over median follow-up of 10.1 years (range, 0.02-11.5 years), 741 participants experienced a composite event. Compared with no FH, any FH was associated with incident CHD, angina, and composite ASCVD (hazard ratios [95% CIs]: 1.4 [1.1-1.8], 1.6 [1.2-2.1], and 1.3 [1.1-1.5], respectively). Similar results were obtained for premature FH compared with no FH and for strong compared with weak FRA for these 3 outcomes. There was no association between the FH definitions and noncoronary cardiovascular events. Compared with traditional risk factors (C statistic = 0.740), any FH, premature FH, and FRA all improved discrimination of composite ASCVD (all P \u003c .01); however, the differences in C statistics among any FH (0.743), premature FH (0.742), and FRA (0.744) were numerically small, as were differences in the net reclassification index.\n\nCONCLUSION:\nA single question regarding the presence of FH in any first-degree relative performs just as well as more complicated assessments in predicting CHD.\n\nTRIAL REGISTRATION:\nclinicaltrials.gov Identifier: NCT00005487." + }, + "questions": [ + { + "id": "6b233259-df39-489f-9dee-60a2d8914680", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1782, + "text": "presence of FH in any first-degree relative" + } + ] + } + ] +} \ No newline at end of file diff --git a/40b1d1d5-bf37-4b48-92fc-ea4e7dec9944.json b/40b1d1d5-bf37-4b48-92fc-ea4e7dec9944.json new file mode 100644 index 0000000000000000000000000000000000000000..d35d0c7dd4c14139346a874cb54d160e5f88d515 --- /dev/null +++ b/40b1d1d5-bf37-4b48-92fc-ea4e7dec9944.json @@ -0,0 +1,34 @@ +{ + "id": "40b1d1d5-bf37-4b48-92fc-ea4e7dec9944", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "17093250", + "text": "BACKGROUND:\nLow-carbohydrate diets have been advocated for weight loss and to prevent obesity, but the long-term safety of these diets has not been determined.\n\nMETHODS:\nWe evaluated data on 82,802 women in the Nurses' Health Study who had completed a validated food-frequency questionnaire. Data from the questionnaire were used to calculate a low-carbohydrate-diet score, which was based on the percentage of energy as carbohydrate, fat, and protein (a higher score reflects a higher intake of fat and protein and a lower intake of carbohydrate). The association between the low-carbohydrate-diet score and the risk of coronary heart disease was examined.\n\nRESULTS:\nDuring 20 years of follow-up, we documented 1994 new cases of coronary heart disease. After multivariate adjustment, the relative risk of coronary heart disease comparing highest and lowest deciles of the low-carbohydrate-diet score was 0.94 (95% confidence interval [CI], 0.76 to 1.18; P for trend=0.19). The relative risk comparing highest and lowest deciles of a low-carbohydrate-diet score on the basis of the percentage of energy from carbohydrate, animal protein, and animal fat was 0.94 (95% CI, 0.74 to 1.19; P for trend=0.52), whereas the relative risk on the basis of the percentage of energy from intake of carbohydrates, vegetable protein, and vegetable fat was 0.70 (95% CI, 0.56 to 0.88; P for trend=0.002). A higher glycemic load was strongly associated with an increased risk of coronary heart disease (relative risk comparing highest and lowest deciles, 1.90; 95% CI, 1.15 to 3.15; P for trend=0.003).\n\nCONCLUSIONS:\nOur findings suggest that diets lower in carbohydrate and higher in protein and fat are not associated with increased risk of coronary heart disease in women. When vegetable sources of fat and protein are chosen, these diets may moderately reduce the risk of coronary heart disease." + }, + "questions": [ + { + "id": "dcdd7bd4-388b-4e94-a978-c91e2d42a926", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1390, + "text": "A higher glycemic load" + } + ] + } + ] +} \ No newline at end of file diff --git a/41072f21-2a04-412f-8a8e-f17096fdc35e.json b/41072f21-2a04-412f-8a8e-f17096fdc35e.json new file mode 100644 index 0000000000000000000000000000000000000000..e517094436b2c98db5c0afbddc7fffb6fb527f05 --- /dev/null +++ b/41072f21-2a04-412f-8a8e-f17096fdc35e.json @@ -0,0 +1,39 @@ +{ + "id": "41072f21-2a04-412f-8a8e-f17096fdc35e", + "disease": { + "id": "H00056", + "names": [ + "Alzheimer disease", + "Dementia due to Alzheimer disease" + ], + "dbLinks": { + "icd10": [ + "G30" + ], + "mesh": [ + "D000544" + ] + }, + "category": "Neurodegenerative disease" + }, + "article": { + "id": "19358976", + "text": "BACKGROUND:\nLate-onset Alzheimer's disease (AD) is a multifactorial and heterogeneous disorder with major risk factors including advanced age, presence of an apolipoprotein E epsilon4 (APOE4) allele, and family history of AD. Other risk factors may be obesity and diabetes and related disorders, which are highly prevalent.\n\nMETHODS:\nWe reviewed longitudinal epidemiological studies of body mass, diabetes, metabolic syndrome, and glucose and insulin levels on risk for AD. We conducted meta-analyses of the results from these studies.\n\nRESULTS:\nFor obesity assessed by body mass index, the pooled effect size for AD was 1.59 (95% confidence interval [CI] 1.02-2.5; z = 2.0; p = .042), and for diabetes, the pooled effect size for AD was 1.54 (95% CI 1.33-1.79; z = 5.7; p \u003c .001). Egger's test did not find significant evidence for publication bias in the meta-analysis for obesity (t = -1.4, p = .21) or for diabetes (t = -.86, p = .42). Since these disorders are highly comorbid, we conducted a meta-analysis combining all studies of obesity, diabetes, and abnormal glucose or insulin levels, which yielded a highly significant pooled effect size for AD of 1.63 (95% CI 1.39-1.92; z = 5.9; p \u003c .001).\n\nCONCLUSIONS:\nObesity and diabetes significantly and independently increase risk for AD. Though the level of risk is less than that with the APOE4 allele, the high prevalence of these disorders may result in substantial increases in future incidence of AD. Physiological changes common to obesity and diabetes plausibly promote AD." + }, + "questions": [ + { + "id": "077dc374-9bd6-4569-bed9-a6dee646e068", + "text": "What are the risk factors of Alzheimer disease?", + "answers": [ + { + "answer_start": 1218, + "text": "Obesity" + }, + { + "answer_start": 1230, + "text": "diabetes" + } + ] + } + ] +} \ No newline at end of file diff --git a/41155da4-4b0d-4054-8ad3-cdf3b8609417.json b/41155da4-4b0d-4054-8ad3-cdf3b8609417.json new file mode 100644 index 0000000000000000000000000000000000000000..373b097544763fd4da06269d7c04abccd8f7bb1b --- /dev/null +++ b/41155da4-4b0d-4054-8ad3-cdf3b8609417.json @@ -0,0 +1,35 @@ +{ + "id": "41155da4-4b0d-4054-8ad3-cdf3b8609417", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "18805332", + "text": "BACKGROUND:\nExposure to paracetamol during intrauterine life, childhood, and adult life may increase the risk of developing asthma. We studied 6-7-year-old children from Phase Three of the International Study of Asthma and Allergies in Childhood (ISAAC) programme to investigate the association between paracetamol consumption and asthma.\n\nMETHODS:\nAs part of Phase Three of ISAAC, parents or guardians of children aged 6-7 years completed written questionnaires about symptoms of asthma, rhinoconjunctivitis, and eczema, and several risk factors, including the use of paracetamol for fever in the child's first year of life and the frequency of paracetamol use in the past 12 months. The primary outcome variable was the odds ratio (OR) of asthma symptoms in these children associated with the use of paracetamol for fever in the first year of life, as calculated by logistic regression.\n\nFINDINGS:\n205 487 children aged 6-7 years from 73 centres in 31 countries were included in the analysis. In the multivariate analyses, use of paracetamol for fever in the first year of life was associated with an increased risk of asthma symptoms when aged 6-7 years (OR 1.46 [95% CI 1.36-1.56]). Current use of paracetamol was associated with a dose-dependent increased risk of asthma symptoms (1.61 [1.46-1.77] and 3.23 [2.91-3.60] for medium and high use vs no use, respectively). Use of paracetamol was similarly associated with the risk of severe asthma symptoms, with population-attributable risks between 22% and 38%. Paracetamol use, both in the first year of life and in children aged 6-7 years, was also associated with an increased risk of symptoms of rhinoconjunctivitis and eczema.\n\nINTERPRETATION:\nUse of paracetamol in the first year of life and in later childhood, is associated with risk of asthma, rhinoconjunctivitis, and eczema at age 6 to 7 years. We suggest that exposure to paracetamol might be a risk factor for the development of asthma in childhood." + }, + "questions": [ + { + "id": "d2dccf89-4462-4d4e-adcc-db186a994ff3", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1702, + "text": "Use of paracetamol in the first year of life and in later childhood" + } + ] + } + ] +} \ No newline at end of file diff --git a/41701683-8925-4272-ab41-30be42003ec5.json b/41701683-8925-4272-ab41-30be42003ec5.json new file mode 100644 index 0000000000000000000000000000000000000000..54b8c5042faeeb855b522cff7e5d2671b77f2ef7 --- /dev/null +++ b/41701683-8925-4272-ab41-30be42003ec5.json @@ -0,0 +1,34 @@ +{ + "id": "41701683-8925-4272-ab41-30be42003ec5", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "18623081", + "text": "Experimental studies suggest that increased urination frequency may reduce bladder cancer risk if carcinogens are present in the urine. Only 2 small studies of the effect of increased urination frequency on bladder cancer risk in humans have been conducted with conflicting results. Our purpose was to evaluate the effect of urination frequency on risk of bladder cancer in a large, multicenter case-control study. We analyzed data based on interviews conducted with 884 patients with newly diagnosed, bladder cancer and 996 controls from 1998 to 2001 in Spain. We observed a consistent, inverse trend in risk with increasing nighttime voiding frequency in both men (p = 0.0003) and women (p = 0.07); voiding at least 2 times per night was associated with a significant, 40-50% risk reduction. The protective effect of nocturia was apparent among study participants with low, moderate and high water consumption. The risk associated with cigarette smoking was reduced by nocturia. Compared with nonsmokers who did not urinate at night, current smokers who did not urinate at night had an OR of 7.0 (95% CI = 4.7-10.2), whereas those who voided at least twice per night had an OR of 3.3 (95% CI = 1.9-5.8) (p value for trend = 0.0005). Our findings suggest a strong protective effect of nocturia on bladder cancer risk, providing evidence in humans that bladder cancer risk is related to the contact time of the urothelium with carcinogens in urine. Increased urination frequency, coupled with possible dilution of the urine from increased water intake, may diminish the effect of urinary carcinogens on bladder cancer risk." + }, + "questions": [ + { + "id": "6a1d9c5a-83b6-4d33-af57-9d2352bb139d", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 1036, + "text": "current smokers who did not urinate at night" + } + ] + } + ] +} \ No newline at end of file diff --git a/422e8c51-db13-4d8a-81bb-50ccd25391bf.json b/422e8c51-db13-4d8a-81bb-50ccd25391bf.json new file mode 100644 index 0000000000000000000000000000000000000000..f00ed2f7d16fb0d9c9f931070add82d8fc044695 --- /dev/null +++ b/422e8c51-db13-4d8a-81bb-50ccd25391bf.json @@ -0,0 +1,37 @@ +{ + "id": "422e8c51-db13-4d8a-81bb-50ccd25391bf", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "30221595", + "text": "BACKGROUND:\nIn the primary analysis of the Aspirin in Reducing Events in the Elderly (ASPREE) trial, now published in the Journal, we report that the daily use of aspirin did not provide a benefit with regard to the primary end point of disability-free survival among older adults. A numerically higher rate of the secondary end point of death from any cause was observed with aspirin than with placebo.\n\nMETHODS:\nFrom 2010 through 2014, we enrolled community-dwelling persons in Australia and the United States who were 70 years of age or older (or ≥65 years of age among blacks and Hispanics in the United States) and did not have cardiovascular disease, dementia, or disability. Participants were randomly assigned to receive 100 mg of enteric-coated aspirin or placebo. Deaths were classified according to the underlying cause by adjudicators who were unaware of trial-group assignments. Hazard ratios were calculated to compare mortality between the aspirin group and the placebo group, and post hoc exploratory analyses of specific causes of death were performed.\n\nRESULTS:\nOf the 19,114 persons who were enrolled, 9525 were assigned to receive aspirin and 9589 to receive placebo. A total of 1052 deaths occurred during a median of 4.7 years of follow-up. The risk of death from any cause was 12.7 events per 1000 person-years in the aspirin group and 11.1 events per 1000 person-years in the placebo group (hazard ratio, 1.14; 95% confidence interval [CI], 1.01 to 1.29). Cancer was the major contributor to the higher mortality in the aspirin group, accounting for 1.6 excess deaths per 1000 person-years. Cancer-related death occurred in 3.1% of the participants in the aspirin group and in 2.3% of those in the placebo group (hazard ratio, 1.31; 95% CI, 1.10 to 1.56).\n\nCONCLUSIONS:\nHigher all-cause mortality was observed among apparently healthy older adults who received daily aspirin than among those who received placebo and was attributed primarily to cancer-related death. In the context of previous studies, this result was unexpected and should be interpreted with caution. (Funded by the National Institute on Aging and others; ASPREE ClinicalTrials.gov number, NCT01038583 .)." + }, + "questions": [ + { + "id": "22c1a911-f255-4df8-bb46-7f42257cf6e3", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1851, + "text": "healthy older adults who received daily aspirin" + } + ] + } + ] +} \ No newline at end of file diff --git a/424902ba-f25f-44f0-863f-7e02d6dc3494.json b/424902ba-f25f-44f0-863f-7e02d6dc3494.json new file mode 100644 index 0000000000000000000000000000000000000000..b207fb2d087fcde2045f881a2d3ab1e3eaed3555 --- /dev/null +++ b/424902ba-f25f-44f0-863f-7e02d6dc3494.json @@ -0,0 +1,41 @@ +{ + "id": "424902ba-f25f-44f0-863f-7e02d6dc3494", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "7593429", + "text": "Patients with acromegaly are reported to be at risk of developing adenomatous colonic polyps, which are considered to be preneoplastic lesions. This assumption is, however, usually drawn from results obtained in rather small series of patients or without a control group. We, therefore, undertook a prospective colonoscopic and pathological study comprising 103 acromegalic patients and 138 nonacromegalic control subjects referred for irritable bowel syndrome. The prevalence of adenomatous colonic polyps was significantly increased in acromegalic patients compared to that in control subjects (22.3% vs. 8.0%; P = 0.0024). The significance was similarly present in male acromegalic patients (28.6% vs. 5.5% in male control subjects; P = 0.0026), but was absent in female acromegalic patients. The prevalence of colonic polyps was also significantly increased in the group of acromegalic patients under 55 yr of age (20.0% vs. 3.0% in the control group of the same age; P = 0.0026). Other characteristics of adenomatous colonic polyps in acromegaly were the multiplicity and the presence proximal to the splenic flexure. No difference in the duration of acromegaly was found between patients with or without adenomatous polyps. The prevalence of hyperplastic colonic polyps was also significantly increased to 24.3% in acromegalic patients vs 4.4% in control subjects (P \u003c 0.001). In conclusion, in view of the increased incidence of adenomatous colonic polyps, colonoscopy should be part of the follow-up examination in acromegaly." + }, + "questions": [ + { + "id": "e26d8111-27f8-4ee4-85bb-ae12bf73cb5f", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 668, + "text": "male acromegalic patients" + }, + { + "answer_start": 878, + "text": "acromegalic patients under 55 yr of age" + } + ] + } + ] +} \ No newline at end of file diff --git a/42540fa8-a65c-4d3c-9c74-c4d1b7686cd0.json b/42540fa8-a65c-4d3c-9c74-c4d1b7686cd0.json new file mode 100644 index 0000000000000000000000000000000000000000..60672fc554cad842d80658357d2fac31baac285f --- /dev/null +++ b/42540fa8-a65c-4d3c-9c74-c4d1b7686cd0.json @@ -0,0 +1,34 @@ +{ + "id": "42540fa8-a65c-4d3c-9c74-c4d1b7686cd0", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "12860911", + "text": "BACKGROUND:\nThe National Cholesterol Education Program (NCEP) recently proposed a simple definition for metabolic syndrome. Information on the prospective association of this definition for coronary heart disease (CHD) and type 2 diabetes is currently limited.\n\nMETHODS AND RESULTS:\nWe used a modified NCEP definition with body mass index in place of waist circumference. Baseline assessments in the West of Scotland Coronary Prevention Study were available for 6447 men to predict CHD risk and for 5974 men to predict incident diabetes over 4.9 years of follow-up. Mean LDL cholesterol was similar but C-reactive protein was higher (P\u003c0.0001) in the 26% of men with the syndrome compared with those without. Metabolic syndrome increased the risk for a CHD event [univariate hazard ratio (HR)=1.76 (95% CI, 1.44 to 2.15)] and for diabetes [univariate HR=3.50 (95% CI 2.51 to 4.90)]. Metabolic syndrome continued to predict CHD events (HR=1.30, 95% CI, 1.00 to 1.67, P=0.045) in a multivariate model incorporating conventional risk factors. Men with 4 or 5 features of the syndrome had a 3.7-fold increase in risk for CHD and a 24.5-fold increase for diabetes compared with men with none (both P\u003c0.0001). C-reactive protein enhanced prognostic information for both outcomes. With pravastatin, men with the syndrome had similar risk reduction for CHD as compared with those without (HR, 0.73 and 0.69; pravastatin versus placebo).\n\nCONCLUSIONS:\nA modified NCEP metabolic syndrome definition predicts CHD events, and, more strikingly, new-onset diabetes, and thus helps identify individuals who may receive particular benefit from lifestyle measures to prevent these diseases." + }, + "questions": [ + { + "id": "4952f733-c1b6-4e10-bd5e-378e34859285", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 709, + "text": "Metabolic syndrome" + } + ] + } + ] +} \ No newline at end of file diff --git a/42c209bf-99bb-4fc3-bb20-16322b5cbda3.json b/42c209bf-99bb-4fc3-bb20-16322b5cbda3.json new file mode 100644 index 0000000000000000000000000000000000000000..e726292d63fc14e78f5a5dab9c30da209e8024f5 --- /dev/null +++ b/42c209bf-99bb-4fc3-bb20-16322b5cbda3.json @@ -0,0 +1,39 @@ +{ + "id": "42c209bf-99bb-4fc3-bb20-16322b5cbda3", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "12548605", + "text": "BACKGROUND:\nThe results of several studies have provided evidence that patients diagnosed with cutaneous melanoma (CM) are at a higher risk of developing a second primary CM than the general population. In this study, the authors examined how the risk of a second primary tumor varied with time from diagnosis of CM and examined the patient-specific factors that modify a CM patient's risk of developing a second primary tumor.\n\nMETHODS:\nSurvival curves for time from first CM to second CM were calculated using the Kaplan-Meier method. The Cox proportional hazards model was used to determine which demographic- and disease-related factors influence the risk of a second CM.\n\nRESULTS:\nApproximately 0.5% of Surveillance, Epidemiology, and End Results (SEER) CM patients were found to have synchronous second primaries. The estimated cumulative probability of having a second primary CM was 0.99% at 1 year after initial CM diagnosis, 2.06% at 5 years, 3.17% at 10 years, and 5.34% at 20 years. Risk was significantly greater for males; older patients; patients with first CM on the face, neck, or trunk; those from the Atlanta, Hawaii, or Connecticut registries; and more recently diagnosed patients. Risk was lower for patients from the Utah registry and those with Stage IV disease.\n\nCONCLUSIONS:\nThe elevated risk for CM among CM survivors appears to be greatest in the first few months, and then subsequently declines. However, the risk for a second CM among CM survivors was found to remain substantially higher than the risk for a first CM in the general population throughout the observation period (\u003e 20 years). Demographic- and disease-related factors substantially modify the risk of a second primary CM." + }, + "questions": [ + { + "id": "0a7f1394-343c-493b-bcf7-13ad2145ce63", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 1464, + "text": "CM survivors" + }, + { + "answer_start": 95, + "text": "cutaneous melanoma (CM)" + } + ] + } + ] +} \ No newline at end of file diff --git a/43434e37-c3f4-4491-8f96-a46e2402f826.json b/43434e37-c3f4-4491-8f96-a46e2402f826.json new file mode 100644 index 0000000000000000000000000000000000000000..28dfaaeac06c69cf56be42a413e83e58bffe056c --- /dev/null +++ b/43434e37-c3f4-4491-8f96-a46e2402f826.json @@ -0,0 +1,38 @@ +{ + "id": "43434e37-c3f4-4491-8f96-a46e2402f826", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "17977935", + "text": "OBJECTIVE:\nTo investigate the association between serum uric acid level and risk of type 2 diabetes.\n\nRESEARCH DESIGN AND METHODS:\nThe population for analysis consisted of 4,536 subjects free from diabetes at baseline. During a mean of 10.1 years of follow-up, 462 subjects developed diabetes.\n\nRESULTS:\nThe age- and sex-adjusted hazard ratios (HRs) (95% CIs) for diabetes were 1.30 (0.96-1.76) for the second, 1.63 (1.21-2.19) for the third, and 2.83 (2.13-3.76) for the fourth quartile of serum uric acid, in comparison with the first quartile. After adjustment for BMI, waist circumference, systolic and diastolic blood pressure, and HDL cholesterol, the HRs decreased to 1.08 (0.78-1.49), 1.12 (0.81-1.53), and 1.68 (1.22-2.30), respectively.\n\nCONCLUSIONS:\nThe results of this population-based study suggest that serum uric acid is a strong and independent risk factor for diabetes." + }, + "questions": [ + { + "id": "154b7f21-6a5e-4d5a-b00b-03ffe3d47994", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 491, + "text": "serum uric acid" + }, + { + "answer_start": 817, + "text": "serum uric acid" + } + ] + } + ] +} \ No newline at end of file diff --git a/43ba678d-f3b1-48f3-9f1f-fb3d454646b1.json b/43ba678d-f3b1-48f3-9f1f-fb3d454646b1.json new file mode 100644 index 0000000000000000000000000000000000000000..e58317ef7beb623d7467809611a6706852394b72 --- /dev/null +++ b/43ba678d-f3b1-48f3-9f1f-fb3d454646b1.json @@ -0,0 +1,54 @@ +{ + "id": "43ba678d-f3b1-48f3-9f1f-fb3d454646b1", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "7988316", + "text": "OBJECTIVE:\nTo investigate the relation between obesity, fat distribution, and weight gain through adulthood and the risk of non-insulin-dependent diabetes mellitus (NIDDM).\n\nRESEARCH DESIGN AND METHODS:\nWe analyzed data from a cohort of 51,529 U.S. male health professionals, 40-75 years of age in 1986, who completed biennial questionnaires sent out in 1986, 1988, 1990, and 1992. During 5 years of follow-up (1987-1992), 272 cases of NIDDM were diagnosed among men without a history of diabetes, heart disease, and cancer in 1986 and who provided complete health information. Relative risks (RRs) associated with different anthropometric measures were calculated controlling for age, and multivariate RRs were calculated controlling for smoking, family history of diabetes, and age.\n\nRESULTS:\nWe found a strong positive association between overall obesity as measured by body mass index (BMI) and risk of diabetes. Men with a BMI of \u003e or = 35 kg/m2 had a multivariate RR of 42.1 (95% confidence interval [CI] 22.0-80.6) compared with men with a BMI \u003c 23.0 kg/m2. BMI at age 21 and absolute weight gain throughout adulthood were also significant independent risk factors for diabetes. Fat distribution, measured by waist-to-hip ratio (WHR), was a good predictor of diabetes only among the top 5%, while waist circumference was positively associated with the risk of diabetes among the top 20% of the cohort.\n\nCONCLUSIONS:\nThese data suggest that waist circumference may be a better indicator than WHR of the relationship between abdominal adiposity and risk of diabetes. Although early obesity, absolute weight gain throughout adulthood, and waist circumference were good predictors of diabetes, attained BMI was the dominant risk factor for NIDDM; even men of average relative weight had significantly elevated RRs." + }, + "questions": [ + { + "id": "b98bd0b1-723d-4b3d-821d-174d94553b6c", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 124, + "text": "non-insulin-dependent diabetes mellitus (NIDDM)" + }, + { + "answer_start": 1697, + "text": "attained BMI" + }, + { + "answer_start": 842, + "text": "overall obesity as measured by body mass index (BMI)" + }, + { + "answer_start": 917, + "text": "Men with a BMI of \u003e or = 35 kg/m2" + }, + { + "answer_start": 1065, + "text": "BMI at age 21" + }, + { + "answer_start": 1083, + "text": "absolute weight gain throughout adulthood" + } + ] + } + ] +} \ No newline at end of file diff --git a/447794a9-76ad-47bc-b8d1-444204617fc8.json b/447794a9-76ad-47bc-b8d1-444204617fc8.json new file mode 100644 index 0000000000000000000000000000000000000000..81e6bbf72f57ab69b8123e8429a9cecc33ceeb96 --- /dev/null +++ b/447794a9-76ad-47bc-b8d1-444204617fc8.json @@ -0,0 +1,35 @@ +{ + "id": "447794a9-76ad-47bc-b8d1-444204617fc8", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "28679610", + "text": "The possible role of maternal consumption of free sugar during pregnancy in the inception of respiratory and atopic diseases has not been studied. We aimed to study the relationship between maternal intake of free sugar during pregnancy and respiratory and atopic outcomes in the offspring in a population-based birth cohort, the Avon Longitudinal Study of Parents and Children.We analysed associations between maternal intake of free sugar in pregnancy (estimated by a food frequency questionnaire), and current doctor-diagnosed asthma, wheezing, hay fever, eczema, atopy, serum total IgE and lung function in children aged 7-9 years (n=8956 with information on maternal diet in pregnancy and at least one outcome of interest).After controlling for potential confounders, maternal intake of free sugar was positively associated with atopy (OR for highest lowest quintile of sugar intake 1.38, 95% CI 1.06-1.78; per quintile p-trend=0.006) and atopic asthma (OR 2.01, 95% CI 1.23-3.29; per quintile p-trend=0.004). These associations were not confounded by intake of sugar in early childhood, which was unrelated to these outcomes.Our results suggest that a higher maternal intake of free sugar during pregnancy is associated with an increased risk of atopy and atopic asthma in the offspring, independently of sugar intake in early childhood." + }, + "questions": [ + { + "id": "40ca5213-3c49-4641-b8de-5d37059e10bc", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1158, + "text": "higher maternal intake of free sugar during pregnancy" + } + ] + } + ] +} \ No newline at end of file diff --git a/44982920-e21a-4227-9a9a-35e1af357595.json b/44982920-e21a-4227-9a9a-35e1af357595.json new file mode 100644 index 0000000000000000000000000000000000000000..6b7ad0807d716ffc7b1a8b509c9decbb0ccabab1 --- /dev/null +++ b/44982920-e21a-4227-9a9a-35e1af357595.json @@ -0,0 +1,34 @@ +{ + "id": "44982920-e21a-4227-9a9a-35e1af357595", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "17891891", + "text": "Using the fixed-effect model, the author quantitatively estimated the risks of cancers of the colon, bladder, kidneys, and brain as well as non-Hodgkin's lymphoma and leukemia among firefighters. The risk of these six cancers was not markedly elevated when cohort mortality studies were considered. When all mortality studies were considered, however, there was a mild increase in risk for kidney cancer and non-Hodgkin's lymphoma, with a summary relative risk (sumRR) of 1.22 (95% confidence interval [CI] = 1.02-1.43) and 1.40 (95% CI = 1.20-1.60), respectively. A subcohort analysis based on duration of employment revealed that firefighters with 30 or more years of employment had a significantly increased mortality risk for colon cancer, sumRR of 1.51 (95% CI = 1.05-2.11); kidney cancer, sumRR of 6.25 (95% CI = 1.70-16.00); brain cancer, sumRR of 2.53 (95% CI = 1.27 7.07); and leukemia, sumRR of 2.87 (95% CI = 1.43-5.14). After firefighters had 40 or more years of employment, their risk of mortality was significantly increased for colon cancer, sumRR of 4.71 (95% CI = 2.03-9.27); kidney cancer, sumRR of 36.12 (95% CI = 4.03-120.42); and bladder cancer, sumRR of 5.7 (95% CI = 1.56-14.63). The risk for non-Hodgkin's lymphoma was elevated but not significantly so among firefighters with 20 or more years of employment, with sumRR of 1.72 (95% CI = 0.90-3.31). Kidney cancer risk was significantly elevated as early as the second decade of employment." + }, + "questions": [ + { + "id": "e046ec1c-1757-4450-abff-e0d0f3991aab", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 939, + "text": "irefighters had 40 or more years of employment" + } + ] + } + ] +} \ No newline at end of file diff --git a/44e1bae2-5da9-4bc8-96a3-584f7a5938b1.json b/44e1bae2-5da9-4bc8-96a3-584f7a5938b1.json new file mode 100644 index 0000000000000000000000000000000000000000..ff5716e40d896e694ae0f12e65a4f66151229343 --- /dev/null +++ b/44e1bae2-5da9-4bc8-96a3-584f7a5938b1.json @@ -0,0 +1,52 @@ +{ + "id": "44e1bae2-5da9-4bc8-96a3-584f7a5938b1", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "24557573", + "text": "BACKGROUND:\nStudies show that the incidence of COPD has remained high in southwest China despite the 1976 National Stove Improvement Program for indoor air quality. Chinese water-pipe tobacco smoking (commonly referred to as water-pipe smoking), which is thought to be less harmful under the assumption that no charcoal is used and water filters tobacco smoke, is popular in China. We investigated whether Chinese water-pipe use and exposure are associated with the risk of COPD.\n\nMETHODS:\nThis multicenter, cross-sectional study enrolled 1,238 individuals from 10 towns in the Fuyuan area, Yunnan Province, China. A matched design was used to estimate the impact of active and passive exposure to Chinese water-pipe smoking on COPD risk; multivariate analyses adjusted for other risk factors. We also collected the water from Chinese water pipes to assess the mutagenicity of its major components and simulated Chinese water-pipe smoke exposure fine particulate 2.5 (PM2.5) by using the High Volume Air Sampler and individuals' sera to search for the potential protein biomarkers of COPD.\n\nRESULTS:\nThe increased risk of COPD was profound for Chinese water-pipe smokers (adjusted OR, 10.61; 95% CI, 6.89-16.34), Chinese water-pipe passive smokers (adjusted OR, 5.50; 95% CI, 3.61-8.38), cigarette smokers (adjusted OR, 3.18; 95% CI, 2.06-4.91), and cigarette passive smokers (adjusted OR, 2.52; 95% CI, 1.62-3.91) compared with never-smoking control subjects. Chinese water-pipe use aggravates lungs with more PM2.5 compared with cigarettes. ChemR23 and tissue inhibitor of metalloproteinase-1 may be potential protein biomarkers of COPD.\n\nCONCLUSIONS:\nChinese water-pipe smoking significantly increases the risk of COPD, including the risk to women who are exposed to the water-pipe smoke.\n\nTRIAL REGISTRY:\nChinese Clinical Trial Registry; No.: ChiCTR-CCH-12002235; URL: www.chictr.org/cn/" + }, + "questions": [ + { + "id": "6373e4d4-9cae-4a9a-9667-e8f86568d45f", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 1144, + "text": "Chinese water-pipe smokers" + }, + { + "answer_start": 1213, + "text": "Chinese water-pipe passive smokers" + }, + { + "answer_start": 1288, + "text": "cigarette smokers" + }, + { + "answer_start": 1350, + "text": "cigarette passive smokers" + }, + { + "answer_start": 1654, + "text": "Chinese water-pipe smoking" + } + ] + } + ] +} \ No newline at end of file diff --git a/44f7d7bd-fd1b-4597-94c9-1331b8e54a75.json b/44f7d7bd-fd1b-4597-94c9-1331b8e54a75.json new file mode 100644 index 0000000000000000000000000000000000000000..f6283239dbc0099dbb9f14b58626a8d43fa7b2f6 --- /dev/null +++ b/44f7d7bd-fd1b-4597-94c9-1331b8e54a75.json @@ -0,0 +1,34 @@ +{ + "id": "44f7d7bd-fd1b-4597-94c9-1331b8e54a75", + "disease": { + "id": "H00408", + "names": [ + "Type 1 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E10" + ], + "mesh": [ + "D003922" + ] + }, + "category": "Metabolic disease; Immune system disease; Endocrine disease" + }, + "article": { + "id": "11705562", + "text": "BACKGROUND:\nDietary vitamin D supplementation is associated with reduced risk of type 1 diabetes in animals. Our aim was to ascertain whether or not vitamin D supplementation or deficiency in infancy could affect development of type 1 diabetes.\n\nMETHODS:\nA birth-cohort study was done, in which all pregnant women (n=12055) in Oulu and Lapland, northern Finland, who were due to give birth in 1966 were enrolled. Data was collected in the first year of life about frequency and dose of vitamin D supplementation and presence of suspected rickets. Our primary outcome measure was diagnosis of type 1 diabetes by end of December, 1997.\n\nFINDINGS:\n12058 of 12231 represented live births, and 10821 (91% of those alive) children were followed-up at age 1 year. Of the 10366 children included in analyses, 81 were diagnosed with diabetes during the study. Vitamin D supplementation was associated with a decreased frequency of type 1 diabetes when adjusted for neonatal, anthropometric, and social characteristics (rate ratio [RR] for regular vs no supplementation 0.12, 95% CI 0.03-0.51, and irregular vs no supplementation 0.16, 0.04-0.74. Children who regularly took the recommended dose of vitamin D (2000 IU daily) had a RR of 0.22 (0.05-0.89) compared with those who regularly received less than the recommended amount. Children suspected of having rickets during the first year of life had a RR of 3.0 (1.0-9.0) compared with those without such a suspicion.\n\nINTERPRETATION:\nDietary vitamin D supplementation is associated with reduced risk of type 1 diabetes. Ensuring adequate vitamin D supplementation for infants could help to reverse the increasing trend in the incidence of type 1 diabetes." + }, + "questions": [ + { + "id": "dc171b7a-a551-4cbe-9368-a312d8d7ec66", + "text": "What are the risk factors of Type 1 diabetes mellitus?", + "answers": [ + { + "answer_start": 1321, + "text": "Children suspected of having rickets during the first year of life" + } + ] + } + ] +} \ No newline at end of file diff --git a/4598f1dc-2012-4d6a-9533-77bcb6e27376.json b/4598f1dc-2012-4d6a-9533-77bcb6e27376.json new file mode 100644 index 0000000000000000000000000000000000000000..430f85c9646b450848de68295147dafeaf7537d9 --- /dev/null +++ b/4598f1dc-2012-4d6a-9533-77bcb6e27376.json @@ -0,0 +1,34 @@ +{ + "id": "4598f1dc-2012-4d6a-9533-77bcb6e27376", + "disease": { + "id": "H00408", + "names": [ + "Type 1 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E10" + ], + "mesh": [ + "D003922" + ] + }, + "category": "Metabolic disease; Immune system disease; Endocrine disease" + }, + "article": { + "id": "12378375", + "text": "Viruses have long been considered a major environmental factor in the aetiology of Type I (insulin-dependent) diabetes mellitus and recent work has greatly confirmed and extended this role. In addition to the enteroviruses, there are several other viruses which, from time to time, have been considered potential causal agents for human diabetes. With the exception of rubella, their role is not clear. The relation of enteroviruses with Type I diabetes has only been properly clarified by the use of new technologies, especially those based on polymerase chain reaction methods to identify them in blood. It is now evident from studies in several countries that enterovirus infection accompanies or precedes the onset of diabetes in many children. It is less certain whether this is true for older persons or for other types of diabetes. Enterovirus infection in pregnancy has also been suggested to cause diabetes in children. The infection with enteroviruses seems to be linked to the induction of islet-cell autoantibodies as well as to the expression of interferon-alpha. Both of these events are connected with islet-cell destruction. It has become increasingly important to establish the nature of the infecting virus in the early stages of diabetes. It seems likely that a number of viruses of the coxsackie or echovirus type are involved, although the nature of the nucleotide sequences responsible for diabetogenicity remains elusive." + }, + "questions": [ + { + "id": "b04ca3a5-843a-4cc4-86f9-9dba686f4acf", + "text": "What are the risk factors of Type 1 diabetes mellitus?", + "answers": [ + { + "answer_start": 1291, + "text": "viruses of the coxsackie or echovirus type" + } + ] + } + ] +} \ No newline at end of file diff --git a/45b034b6-2623-4813-a50d-e085402c73e4.json b/45b034b6-2623-4813-a50d-e085402c73e4.json new file mode 100644 index 0000000000000000000000000000000000000000..0f8d4a203e8febaa948cf7373fa152bf8db5b294 --- /dev/null +++ b/45b034b6-2623-4813-a50d-e085402c73e4.json @@ -0,0 +1,34 @@ +{ + "id": "45b034b6-2623-4813-a50d-e085402c73e4", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "20200384", + "text": "BACKGROUND:\nFasting glucose is the standard measure used to diagnose diabetes in the United States. Recently, glycated hemoglobin was also recommended for this purpose.\n\nMETHODS:\nWe compared the prognostic value of glycated hemoglobin and fasting glucose for identifying adults at risk for diabetes or cardiovascular disease. We measured glycated hemoglobin in whole-blood samples from 11,092 black or white adults who did not have a history of diabetes or cardiovascular disease and who attended the second visit (occurring in the 1990-1992 period) of the Atherosclerosis Risk in Communities (ARIC) study.\n\nRESULTS:\nThe glycated hemoglobin value at baseline was associated with newly diagnosed diabetes and cardiovascular outcomes. For glycated hemoglobin values of less than 5.0%, 5.0 to less than 5.5%, 5.5 to less than 6.0%, 6.0 to less than 6.5%, and 6.5% or greater, the multivariable-adjusted hazard ratios (with 95% confidence intervals) for diagnosed diabetes were 0.52 (0.40 to 0.69), 1.00 (reference), 1.86 (1.67 to 2.08), 4.48 (3.92 to 5.13), and 16.47 (14.22 to 19.08), respectively. For coronary heart disease, the hazard ratios were 0.96 (0.74 to 1.24), 1.00 (reference), 1.23 (1.07 to 1.41), 1.78 (1.48 to 2.15), and 1.95 (1.53 to 2.48), respectively. The hazard ratios for stroke were similar. In contrast, glycated hemoglobin and death from any cause were found to have a J-shaped association curve. All these associations remained significant after adjustment for the baseline fasting glucose level. The association between the fasting glucose levels and the risk of cardiovascular disease or death from any cause was not significant in models with adjustment for all covariates as well as glycated hemoglobin. For coronary heart disease, measures of risk discrimination showed significant improvement when glycated hemoglobin was added to models including fasting glucose.\n\nCONCLUSIONS:\nIn this community-based population of nondiabetic adults, glycated hemoglobin was similarly associated with a risk of diabetes and more strongly associated with risks of cardiovascular disease and death from any cause as compared with fasting glucose. These data add to the evidence supporting the use of glycated hemoglobin as a diagnostic test for diabetes." + }, + "questions": [ + { + "id": "b19dc8d5-5533-449b-aed2-2b909bcb64d5", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 737, + "text": "glycated hemoglobin" + } + ] + } + ] +} \ No newline at end of file diff --git a/45c89945-d985-4717-b193-5934bba6943d.json b/45c89945-d985-4717-b193-5934bba6943d.json new file mode 100644 index 0000000000000000000000000000000000000000..b296fe1570c65122a9d4ccddb68610294b752f1c --- /dev/null +++ b/45c89945-d985-4717-b193-5934bba6943d.json @@ -0,0 +1,42 @@ +{ + "id": "45c89945-d985-4717-b193-5934bba6943d", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "10333916", + "text": "OBJECTIVE:\nNIDDM occurs commonly among women with polycystic ovary syndrome (PCOS). The prevalence and natural history of its precursor, impaired glucose tolerance (IGT), is less well known. The objective of this study was to characterize the prevalence and incidence of glucose intolerance in a large cohort of women with well-characterized PCOS.\n\nRESEARCH DESIGN AND METHODS:\nA total of 122 women with clinical and hormonal evidence of PCOS were recruited from the Medicine, Endocrinology, Gynecology, and Pediatrics Clinics at the University of Chicago. All women had a standard oral glucose tolerance test (OGTT) with measurement of glucose and insulin levels. A subset of 25 women were subsequently restudied with the aim of characterizing the natural history of glucose tolerance in PCOS.\n\nRESULTS:\nGlucose tolerance was abnormal in 55 (45%) of the 122 women: 43 (35%) had IGT and 12 (10%) had NIDDM at the time of initial study. The women with NIDDM differed from those with normal glucose tolerance in that they had a 2.6-fold higher prevalence of first-degree relatives with NIDDM (83 vs. 31%, P \u003c 0.01 by chi 2) and were significantly more obese (BMI 41.0 +/- 2.4 vs. 33.4 +/- 1.1 kg/m2, P \u003c 0.01). For the entire cohort of 122 women, there was a significant correlation between fasting and 2-h glucose concentrations (r = 0.76, P \u003c 0.0001); among the subset with IGT, the fasting glucose concentration was poorly predictive of the 2-h level (r = 0.25, NS). After a mean follow-up of 2.4 +/- 0.3 years (range 0.5-6.3), 25 women had a second OGTT. The glucose concentration at 2 h during the second glucose tolerance test was significantly higher than the 2-h concentration during the first study (161 +/- 9 vs. 139 +/- 6 mg/dl, P \u003c 0.02).\n\nCONCLUSIONS:\nThe prevalence of IGT and NIDDM in women with PCOS is substantially higher than expected when compared with age- and weight-matched populations of women without PCOS. The conversion from IGT to NIDDM is accelerated in PCOS. The fasting glucose concentration does not reliably predict the glucose concentration at 2 h after an oral glucose challenge, particularly among those with IGT, the subgroup at highest risk for subsequent development of NIDDM. We conclude that women with PCOS should periodically have an OGTT and must be closely monitored for deterioration in glucose tolerance." + }, + "questions": [ + { + "id": "796c1dbf-4857-48e6-a236-9e11e7ca342f", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1798, + "text": "women with PCOS" + }, + { + "answer_start": 50, + "text": "polycystic ovary syndrome (PCOS)" + }, + { + "answer_start": 2231, + "text": "women with PCOS" + } + ] + } + ] +} \ No newline at end of file diff --git a/462bf7f6-9259-47a5-8330-9b498db0a857.json b/462bf7f6-9259-47a5-8330-9b498db0a857.json new file mode 100644 index 0000000000000000000000000000000000000000..809d211148538b77284b03b567d3464e1a254b57 --- /dev/null +++ b/462bf7f6-9259-47a5-8330-9b498db0a857.json @@ -0,0 +1,40 @@ +{ + "id": "462bf7f6-9259-47a5-8330-9b498db0a857", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "19201711", + "text": "BACKGROUND:\nCOPD is a major cause of chronic morbidity and mortality throughout the world. Although the prevalence of COPD is already well documented, there are only few studies regarding the incidence of COPD.\n\nMETHODS:\nIn a prospective population-based cohort study among subjects aged \u003eor= 55 years, COPD was diagnosed with an algorithm based on the validation of hospital discharge letters, files from the general practitioner, and spirometry reports.\n\nRESULTS:\nIn this study cohort of 7,983 participants, 648 cases were identified with incident COPD after a median follow-up time of 11 years (interquartile range, 7.8 years). This resulted in an overall incidence rate (IR) of 9.2/1,000 person-years (PY) [95% confidence interval (CI), 8.5 to 10.0]. The IR of COPD was higher among men (14.4/1,000 PY; 95% CI, 13.0 to 16.0) than among women (6.2/1,000 PY; 95% CI, 5.5 to 7.0), and higher in smokers than in never-smokers (12.8/1,000 PY; 95% CI, 11.7 to 13.9 and 3.9/1,000 PY; 95% CI, 3.2 to 4.7, respectively). Remarkable was the high incidence in the youngest female age category of 55 to 59 years (7.4/1,000 PY; 95% CI, 4.1 to 12.6). For a 55-year-old man and woman still free of COPD at cohort entry, the risk for the development of COPD over the coming 40 years was 24% and 16%, respectively.\n\nCONCLUSION:\nThe overall incidence of COPD in an elderly population is 9.2/1,000 PY, with a remarkably high incidence in the youngest women, suggesting a further shift toward the female sex in the gender distribution of COPD. During their further lives, one of four men and one of six women free of COPD at the age of 55 years will have COPD develop." + }, + "questions": [ + { + "id": "d0afd3d1-0dd3-43b4-94e0-76cca663471e", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 787, + "text": "men" + }, + { + "answer_start": 896, + "text": "smokers" + } + ] + } + ] +} \ No newline at end of file diff --git a/46840d98-685e-47b1-9e3c-f4b9c69becab.json b/46840d98-685e-47b1-9e3c-f4b9c69becab.json new file mode 100644 index 0000000000000000000000000000000000000000..35b3ca23631c4dd43c24b9842230301297aea84c --- /dev/null +++ b/46840d98-685e-47b1-9e3c-f4b9c69becab.json @@ -0,0 +1,42 @@ +{ + "id": "46840d98-685e-47b1-9e3c-f4b9c69becab", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "8892715", + "text": "OBJECTIVE:\nTo test the hypothesis that bone mineral density (BMD) is associated with the risk of developing breast cancer in older women.\n\nDESIGN:\nProspective cohort study with mean (SD) follow-up of 3.2 (1.6) years.\n\nSETTING:\nFour clinical centers, one each located in the following areas: Baltimore, Md; Minneapolis, Minn; Portland, Ore; and the Monongahela Valley in Pennsylvania.\n\nPARTICIPANTS:\nA total of 6854 nonblack women who were 65 years of age or older and enrolled in the Study of Osteoporotic Fractures.\n\nMEASUREMENTS:\nRadius and calcaneus BMD by single photon absorptiometry at baseline; hip and spine BMD by dual-energy x-ray absorptiometry 2 years later.\n\nMAIN OUTCOME MEASURE:\nBreast cancer confirmed by medical record review.\n\nRESULTS:\nA total of 97 women developed breast cancer. In the multivariate model, adjusting for age, the degree of obesity, and other important covariates, the risk of breast cancer was about 30% to 50% higher per 1 SD increase in BMD (relative risk, distal radius BMD=1.50; 95% confidence interval, 1.16-1.95). The age-adjusted incidence rate of breast cancer per 1000 person-years among women in the lowest quartile of distal radius BMD was 2.46, compared with 5.99 among women with the highest BMD. Women with BMD above the 25th percentile were at 2.0 to 2.5 times increased risk of breast cancer compared with women below the 25th percentile. Results were consistent across all BMD sites.\n\nCONCLUSIONS:\nBone mineral density predicts the risk of breast cancer in older women. The magnitude of the association is similar to that observed between BMD and all fractures. Our findings suggest a link between 2 of the most common conditions affecting a woman's health. Identifying a common denominator for these conditions should substantially improve our understanding of their etiology and prevention." + }, + "questions": [ + { + "id": "f3290584-380b-4b3c-ba90-0229fb3530c8", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 958, + "text": "1 SD increase in BMD" + }, + { + "answer_start": 39, + "text": "bone mineral density (BMD)" + }, + { + "answer_start": 1451, + "text": "Bone mineral density " + } + ] + } + ] +} \ No newline at end of file diff --git a/46a43899-c6b9-436a-a6e8-227225526000.json b/46a43899-c6b9-436a-a6e8-227225526000.json new file mode 100644 index 0000000000000000000000000000000000000000..42b2d720ddbb0bcdfe3fdd00d6a2a6ea2e34c49f --- /dev/null +++ b/46a43899-c6b9-436a-a6e8-227225526000.json @@ -0,0 +1,55 @@ +{ + "id": "46a43899-c6b9-436a-a6e8-227225526000", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "28795508", + "text": "OBJECTIVE:\nEnvironmental factors are of importance for the etiology of rheumatoid arthritis (RA), but much remains unknown concerning the contributions from distinct occupational hazards. We explored the association between occupation and the risk of anti-citrullinated protein antibody (ACPA)+ RA or ACPA- RA.\n\nMETHODS:\nWe analyzed 3,522 cases and 5,580 controls from the Swedish population-based Epidemiological Investigation of Rheumatoid Arthritis case-control study. A questionnaire was used to obtain information on work history and lifestyle factors. Blood samples were drawn for serologic analyses. Unconditional logistic regression was used to calculate the odds ratio (OR) of RA associated with the last occupation before study inclusion. Analyses were performed with adjustments for known environmental exposures and lifestyle factors, including pack-years of cigarette smoking, alcohol use, body mass index, and education.\n\nRESULTS:\nAmong men, bricklayers and concrete workers (OR 2.9, 95% confidence interval [95% CI] 1.4-5.7), material handling operators (OR 2.4, 95% CI 1.3-4.4), and electrical and electronics workers (OR 2.1, 95% CI 1.1-3.8) had an increased risk of ACPA+ RA. For ACPA- RA, bricklayers and concrete workers (OR 2.4, 95% CI 1.0-5.7) and electrical and electronics workers (OR 2.6, 95% CI 1.3-5.0) had an increased risk. Among women, assistant nurses and attendants had a moderately increased risk of ACPA+ RA (OR 1.3, 95% CI 1.1-1.6). No occupations were significantly associated with ACPA- RA among women.\n\nCONCLUSION:\nMainly occupations related to potential noxious airborne agents were associated with an increased risk of ACPA+ or ACPA- RA, after adjustments for previously known confounders." + }, + "questions": [ + { + "id": "a6be3e91-4e94-4001-86a0-60b1bbfa960f", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 956, + "text": "bricklayers and concrete workers" + }, + { + "answer_start": 1041, + "text": "material handling operators" + }, + { + "answer_start": 1099, + "text": "electrical and electronics workers" + }, + { + "answer_start": 1208, + "text": "bricklayers and concrete workers" + }, + { + "answer_start": 1270, + "text": "electrical and electronics workers" + }, + { + "answer_start": 1353, + "text": "Among women, assistant nurses and attendants" + } + ] + } + ] +} \ No newline at end of file diff --git a/46ddc218-da5b-4259-ab27-ea4489dd0afe.json b/46ddc218-da5b-4259-ab27-ea4489dd0afe.json new file mode 100644 index 0000000000000000000000000000000000000000..69f41c552e93bbf8db9c74d040b76ece930e23ee --- /dev/null +++ b/46ddc218-da5b-4259-ab27-ea4489dd0afe.json @@ -0,0 +1,37 @@ +{ + "id": "46ddc218-da5b-4259-ab27-ea4489dd0afe", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "10088625", + "text": "BACKGROUND:\nThe remarkable similarity of lifestyle and environmental risk factors for type 2 (non-insulin-dependent) diabetes mellitus and colon cancer has led to the hypothesis that diabetes may increase the risk of this cancer. We prospectively examined the relationship between diabetes and risk of colorectal cancer in a cohort of 118403 women aged 30 through 55 years who were without previously diagnosed cancer at baseline in 1976.\n\nMETHODS:\nThe women, who were enrolled in the Nurses' Health Study, were assessed for history of diabetes at baseline and during follow-up by use of biennial questionnaires. Self-reported diabetes was validated by information obtained from a supplemental questionnaire on symptoms and treatment and was confirmed by medical record review in a sample of the participants. Incident cases of colorectal cancer were ascertained through medical record review. All reported P values are two-sided.\n\nRESULTS:\nDuring 18 years of follow-up (201061 person-years), we documented 892 new cases of colorectal cancer. After adjustment for age, body mass index (weight in kg/height in m2), physical activity, and other covariates, relative risks (RRs) were 1.43 (95% confidence interval [CI] = 1.10-1.87; P = .009) for colorectal cancer, 1.49 (95% CI = 1.09-2.06; P = .01) for colon cancer, 1.11 (95% CI = 0.56-2.21; P = .76) for rectal cancer, 1.56 (95% CI = 1.07-2.28; P = .02) for advanced colorectal cancer, and 2.39 (95% CI = 1.46-3.92; P = .0005) for fatal colorectal cancer.\n\nCONCLUSION:\nOur data provide support for the hypothesis that diabetes is associated with an increased risk of colorectal cancer in women." + }, + "questions": [ + { + "id": "3630df0e-5674-489b-8452-a574f2a4165e", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1568, + "text": "diabetes" + } + ] + } + ] +} \ No newline at end of file diff --git a/477195b6-857e-4d27-8893-e6ce2fb49b75.json b/477195b6-857e-4d27-8893-e6ce2fb49b75.json new file mode 100644 index 0000000000000000000000000000000000000000..702ec85e4a6c5a3179911fa2022a857dbff71949 --- /dev/null +++ b/477195b6-857e-4d27-8893-e6ce2fb49b75.json @@ -0,0 +1,51 @@ +{ + "id": "477195b6-857e-4d27-8893-e6ce2fb49b75", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "11421892", + "text": "BACKGROUND:\nIt has been suggested that pregnancy and early life may influence the development of asthma in the offspring, but published studies have not carefully controlled for potential biases.\n\nMETHODS:\nIn a large British birth cohort of 4065 natural children of 2583 mothers, we investigated whether in utero and perinatal influences contribute to the development and the severity of asthma in childhood, allowing for possible confounders of the relationship, and considering the nonindependence of familial data.\n\nRESULTS:\nChild asthma (10.1%) was more frequently reported by mothers when there had been health complications during pregnancy (prevalence =14.3%; adjusted odds ratio [ORadj] =2.01; 95% confidence interval, 1.52-2.67), labor, or delivery (19.3%, ORadj =1.35, 1.01-1.81); child illness or health complications during the first week of life (22.6%, ORadj =1.35, 1.01-1.82); and birth weight of \u003c 2.5 kg (7.0%, ORadj =1.57, 1.10-2.25). Specific causes of health complications during pregnancy which significantly related to asthma were early or threatened labor (ICD: 644) (4.8%, ORadj =1.58, 1.03-2.40) and the malposition or malpresentation of the fetus (ICD: 652) (1.6%, ORadj =3.63, 1.47-8.91).\n\nCONCLUSION:\nThe results provide further evidence that in utero and perinatal factors may increase the risk of developing asthma." + }, + "questions": [ + { + "id": "4fec9825-fd69-464a-ab8c-c4dcd8246d80", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 609, + "text": "health complications during pregnancy" + }, + { + "answer_start": 791, + "text": "child illness or health complications during the first week of life" + }, + { + "answer_start": 896, + "text": "birth weight of \u003c 2.5 kg" + }, + { + "answer_start": 1053, + "text": "early or threatened labor (ICD: 644)" + }, + { + "answer_start": 1129, + "text": "malposition or malpresentation of the fetus (ICD: 652)" + } + ] + } + ] +} \ No newline at end of file diff --git a/47dc2d94-9c73-4ff8-b3f9-52bb63fd5c4e.json b/47dc2d94-9c73-4ff8-b3f9-52bb63fd5c4e.json new file mode 100644 index 0000000000000000000000000000000000000000..9492cca06669417a5aa182b6d801f4e84b9e6213 --- /dev/null +++ b/47dc2d94-9c73-4ff8-b3f9-52bb63fd5c4e.json @@ -0,0 +1,42 @@ +{ + "id": "47dc2d94-9c73-4ff8-b3f9-52bb63fd5c4e", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "18799442", + "text": "CONTEXT:\nBisphenol A (BPA) is widely used in epoxy resins lining food and beverage containers. Evidence of effects in animals has generated concern over low-level chronic exposures in humans.\n\nOBJECTIVE:\nTo examine associations between urinary BPA concentrations and adult health status.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nCross-sectional analysis of BPA concentrations and health status in the general adult population of the United States, using data from the National Health and Nutrition Examination Survey 2003-2004. Participants were 1455 adults aged 18 through 74 years with measured urinary BPA and urine creatinine concentrations. Regression models were adjusted for age, sex, race/ethnicity, education, income, smoking, body mass index, waist circumference, and urinary creatinine concentration. The sample provided 80% power to detect unadjusted odds ratios (ORs) of 1.4 for diagnoses of 5% prevalence per 1-SD change in BPA concentration, or standardized regression coefficients of 0.075 for liver enzyme concentrations, at a significance level of P \u003c .05.\n\nMAIN OUTCOME MEASURES:\nChronic disease diagnoses plus blood markers of liver function, glucose homeostasis, inflammation, and lipid changes.\n\nRESULTS:\nHigher urinary BPA concentrations were associated with cardiovascular diagnoses in age-, sex-, and fully adjusted models (OR per 1-SD increase in BPA concentration, 1.39; 95% confidence interval [CI], 1.18-1.63; P = .001 with full adjustment). Higher BPA concentrations were also associated with diabetes (OR per 1-SD increase in BPA concentration, 1.39; 95% confidence interval [CI], 1.21-1.60; P \u003c .001) but not with other studied common diseases. In addition, higher BPA concentrations were associated with clinically abnormal concentrations of the liver enzymes gamma-glutamyltransferase (OR per 1-SD increase in BPA concentration, 1.29; 95% CI, 1.14-1.46; P \u003c .001) and alkaline phosphatase (OR per 1-SD increase in BPA concentration, 1.48; 95% CI, 1.18-1.85; P = .002).\n\nCONCLUSION:\nHigher BPA exposure, reflected in higher urinary concentrations of BPA, may be associated with avoidable morbidity in the community-dwelling adult population." + }, + "questions": [ + { + "id": "cc47d44a-ae08-4175-9ae3-224d0b9bb492", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 2011, + "text": "Higher BPA exposure" + }, + { + "answer_start": 9, + "text": "Bisphenol A (BPA)" + }, + { + "answer_start": 1466, + "text": "Higher BPA concentrations" + } + ] + } + ] +} \ No newline at end of file diff --git a/480a4011-3590-419c-ace0-2764c922d262.json b/480a4011-3590-419c-ace0-2764c922d262.json new file mode 100644 index 0000000000000000000000000000000000000000..424bdbdb573f740b44434cc076d8abbf2d718a71 --- /dev/null +++ b/480a4011-3590-419c-ace0-2764c922d262.json @@ -0,0 +1,34 @@ +{ + "id": "480a4011-3590-419c-ace0-2764c922d262", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "21330633", + "text": "BACKGROUND:\nEndogenous sex hormone levels are associated with risks of breast cancer overall and estrogen receptor (ER)-positive breast tumors; however, their associations with ER-negative tumors remain unclear.\n\nMETHODS:\nIn a case-cohort study within the Women's Health Initiative Observational Study among postmenopausal women aged 50-79 years, we examined associations between endogenous testosterone and estradiol levels and the risks of ER-negative and ER-positive breast cancers. Serum levels of bioavailable testosterone and estradiol were assessed at the baseline visit in 317 invasive breast cancer case subjects and in a subcohort of 594 women. Bioavailable sex hormone levels were calculated using the total hormone level and the sex hormone-binding globulin concentration (measured by radioimmunoassays and a chemiluminescent immunoassay, respectively). Cox proportional hazards regression was used for statistical analysis. All statistical tests were two-sided.\n\nRESULT:\nThe unadjusted absolute rates of ER-negative breast cancer for testosterone quartiles 1-4 were 0.34, 0.20, 0.23, and 0.21 per 10,000 person-years, respectively. Compared with women in the lowest quartile of testosterone level, those in quartile 2 had a 56% lower risk of ER-negative cancer (hazard ratio [HR] = 0.44, 95% confidence interval [CI] = 0.23 to 0.85), those in quartile 3 had a 45% lower risk (HR = 0.55, 95% CI = 0.30 to 1.01), and those in quartile 4 had a 49% lower risk (HR = 0.51, 95% CI = 0.28 to 0.94), independent of other risk factors. Estradiol level was not associated with ER-negative breast cancer. ER-positive breast cancer risk increased with higher testosterone levels (P(trend) = .04), but this trend was not statistically significant after adjustment for estradiol (P(trend) = .15). ER-positive cancer risk was approximately twofold higher in women with estradiol levels in quartiles 2-4 compared with women in quartile 1, independent of risk factors.\n\nCONCLUSION:\nHigher serum levels of bioavailable testosterone are associated with lower risks of ER-negative breast cancer in postmenopausal women." + }, + "questions": [ + { + "id": "30f3d3d6-9c03-4519-8c93-44c7e10648f7", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1856, + "text": "women with estradiol levels in quartiles 2-4 compared with women in quartile 1" + } + ] + } + ] +} \ No newline at end of file diff --git a/4816652e-aac2-4e49-9cef-0c0162366e19.json b/4816652e-aac2-4e49-9cef-0c0162366e19.json new file mode 100644 index 0000000000000000000000000000000000000000..4a2da275c2d41bf5e05f40633c0394aad4f7664f --- /dev/null +++ b/4816652e-aac2-4e49-9cef-0c0162366e19.json @@ -0,0 +1,42 @@ +{ + "id": "4816652e-aac2-4e49-9cef-0c0162366e19", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "15328324", + "text": "CONTEXT:\nSugar-sweetened beverages like soft drinks and fruit punches contain large amounts of readily absorbable sugars and may contribute to weight gain and an increased risk of type 2 diabetes, but these relationships have been minimally addressed in adults.\n\nOBJECTIVE:\nTo examine the association between consumption of sugar-sweetened beverages and weight change and risk of type 2 diabetes in women.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nProspective cohort analyses conducted from 1991 to 1999 among women in the Nurses' Health Study II. The diabetes analysis included 91,249 women free of diabetes and other major chronic diseases at baseline in 1991. The weight change analysis included 51,603 women for whom complete dietary information and body weight were ascertained in 1991, 1995, and 1999. We identified 741 incident cases of confirmed type 2 diabetes during 716,300 person-years of follow-up.\n\nMAIN OUTCOME MEASURES:\nWeight gain and incidence of type 2 diabetes.\n\nRESULTS:\nThose with stable consumption patterns had no difference in weight gain, but weight gain over a 4-year period was highest among women who increased their sugar-sweetened soft drink consumption from 1 or fewer drinks per week to 1 or more drinks per day (multivariate-adjusted means, 4.69 kg for 1991 to 1995 and 4.20 kg for 1995 to 1999) and was smallest among women who decreased their intake (1.34 and 0.15 kg for the 2 periods, respectively) after adjusting for lifestyle and dietary confounders. Increased consumption of fruit punch was also associated with greater weight gain compared with decreased consumption. After adjustment for potential confounders, women consuming 1 or more sugar-sweetened soft drinks per day had a relative risk [RR] of type 2 diabetes of 1.83 (95% confidence interval [CI], 1.42-2.36; P\u003c.001 for trend) compared with those who consumed less than 1 of these beverages per month. Similarly, consumption of fruit punch was associated with increased diabetes risk (RR for \u003e or =1 drink per day compared with \u003c1 drink per month, 2.00; 95% CI, 1.33-3.03; P =.001).\n\nCONCLUSION:\nHigher consumption of sugar-sweetened beverages is associated with a greater magnitude of weight gain and an increased risk for development of type 2 diabetes in women, possibly by providing excessive calories and large amounts of rapidly absorbable sugars." + }, + "questions": [ + { + "id": "06c5d9db-f5ea-4dce-83df-f97192f92446", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1649, + "text": "women consuming 1 or more sugar-sweetened soft drinks per day" + }, + { + "answer_start": 1909, + "text": "consumption of fruit punch" + }, + { + "answer_start": 2092, + "text": "Higher consumption of sugar-sweetened beverages" + } + ] + } + ] +} \ No newline at end of file diff --git a/49484e22-6a75-42c8-878b-a8788d0f217e.json b/49484e22-6a75-42c8-878b-a8788d0f217e.json new file mode 100644 index 0000000000000000000000000000000000000000..390ffe5660256b11cd8bc9ab446a947aa25b6a53 --- /dev/null +++ b/49484e22-6a75-42c8-878b-a8788d0f217e.json @@ -0,0 +1,39 @@ +{ + "id": "49484e22-6a75-42c8-878b-a8788d0f217e", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "20709817", + "text": "RATIONALE:\nThere is epidemiological evidence that the use of acetaminophen may increase the risk of developing asthma.\n\nOBJECTIVES:\nTo investigate the risk of asthma and other allergic disorders associated with the current use of acetaminophen in 13- to 14-year-old children in different populations worldwide.\n\nMETHODS:\nAs part of the International Study of Asthma and Allergies in Childhood (ISAAC) Phase Three, 13- to 14-year-old children completed written and video questionnaires obtaining data on current symptoms of asthma, rhinoconjunctivitis, and eczema, and a written environmental questionnaire obtaining data on putative risk factors, including acetaminophen use in the past 12 months.\n\nMEASUREMENTS AND MAIN RESULTS:\nThe primary outcome measure was the odds ratio (OR) of current asthma symptoms associated with acetaminophen use calculated by logistic regression. A total of 322,959 adolescent children from 113 centers in 50 countries participated. In the multivariate analyses the recent use of acetaminophen was associated with an exposure-dependent increased risk of current asthma symptoms (OR, 1.43 [95% confidence interval, 1.33-1.53] and 2.51 [95% confidence interval, 2.33-2.70] for medium and high versus no use, respectively). Acetaminophen use was also associated with an exposure-dependent increased risk of current symptoms of rhinoconjunctivitis and eczema.\n\nCONCLUSIONS:\nAcetaminophen use may represent an important risk factor for the development and/or maintenance of asthma, rhinoconjunctivitis, and eczema in adolescent children." + }, + "questions": [ + { + "id": "05a497e8-72d8-419c-bb80-cdcb8c180f55", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 997, + "text": "recent use of acetaminophen" + }, + { + "answer_start": 1401, + "text": "Acetaminophen use" + } + ] + } + ] +} \ No newline at end of file diff --git a/49e357a3-288a-479a-8877-3f7c8c4864e5.json b/49e357a3-288a-479a-8877-3f7c8c4864e5.json new file mode 100644 index 0000000000000000000000000000000000000000..8fc38b955c4a19a7b05ab7e17b487fc9a369e939 --- /dev/null +++ b/49e357a3-288a-479a-8877-3f7c8c4864e5.json @@ -0,0 +1,34 @@ +{ + "id": "49e357a3-288a-479a-8877-3f7c8c4864e5", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "11923036", + "text": "OBJECTIVES:\nThe goal of this study was to assess soluble intercellular adhesion molecule-1 (sICAM-1) level as a predictor of future acute coronary events in patients with chronic coronary heart disease (CHD).\n\nBACKGROUND:\nIncreased sICAM-1 concentration has been shown to be associated with the incidence of CHD in healthy persons. Its significance in patients with CHD has been scarcely investigated.\n\nMETHODS:\nWe designed a prospective, nested case-control study. Sera were collected from patients with CHD enrolled in a secondary prevention trial that evaluated the efficacy of bezafibrate in reducing coronary events. We measured baseline sICAM-1 concentration in the sera of patients who developed subsequent cardiovascular events (cases: n = 136) during follow-up (mean: 6.2 years) and in age- and gender-matched controls (without events: n = 136).\n\nRESULTS:\nBaseline serum concentrations of sICAM-1 were significantly higher in cases versus controls (375 vs. 350 ng/ml; p \u003c 0.05). Each 100 ng/ml increase in sICAM-1 concentration was associated with 1.27 (95% confidence interval [CI]: 1.00 to 1.63) higher relative odds of coronary events. Soluble ICAM-1 concentration in the highest quartile (\u003e394 ng/ml) was associated with significantly higher odds of coronary events (compared with the lowest quartile), even after multivariate adjustment (2.31, 95% CI: 1.02 to 5.50). After adding fibrinogen and total white blood cell count to the multivariate model, the relative odds were 2.12 (95% CI: 0.88 to 5.35) and 2.70 (95% CI: 1.10 to 7.05), respectively.\n\nCONCLUSIONS:\nElevated sICAM-1 concentration in CHD patients is associated with increased risk of future coronary events independent of other traditional risk factors." + }, + "questions": [ + { + "id": "b22526d6-8286-4667-b31c-51f45261c3de", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1577, + "text": "Elevated sICAM-1" + } + ] + } + ] +} \ No newline at end of file diff --git a/4a44e6d3-5b76-4c7c-9359-f366d509b616.json b/4a44e6d3-5b76-4c7c-9359-f366d509b616.json new file mode 100644 index 0000000000000000000000000000000000000000..bad11bbcc1b59b102fed1418d6c7aee060f94f37 --- /dev/null +++ b/4a44e6d3-5b76-4c7c-9359-f366d509b616.json @@ -0,0 +1,38 @@ +{ + "id": "4a44e6d3-5b76-4c7c-9359-f366d509b616", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "11522704", + "text": "OBJECTIVE:\nTo examine the effects of cigarette smoking, giving up smoking, and primary or secondary pipe or cigar smoking on the risk of type 2 diabetes.\n\nRESEARCH DESIGN AND METHODS:\nA prospective study followed 7,735 men aged 40-59 years from general practices in 24 British towns for an average of 16.8 years. Incident cases of physician-diagnosed diabetes were ascertained by repeated postal questionnaires and systematic reviews of primary care records.\n\nRESULTS:\nA total of 290 incident cases of diabetes were found in 7,124 men with no history of diabetes, coronary heart disease, or stroke. Cigarette smoking was associated with a significant increase in risk of diabetes, even after adjustment for age, BMI, and other potential confounders. The benefit of giving up smoking was only apparent after 5 years of smoking cessation, and risk reverted to that of never-smokers only after 20 years. The risk of diabetes in those who switched from smoking cigarettes to pipe or cigars remained equal to the risk in continuing cigarette smokers. Men who gave up smoking during the first 5 years of follow-up showed significant weight gain and subsequently higher risk of diabetes than continuing smokers.\n\nCONCLUSIONS:\nCigarette smoking is an independent and modifiable risk factor for type 2 diabetes. Smoking cessation is associated with weight gain and a subsequent increase in risk of diabetes, but in the long term, the benefits of giving up smoking outweigh the adverse effects of early weight gain." + }, + "questions": [ + { + "id": "7df46c23-76a4-47ca-88f1-8885a8a5748e", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1219, + "text": "Cigarette smoking" + }, + { + "answer_start": 1303, + "text": "Smoking cessation" + } + ] + } + ] +} \ No newline at end of file diff --git a/4a69167c-8bf6-41c1-bc89-8f64317a2a8f.json b/4a69167c-8bf6-41c1-bc89-8f64317a2a8f.json new file mode 100644 index 0000000000000000000000000000000000000000..1d2fa1b376f229182f79535b3074317fe9314958 --- /dev/null +++ b/4a69167c-8bf6-41c1-bc89-8f64317a2a8f.json @@ -0,0 +1,41 @@ +{ + "id": "4a69167c-8bf6-41c1-bc89-8f64317a2a8f", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "25888582", + "text": "Results from cohort studies of adult weight gain and risk of colorectal cancer are inconsistent. We conducted a systematic review and meta-analysis of prospective studies assessing the association of change in weight/body mass index with colorectal cancer risk. We searched Scopus and Web of Science up to June 2014 and supplemented the search with manual searches of the reference lists of the identified articles. Thirteen studies published between 1997 and 2014 were pooled by using a random-effects model, and potential heterogeneity was explored by fitting meta-regression models. The highest weight gain category, measured by weight/body mass index, compared with a reference category, was associated with increased risk of colorectal cancer (hazard ratio (HR) = 1.16, 95% confidence interval (CI): 1.08, 1.24), whereas no association was found for weight loss (HR = 0.96, 95% CI: 0.89, 1.05). There was no suggestion of heterogeneity across studies. For dose response, a 5-kg weight gain was associated with a slightly increased risk of colorectal cancer (HR = 1.03, 95% CI: 1.02, 1.05), with some heterogeneity observed (I(2) = 42%; P = 0.02), which was partially explained by sex (ratio of HRs = 1.03, 95% CI: 1.00, 1.07). In this meta-analysis, gain in weight/body mass index was positively associated with colorectal cancer risk." + }, + "questions": [ + { + "id": "5d9a2898-c61a-4097-87d9-145d67d46c97", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1255, + "text": "gain in weight/body mass index" + }, + { + "answer_start": 590, + "text": "highest weight gain category, measured by weight/body mass index" + } + ] + } + ] +} \ No newline at end of file diff --git a/4b1d471a-9e45-4c0e-a55b-bb7f5ab99fa9.json b/4b1d471a-9e45-4c0e-a55b-bb7f5ab99fa9.json new file mode 100644 index 0000000000000000000000000000000000000000..ed0ab960b810fcdb1f8f6f74d175190b73d9b812 --- /dev/null +++ b/4b1d471a-9e45-4c0e-a55b-bb7f5ab99fa9.json @@ -0,0 +1,35 @@ +{ + "id": "4b1d471a-9e45-4c0e-a55b-bb7f5ab99fa9", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "16718266", + "text": "Since the early 1970s, a number of case reports have suggested that levodopa therapy for Parkinson's disease increases the risk of cutaneous malignant melanoma. As yet, no formal epidemiological study has been conducted to verify this hypothesis. To elucidate the relationship between levodopa and the risk of cutaneous malignant melanoma, a systematic literature search using computerized bibliographic databases was done. This review presents the case history evidence for and against the hypothesis of a causal association, and explores possible epidemiological, genetic, social, biochemical and toxicological factors that may increase the risk of melanoma in Parkinson's disease patients. All the case reports in the literature were considered. We concluded that (1) there is no epidemiological or experimental evidence of a causal role of levodopa in increasing the risk of melanoma incidence or progression; (2) there is good evidence of an excess risk of melanoma in patients with Parkinson's disease; (3) there is good evidence of a protective effect of tobacco smoking on the risk for Parkinson's disease; (4) there is good evidence of positive correlation between social class and melanoma risk; (5) the relationship between the risk of Parkinson's disease and the risk of melanoma may be due to a common genetic profile or it can be attributed to a confounding role of social class, associated with both melanoma and Parkinson's disease possibly through an inverse relationship with tobacco smoking." + }, + "questions": [ + { + "id": "3e511fa6-0bff-4ff8-815c-6b36c14dd3e0", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 974, + "text": "patients with Parkinson's disease" + } + ] + } + ] +} \ No newline at end of file diff --git a/4b493b9d-1989-4f78-b81e-c53c6c8a6a68.json b/4b493b9d-1989-4f78-b81e-c53c6c8a6a68.json new file mode 100644 index 0000000000000000000000000000000000000000..a9747ad4c11a2bca26bfa7d70239ec386858955e --- /dev/null +++ b/4b493b9d-1989-4f78-b81e-c53c6c8a6a68.json @@ -0,0 +1,42 @@ +{ + "id": "4b493b9d-1989-4f78-b81e-c53c6c8a6a68", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "20160170", + "text": "Soft drinks and other sweetened beverages may contribute to risk of type 2 diabetes and obesity. However, research has not addressed higher risk and Asian populations. The authors examined the association between soft drinks and juice and the risk of type 2 diabetes among Chinese Singaporeans enrolled in a prospective cohort study of 43,580 participants aged 45-74 years and free of diabetes and other chronic diseases at baseline. The incidence of physician-diagnosed type 2 diabetes was assessed by interview and validated; 2,273 participants developed diabetes during follow-up. After adjustment for potential lifestyle and dietary confounders, participants consuming \u003e or =2 soft drinks per week had a relative risk of type 2 diabetes of 1.42 (95% confidence interval (CI): 1.25, 1.62) compared with those who rarely consumed soft drinks. Similarly, consumption of \u003e or =2 juice beverages per week was associated with an increased risk (relative risk (RR) = 1.29, 95% CI: 1.05, 1.58). The association was modified by 5-year weight gain for \u003e or =2 soft drinks per week among those who gained \u003e or =3 kg (RR = 1.70, 95% CI: 1.34, 2.16) compared with those who gained less weight (RR = 1.20, 95% CI: 1.03, 1.41). Relatively frequent intake of soft drinks and juice is associated with an increased risk for development of type 2 diabetes in Chinese men and women." + }, + "questions": [ + { + "id": "56f384ee-5ed9-4c93-b23a-3d5f7094ecba", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 650, + "text": "participants consuming \u003e or =2 soft drinks per week" + }, + { + "answer_start": 856, + "text": "consumption of \u003e or =2 juice beverages per week" + }, + { + "answer_start": 1217, + "text": "Relatively frequent intake of soft drinks and juice" + } + ] + } + ] +} \ No newline at end of file diff --git a/4b9025da-8041-4ba7-89a6-6497817a8ab1.json b/4b9025da-8041-4ba7-89a6-6497817a8ab1.json new file mode 100644 index 0000000000000000000000000000000000000000..a963ec46b10fd03280c65e12dfd1d7f2172320c0 --- /dev/null +++ b/4b9025da-8041-4ba7-89a6-6497817a8ab1.json @@ -0,0 +1,46 @@ +{ + "id": "4b9025da-8041-4ba7-89a6-6497817a8ab1", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "20587727", + "text": "We examined ranges of A1C useful for identifying persons at high risk for diabetes prior to preventive intervention by conducting a systematic review. From 16 included studies, we found that annualized diabetes incidence ranged from 0.1% at A1C \u003c5.0% to 54.1% at A1C \u003eor=6.1%. Findings from 7 studies that examined incident diabetes across a broad range of A1C categories showed 1) risk of incident diabetes increased steeply with A1C across the range of 5.0 to 6.5%; 2) the A1C range of 6.0 to 6.5% was associated with a highly increased risk of incident diabetes, 25 to 50% incidence over 5 years; 3) the A1C range of 5.5 to 6.0% was associated with a moderately increased relative risk, 9 to 25% incidence over 5 years; and 4) the A1C range of 5.0 to 5.5% was associated with an increased incidence relative to those with A1C \u003c5%, but the absolute incidence of diabetes was less than 9% over 5 years. Our systematic review demonstrated that A1C values between 5.5 and 6.5% were associated with a substantially increased risk for developing diabetes." + }, + "questions": [ + { + "id": "dd1dc101-a7bd-4d93-a77a-693b0f1fa753", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 431, + "text": "A1C across the range of 5.0 to 6.5%" + }, + { + "answer_start": 475, + "text": "A1C range of 6.0 to 6.5%" + }, + { + "answer_start": 607, + "text": "A1C range of 5.5 to 6.0%" + }, + { + "answer_start": 944, + "text": "A1C values between 5.5 and 6.5%" + } + ] + } + ] +} \ No newline at end of file diff --git a/4bb3ee36-eec3-4946-bc01-8a41223cb8aa.json b/4bb3ee36-eec3-4946-bc01-8a41223cb8aa.json new file mode 100644 index 0000000000000000000000000000000000000000..ca428ea9fe6eacac953fbbd6634cb3b92c397c06 --- /dev/null +++ b/4bb3ee36-eec3-4946-bc01-8a41223cb8aa.json @@ -0,0 +1,43 @@ +{ + "id": "4bb3ee36-eec3-4946-bc01-8a41223cb8aa", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "8404764", + "text": "Intermittent exposure to sunlight is considered to be an important risk factor for melanoma, but the associations reported in most case-control studies are surprisingly weak. The aim of this study was to evaluate whether the incorporation of a subject's background exposure to the sun and pigmentation characteristics (which are assumed to influence a person's susceptibility to sunlight exposure) could produce stronger associations between sunlight exposure and the risk for melanoma. A population-based case-control study was performed in the mid-eastern part of the Netherlands. The study group comprised 141 patients with a histologically verified melanoma and 183 controls with other malignancies who were registered by the same cancer registry. Patients with a lentigo maligna melanoma or an acrolentiginous melanoma were excluded. Information was collected by interviews and physical examination. We categorized subjects as indoor or outdoor workers on the basis of occupational exposure to the sun. Pigmentation characteristics, which are known to be risk indicators for cutaneous melanoma, were summarized as one sun sensitivity score. We used this score to distinguish between sun-sensitive and sun-resistant persons. The odds ratios associated with sunbathing, vacations spent in sunny countries, and sunburns were higher among the indoor workers than among the outdoor workers. After stratification by the sun sensitivity score, the effect of sunbathing, participating in water sports (swimming excluded), vacations to sunny countries, and a history of sunburn was largest for the sun-sensitive persons. The data show a general trend toward higher relative risks among indoor workers and sun-sensitive individuals. The results of this study support the intermittent sunlight hypothesis." + }, + "questions": [ + { + "id": "97e14271-372a-4373-a4a1-4f366f6829e0", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 1261, + "text": "sunbathing" + }, + { + "answer_start": 1273, + "text": "vacations spent in sunny countries" + }, + { + "answer_start": 1313, + "text": "sunburns" + } + ] + } + ] +} \ No newline at end of file diff --git a/4c278539-416d-4896-addb-3a1b8080c0d5.json b/4c278539-416d-4896-addb-3a1b8080c0d5.json new file mode 100644 index 0000000000000000000000000000000000000000..f3524598fd8cb598c0ab30bd1ed860197cc8fee9 --- /dev/null +++ b/4c278539-416d-4896-addb-3a1b8080c0d5.json @@ -0,0 +1,47 @@ +{ + "id": "4c278539-416d-4896-addb-3a1b8080c0d5", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "17954799", + "text": "BACKGROUND:\nAn association between melanoma and endometriosis has been reported, but most findings relied on case-control studies or a limited number of melanoma cases, and therefore the available evidence is weak. Moreover, the effect of other benign gynecological diseases on melanoma risk is unknown.\n\nMETHODS:\nWe prospectively studied data from the Etude Epidémiologique auprès de femmes de la Mutuelle Générale de l'Education Nationale cohort, which includes 98 995 French women, insured by a national health scheme mostly covering teachers, aged 40 to 65 years at inclusion. Data on history of endometriosis and other benign gynecological diseases were regularly collected, starting in 1990. Relative risks and 95% confidence intervals were computed using Cox proportional hazards regression models.\n\nRESULTS:\nDuring 12 years of follow-up, 363 melanoma cases were ascertained among 91 965 subjects. A history of endometriosis (n = 5949) was significantly associated with a higher risk of melanoma (relative risk, 1.62; 95% confidence interval, 1.15-2.29). There was also a significantly increased risk among women with a history of fibroma (n = 24 375), compared with those who had no such history (relative risk, 1.33; 95% confidence interval, 1.06-1.67). A history of ovarian cyst, uterine polyp, breast adenoma/fibroadenoma, or breast fibrocystic disease was not significantly associated with risk.\n\nCONCLUSIONS:\nThese data provide the strongest evidence to date of a positive association between a history of endometriosis and melanoma risk. The association between fibroma and melanoma, which has not been previously described, warrants further investigation." + }, + "questions": [ + { + "id": "c6e93cbb-016d-4368-b3ec-113575de1cf6", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 905, + "text": "A history of endometriosis" + }, + { + "answer_start": 1113, + "text": " women with a history of fibroma" + }, + { + "answer_start": 1508, + "text": "history of endometriosis" + }, + { + "answer_start": 1576, + "text": "fibroma" + } + ] + } + ] +} \ No newline at end of file diff --git a/4c6c385f-c443-471e-9125-aceb1f3bea7f.json b/4c6c385f-c443-471e-9125-aceb1f3bea7f.json new file mode 100644 index 0000000000000000000000000000000000000000..0e928d39d023db926ebe08c85459503120181e3f --- /dev/null +++ b/4c6c385f-c443-471e-9125-aceb1f3bea7f.json @@ -0,0 +1,39 @@ +{ + "id": "4c6c385f-c443-471e-9125-aceb1f3bea7f", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "17932376", + "text": "RATIONALE:\nRisk factors for asthma among farm women are understudied.\n\nOBJECTIVES:\nWe evaluated pesticide and other occupational exposures as risk factors for adult-onset asthma.\n\nMETHODS:\nStudying 25,814 farm women in the Agricultural Health Study, we used self-reported history of doctor-diagnosed asthma with or without eczema and/or hay fever to create two case groups: patients with atopic asthma and those with nonatopic asthma. We assessed disease-exposure associations with polytomous logistic regression.\n\nMEASUREMENTS AND MAIN RESULTS:\nAt enrollment (1993-1997), 702 women (2.7%) reported a doctor's diagnosis of asthma after age 19 years (282 atopic, 420 nonatopic). Growing up on a farm (61% of all farm women) was protective for atopic asthma (odds ratio [OR], 0.55; 95% confidence interval [CI], 0.43-0.70) and, to a lesser extent, for nonatopic asthma (OR, 0.83; 95%CI, 0.68-1.02; P value for difference = 0.008). Pesticide use was almost exclusively associated with atopic asthma. Any use of pesticides on the farm was associated only with atopic asthma (OR, 1.46; 95% CI, 1.14-1.87). This association with pesticides was strongest among women who had grown up on a farm. Women who grew up on farms and did not apply pesticides had the lowest overall risk of atopic asthma (OR, 0.41; 95% CI, 0.27-0.62) compared with women who neither grew up on farms nor applied pesticides. A total of 7 of 16 insecticides, 2 of 11 herbicides, and 1 of 4 fungicides were significantly associated with atopic asthma; only permethrin use on crops was associated with nonatopic asthma.\n\nCONCLUSIONS:\nThese findings suggest that pesticides may contribute to atopic asthma, but not nonatopic asthma, among farm women." + }, + "questions": [ + { + "id": "e1668eea-c054-420a-8c09-352b42550fb9", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 929, + "text": "Pesticide use" + }, + { + "answer_start": 997, + "text": "Any use of pesticides" + } + ] + } + ] +} \ No newline at end of file diff --git a/4cdb34b7-f48a-46ed-840f-52c1add94e4b.json b/4cdb34b7-f48a-46ed-840f-52c1add94e4b.json new file mode 100644 index 0000000000000000000000000000000000000000..ad033120ea7b0fb4bb5a5ff7577f8c47be7acc6a --- /dev/null +++ b/4cdb34b7-f48a-46ed-840f-52c1add94e4b.json @@ -0,0 +1,70 @@ +{ + "id": "4cdb34b7-f48a-46ed-840f-52c1add94e4b", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "22547473", + "text": "BACKGROUND:\nIdentifying risk factors for breast cancer specific to women in their 40s could inform screening decisions.\n\nPURPOSE:\nTo determine what factors increase risk for breast cancer in women aged 40 to 49 years and the magnitude of risk for each factor.\n\nDATA SOURCES:\nMEDLINE (January 1996 to the second week of November 2011), Cochrane Central Register of Controlled Trials and Cochrane Database of Systematic Reviews (fourth quarter of 2011), Scopus, reference lists of published studies, and the Breast Cancer Surveillance Consortium.\n\nSTUDY SELECTION:\nEnglish-language studies and systematic reviews of risk factors for breast cancer in women aged 40 to 49 years. Additional inclusion criteria were applied for each risk factor.\n\nDATA EXTRACTION:\nData on participants, study design, analysis, follow-up, and outcomes were abstracted. Study quality was rated by using established criteria, and only studies rated as good or fair were included. Results were summarized by using meta-analysis when sufficient studies were available or from the best evidence based on study quality, size, and applicability when meta-analysis was not possible. Data from the Breast Cancer Surveillance Consortium were analyzed with proportional hazards models by using partly conditional Cox regression. Reference groups for comparisons were set at U.S. population means.\n\nDATA SYNTHESIS:\nSixty-six studies provided data for estimates. Extremely dense breasts on mammography or first-degree relatives with breast cancer were associated with at least a 2-fold increase in risk for breast cancer. Prior breast biopsy, second-degree relatives with breast cancer, or heterogeneously dense breasts were associated with a 1.5- to 2.0-fold increased risk; current use of oral contraceptives, nulliparity, and age 30 years or older at first birth were associated with a 1.0- to 1.5-fold increased risk.\n\nLIMITATIONS:\nStudies varied by measures, reference groups, and adjustment for confounders, which could bias combined estimates. Effects of multiple risk factors were not considered.\n\nCONCLUSION:\nExtremely dense breasts and first-degree relatives with breast cancer were each associated with at least a 2-fold increase in risk for breast cancer in women aged 40 to 49 years. Identification of these risk factors may be useful for personalized mammography screening.\n\nPRIMARY FUNDING SOURCE:\nNational Cancer Institute." + }, + "questions": [ + { + "id": "ff3fd2c5-4aa8-4115-9ef1-4edf4971b2a0", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1426, + "text": "Extremely dense breasts on mammography" + }, + { + "answer_start": 1468, + "text": "first-degree relatives with breast cancer" + }, + { + "answer_start": 1585, + "text": "Prior breast biopsy" + }, + { + "answer_start": 1606, + "text": "second-degree relatives with breast cancer" + }, + { + "answer_start": 1653, + "text": "heterogeneously dense breasts" + }, + { + "answer_start": 1739, + "text": "current use of oral contraceptives" + }, + { + "answer_start": 1775, + "text": "nulliparity" + }, + { + "answer_start": 1792, + "text": "age 30 years or older at first birth" + }, + { + "answer_start": 2081, + "text": "Extremely dense breast" + }, + { + "answer_start": 2109, + "text": "first-degree relatives with breast cancer" + } + ] + } + ] +} \ No newline at end of file diff --git a/4cdcadf6-4637-4edf-8b5a-8d02915b989b.json b/4cdcadf6-4637-4edf-8b5a-8d02915b989b.json new file mode 100644 index 0000000000000000000000000000000000000000..a9d143ea171546e779a33738c9daa95940815032 --- /dev/null +++ b/4cdcadf6-4637-4edf-8b5a-8d02915b989b.json @@ -0,0 +1,46 @@ +{ + "id": "4cdcadf6-4637-4edf-8b5a-8d02915b989b", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "10733371", + "text": "BACKGROUND:\nSince inflammation is believed to have a role in the pathogenesis of cardiovascular events, measurement of markers of inflammation has been proposed as a method to improve the prediction of the risk of these events.\n\nMETHODS:\nWe conducted a prospective, nested case-control study among 28,263 apparently healthy postmenopausal women over a mean follow-up period of three years to assess the risk of cardiovascular events associated with base-line levels of markers of inflammation. The markers included high-sensitivity C-reactive protein (hs-CRP), serum amyloid A, interleukin-6, and soluble intercellular adhesion molecule type 1 (sICAM-1). We also studied homocysteine and a variety of lipid and lipoprotein measurements. Cardiovascular events were defined as death from coronary heart disease, nonfatal myocardial infarction or stroke, or the need for coronary-revascularization procedures.\n\nRESULTS:\nOf the 12 markers measured, hs-CRP was the strongest univariate predictor of the risk of cardiovascular events; the relative risk of events for women in the highest as compared with the lowest quartile for this marker was 4.4 (95 percent confidence interval, 2.2 to 8.9). Other markers significantly associated with the risk of cardiovascular events were serum amyloid A (relative risk for the highest as compared with the lowest quartile, 3.0), sICAM-1 (2.6), interleukin-6 (2.2), homocysteine (2.0), total cholesterol (2.4), LDL cholesterol (2.4), apolipoprotein B-100 (3.4), HDL cholesterol (0.3), and the ratio of total cholesterol to HDL cholesterol (3.4). Prediction models that incorporated markers of inflammation in addition to lipids were significantly better at predicting risk than models based on lipid levels alone (P\u003c0.001). The levels of hs-CRP and serum amyloid A were significant predictors of risk even in the subgroup of women with LDL cholesterol levels below 130 mg per deciliter (3.4 mmol per liter), the target for primary prevention established by the National Cholesterol Education Program. In multivariate analyses, the only plasma markers that independently predicted risk were hs-CRP (relative risk for the highest as compared with the lowest quartile, 1.5; 95 percent confidence interval, 1.1 to 2.1) and the ratio of total cholesterol to HDL cholesterol (relative risk, 1.4; 95 percent confidence interval, 1.1 to 1.9).\n\nCONCLUSIONS:\nThe addition of the measurement of C-reactive protein to screening based on lipid levels may provide an improved method of identifying persons at risk for cardiovascular events." + }, + "questions": [ + { + "id": "d2956426-a3ad-4772-9606-feae9dd14342", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1761, + "text": "levels of hs-CRP" + }, + { + "answer_start": 1782, + "text": "serum amyloid A" + }, + { + "answer_start": 945, + "text": "hs-CRP" + }, + { + "answer_start": 2256, + "text": "ratio of total cholesterol to HDL cholesterol" + } + ] + } + ] +} \ No newline at end of file diff --git a/4de7ceb4-e93e-4419-b7b0-06da33c8aac4.json b/4de7ceb4-e93e-4419-b7b0-06da33c8aac4.json new file mode 100644 index 0000000000000000000000000000000000000000..b58d8d395c33ee9b9a7728cf623745fff491c1bf --- /dev/null +++ b/4de7ceb4-e93e-4419-b7b0-06da33c8aac4.json @@ -0,0 +1,52 @@ +{ + "id": "4de7ceb4-e93e-4419-b7b0-06da33c8aac4", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "25241909", + "text": "BACKGROUND:\nChronic bronchitis (CB) is one of the classic phenotypes of COPD. The aims of our study were to investigate genetic variants associated with COPD subjects with CB relative to smokers with normal spirometry, and to assess for genetic differences between subjects with CB and without CB within the COPD population.\n\nMETHODS:\nWe analyzed data from current and former smokers from three cohorts: the COPDGene Study; GenKOLS (Bergen, Norway); and the Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints (ECLIPSE). CB was defined as having a cough productive of phlegm on most days for at least 3 consecutive months per year for at least 2 consecutive years. CB COPD cases were defined as having both CB and at least moderate COPD based on spirometry. Our primary analysis used smokers with normal spirometry as controls; secondary analysis was performed using COPD subjects without CB as controls. Genotyping was performed on Illumina platforms; results were summarized using fixed-effect meta-analysis.\n\nRESULTS:\nFor CB COPD relative to smoking controls, we identified a new genome-wide significant locus on chromosome 11p15.5 (rs34391416, OR = 1.93, P = 4.99 × 10-8) as well as significant associations of known COPD SNPs within FAM13A. In addition, a GWAS of CB relative to those without CB within COPD subjects showed suggestive evidence for association on 1q23.3 (rs114931935, OR = 1.88, P = 4.99 × 10-7).\n\nCONCLUSIONS:\nWe found genome-wide significant associations with CB COPD on 4q22.1 (FAM13A) and 11p15.5 (EFCAB4A, CHID1 and AP2A2), and a locus associated with CB within COPD subjects on 1q23.3 (RPL31P11 and ATF6). This study provides further evidence that genetic variants may contribute to phenotypic heterogeneity of COPD.\n\nTRIAL REGISTRATION:\nClinicalTrials.gov NCT00608764, NCT00292552." + }, + "questions": [ + { + "id": "f75fb41b-a726-4f1f-9e45-f358902fe28c", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 1132, + "text": "locus on chromosome 11p15.5" + }, + { + "answer_start": 1251, + "text": "SNPs within FAM13A" + }, + { + "answer_start": 1519, + "text": "4q22.1 (FAM13A)" + }, + { + "answer_start": 1539, + "text": "11p15.5 (EFCAB4A, CHID1 and AP2A2)" + }, + { + "answer_start": 1630, + "text": "1q23.3 (RPL31P11 and ATF6)" + } + ] + } + ] +} \ No newline at end of file diff --git a/4ebc3a39-6af7-4a4e-8aec-64e5930afcdb.json b/4ebc3a39-6af7-4a4e-8aec-64e5930afcdb.json new file mode 100644 index 0000000000000000000000000000000000000000..16d04f72dbc7a19a85f89c06d264a79220958309 --- /dev/null +++ b/4ebc3a39-6af7-4a4e-8aec-64e5930afcdb.json @@ -0,0 +1,58 @@ +{ + "id": "4ebc3a39-6af7-4a4e-8aec-64e5930afcdb", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "6897634", + "text": "A case-control study was performed on 165 male bladder cancer patients and an equal number of male control persons matched in age and geographic area. Thirty determinants of assumed importance were examined. A multivariate logistic analysis was performed. A significant increment in the relative risk (RR) for bladder cancer was associated with cigarette smoking (RR = 1.89), a history of prostatic surgery (RR = 2.38), nocturia (RR = 2.05), previous venereal disease (RR = 2.42), industrial work (RR = 1.82), work with oil or gasoline (RR = 2.71) and work with various unspecified chemical materials (RR = 1.58)." + }, + "questions": [ + { + "id": "6416baff-47fe-487c-8246-be6cc8f518f4", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 345, + "text": "cigarette smoking" + }, + { + "answer_start": 378, + "text": "history of prostatic surgery" + }, + { + "answer_start": 420, + "text": "nocturia" + }, + { + "answer_start": 442, + "text": "previous venereal disease" + }, + { + "answer_start": 481, + "text": "industrial work" + }, + { + "answer_start": 510, + "text": "work with oil or gasoline" + }, + { + "answer_start": 552, + "text": "work with various unspecified chemical materials" + } + ] + } + ] +} \ No newline at end of file diff --git a/4f87b252-1d68-4ddd-a4ad-3ffe3fcc1737.json b/4f87b252-1d68-4ddd-a4ad-3ffe3fcc1737.json new file mode 100644 index 0000000000000000000000000000000000000000..039ab3102649f02217e36843ad5cad4ad983940e --- /dev/null +++ b/4f87b252-1d68-4ddd-a4ad-3ffe3fcc1737.json @@ -0,0 +1,54 @@ +{ + "id": "4f87b252-1d68-4ddd-a4ad-3ffe3fcc1737", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "17101944", + "text": "BACKGROUND:\nThe association between red meat intake and breast cancer is unclear, but most studies have assessed diet in midlife or later. Although breast tumors differ clinically and biologically by hormone receptor status, few epidemiologic studies of diet have made this distinction.\n\nMETHODS:\nRed meat intake and breast cancer risk were assessed among premenopausal women aged 26 to 46 years in the Nurses' Health Study II. Red meat intake was assessed with a food frequency questionnaire administered in 1991, 1995, and 1999, with respondents followed up through 2003. Breast cancers were self-reported and confirmed by review of pathologic reports.\n\nRESULTS:\nDuring 12 years of follow-up of 90,659 premenopausal women, we documented 1021 cases of invasive breast carcinoma. Greater red meat intake was strongly related to elevated risk of breast cancers that were estrogen and progesterone receptor positive (ER+/PR+; n = 512) but not to those that were estrogen and progesterone receptor negative (ER-/PR-; n = 167). Compared with those eating 3 or fewer servings per week of red meat, the multivariate relative risks (95% confidence intervals) for ER+/PR+ breast cancer with increasing servings of red meat intake were 1.14 (0.90-1.45) for more than 3 to 5 or fewer servings per week, 1.42 (1.06-1.90) for more than 5 per week to 1 or fewer servings per day, 1.20 (0.89-1.63) for more than 1 to 1.5 or fewer servings per day, and 1.97 (1.35-2.88) for more than 1.5 servings per day (test for trend, P = .001). The corresponding relative risks for ER-/PR- breast cancer were 1.34 (0.89-2.00), 1.21 (0.73-2.00), 0.69 (0.39-1.23), and 0.89 (0.43-1.84) (test for trend, P = .28). Higher intakes of several individual red meat items were also strongly related to elevated risk of ER+/PR+ breast cancer.\n\nCONCLUSION:\nHigher red meat intake may be a risk factor for ER+/PR+ breast cancer among premenopausal women." + }, + "questions": [ + { + "id": "62f35f33-6c15-450f-822a-b75b211ab601", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1819, + "text": "Higher red meat intake" + }, + { + "answer_start": 1183, + "text": "increasing servings of red meat intake" + }, + { + "answer_start": 1248, + "text": "more than 3 to 5 or fewer servings per week" + }, + { + "answer_start": 1388, + "text": "more than 1 to 1.5 or fewer servings per day" + }, + { + "answer_start": 1459, + "text": "more than 1.5 servings per day" + }, + { + "answer_start": 1684, + "text": "Higher intakes of several individual red meat items" + } + ] + } + ] +} \ No newline at end of file diff --git a/4f9acef6-1853-4f84-a449-deede3fd13f6.json b/4f9acef6-1853-4f84-a449-deede3fd13f6.json new file mode 100644 index 0000000000000000000000000000000000000000..10655aa59c597d4bf14c61d2465fd43d0f8298fd --- /dev/null +++ b/4f9acef6-1853-4f84-a449-deede3fd13f6.json @@ -0,0 +1,35 @@ +{ + "id": "4f9acef6-1853-4f84-a449-deede3fd13f6", + "disease": { + "id": "H00056", + "names": [ + "Alzheimer disease", + "Dementia due to Alzheimer disease" + ], + "dbLinks": { + "icd10": [ + "G30" + ], + "mesh": [ + "D000544" + ] + }, + "category": "Neurodegenerative disease" + }, + "article": { + "id": "12552037", + "text": "BACKGROUND:\nThree causative genes have been identified for autosomal dominant AD.\n\nOBJECTIVE:\nTo determine the proportion of patients with early onset AD with a positive family history accounted for by mutations in these genes.\n\nMETHODS:\nA mutational analysis of the amyloid precursor protein (APP), presenilin 1 (PSEN1), and presenilin 2 (PSEN2) genes was performed in 31 probands with probable or definite AD from UK families with an age at onset (AAO) \u003c61 years.\n\nRESULTS:\nThe mean AAO was 46.9 years (median 45 years; range 33 to 60 years). The majority of patients (23 of 31; 74%) fulfilled recognized criteria for autosomal dominant inheritance. In 17 (55%) probands the authors identified eight novel PSEN1 sequence variants and eight recognized pathogenic mutations. In 4 (13%) probands the authors identified one novel APP sequence variant (H677R) and two recognized mutations. Thus in this series 21 of 31 (68%) probands were associated with a sequence variant in APP or PSEN1. Nine of the 11 (82%) probands with neuropathologically confirmed AD who additionally fulfilled recognized criteria for autosomal dominant inheritance were associated with a sequence variant in APP or PSEN1. The 10 patients in whom the authors were unable to identify a mutation in APP, PSEN1, or PSEN2 were older than the probands with sequence variants (55.4 vs 44.7 years: p = 0.001).\n\nCONCLUSIONS:\nSequence variants in APP and PSEN1 accounted for the majority of neuropathologically confirmed autosomal dominant early onset AD; no mutations in PSEN2 were detected. There may be a further genetic factor involved in the etiology of autosomal dominant early onset AD." + }, + "questions": [ + { + "id": "05a37c54-e00f-4909-a479-b41c47896f4e", + "text": "What are the risk factors of Alzheimer disease?", + "answers": [ + { + "answer_start": 1389, + "text": "Sequence variants in APP and PSEN1" + } + ] + } + ] +} \ No newline at end of file diff --git a/501c49a2-c4ed-40bf-b070-d61fef5e5b55.json b/501c49a2-c4ed-40bf-b070-d61fef5e5b55.json new file mode 100644 index 0000000000000000000000000000000000000000..d366748c76fe6245122cfb3e3e4aa8e8442217e3 --- /dev/null +++ b/501c49a2-c4ed-40bf-b070-d61fef5e5b55.json @@ -0,0 +1,43 @@ +{ + "id": "501c49a2-c4ed-40bf-b070-d61fef5e5b55", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "20212233", + "text": "OBJECTIVE:\nTo evaluate the possible association of Parkinson disease (PD) and melanoma in North America.\n\nDESIGN, SETTING, AND PATIENTS:\nThirty-one centers enrolled patients with idiopathic PD. At visit 1, a neurologist obtained a medical history. At visit 2, a dermatologist recorded melanoma risk factors, performed a whole-body examination, and performed a biopsy of lesions suggestive of melanoma for evaluation by a central dermatopathology laboratory. We compared overall prevalence of melanoma with prevalence calculated from the US Surveillance Epidemiology and End Results (SEER) cancer database and the American Academy of Dermatology skin cancer screening programs.\n\nRESULTS:\nA total of 2106 patients (mean [SD] age, 68.6 [10.6] years; duration of PD, 7.1 [5.7] years) completed the study. Most (84.8%) had received levodopa. Dermatology examinations revealed 346 pigmented lesions; dermatopathological findings confirmed 20 in situ melanomas (0.9%) and 4 invasive melanomas (0.2%). In addition, histories revealed 68 prior melanomas (3.2%). Prevalence (5-year limited duration) of invasive malignant melanoma in the US cohort of patients with PD (n = 1692) was 2.24-fold higher (95% confidence interval, 1.21-4.17) than expected in age- and sex-matched populations in the US SEER database. Age- or sex-adjusted relative risk of any melanoma for US patients was more than 7 times that expected from confirmed cases in American Academy of Dermatology skin cancer screening programs.\n\nCONCLUSIONS:\nMelanoma prevalence appears to be higher in patients with PD than in the general population. Despite difficulties in comparing other databases with this study population, the study supports increased melanoma screening in patients with PD." + }, + "questions": [ + { + "id": "6a4056f0-8913-4f9f-a814-b173956b0ea4", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 1141, + "text": "patients with PD" + }, + { + "answer_start": 51, + "text": "Parkinson disease (PD)" + }, + { + "answer_start": 1551, + "text": "patients with PD" + } + ] + } + ] +} \ No newline at end of file diff --git a/503e9106-a28c-418f-b446-4fcb86458d1f.json b/503e9106-a28c-418f-b446-4fcb86458d1f.json new file mode 100644 index 0000000000000000000000000000000000000000..57452273e8c8aca3693772336b656412e0112b4a --- /dev/null +++ b/503e9106-a28c-418f-b446-4fcb86458d1f.json @@ -0,0 +1,34 @@ +{ + "id": "503e9106-a28c-418f-b446-4fcb86458d1f", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "14573731", + "text": "BACKGROUND:\nInflammation is linked to adverse outcomes in acute coronary syndromes. Myeloperoxidase, an abundant leukocyte enzyme, is elevated in culprit lesions that have fissured or ruptured in patients with sudden death from cardiac causes. Numerous lines of evidence suggest mechanistic links between myeloperoxidase and both inflammation and cardiovascular disease.\n\nMETHODS:\nWe assessed the value of plasma levels of myeloperoxidase as a predictor of the risk of cardiovascular events in 604 sequential patients presenting to the emergency department with chest pain.\n\nRESULTS:\nInitial plasma myeloperoxidase levels predicted the risk of myocardial infarction, even in patients who are negative for troponin T (\u003c0.1 ng per milliliter) at base line (P\u003c0.001). Myeloperoxidase levels at presentation also predicted the risk of major adverse cardiac events (myocardial infarction, the need for revascularization, or death) within 30 days and 6 months after presentation (P\u003c0.001). In patients without evidence of myocardial necrosis (defined as those who were negative for troponin T), the base-line myeloperoxidase levels independently predicted the risk of major adverse coronary events at 30 days (unadjusted 2nd, 3rd, and 4th quartile odds ratios, 2.2 [95 percent confidence interval, 1.1 to 4.6], 4.2 [95 percent confidence interval, 2.1 to 8.4], and 4.1 [95 percent confidence interval, 2.0 to 8.4], respectively) and at 6 months.\n\nCONCLUSIONS:\nA single initial measurement of plasma myeloperoxidase independently predicts the early risk of myocardial infarction, as well as the risk of major adverse cardiac events in the ensuing 30-day and 6-month periods. Myeloperoxidase levels, in contrast to troponin T, creatine kinase MB isoform, and C-reactive protein levels, identified patients at risk for cardiac events in the absence of myocardial necrosis, highlighting its potential usefulness for risk stratification among patients who present with chest pain." + }, + "questions": [ + { + "id": "92907516-2e6f-4e7a-b180-67805fff07aa", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1454, + "text": "A single initial measurement of plasma myeloperoxidase" + } + ] + } + ] +} \ No newline at end of file diff --git a/508b9617-c64f-4949-afb3-4c452b2eacde.json b/508b9617-c64f-4949-afb3-4c452b2eacde.json new file mode 100644 index 0000000000000000000000000000000000000000..04d2891e9b3befa02aafab309ebb3c9a30a98956 --- /dev/null +++ b/508b9617-c64f-4949-afb3-4c452b2eacde.json @@ -0,0 +1,42 @@ +{ + "id": "508b9617-c64f-4949-afb3-4c452b2eacde", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "16801631", + "text": "PURPOSE:\nWomen who carry germline mutations in the BRCA1 and BRCA2 genes are at greatly increased risk of breast cancer (BC). Numerous studies have shown that moderate to high doses of ionizing radiation are a risk factor for BC. Because of the role of the BRCA proteins in DNA repair, we hypothesized that BRCA carriers might be more sensitive to ionizing radiation than women in the general population.\n\nPATIENTS AND METHODS:\nA retrospective cohort study of 1,601 female BRCA1/2 carriers was performed. Risk of breast cancer from exposure to chest x-rays, as assessed by questionnaire data, was analyzed using a weighted Cox proportional hazards model.\n\nRESULTS:\nIn this cohort, any reported exposure to chest x-rays was associated with an increased risk of BC (hazard ratio [HR] = 1.54; P = .007). This risk was increased in carrier women aged 40 years and younger (HR = 1.97; P \u003c .001) and in women born after 1949 (HR = 2.56; P \u003c .001), particularly those exposed only before the age of 20 years (HR = 4.64; P \u003c .001).\n\nCONCLUSION:\nIn our series of BRCA carriers, we detected a relatively large effect on BC risk with a level of radiation exposure that is at least an order of magnitude lower than in previously studied medical radiation-exposed cohorts. Although part of this increase may be attributable to recall bias, the observed patterns of risk in terms of age at exposure and attained age are consistent with those found in previous studies. If confirmed, the results have important implications for the use of x-ray imaging in young BRCA1/2 carriers." + }, + "questions": [ + { + "id": "0f64033a-84c8-4aac-8c46-db0f79c25811", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 681, + "text": "any reported exposure to chest x-rays" + }, + { + "answer_start": 828, + "text": "carrier women aged 40 years and younger" + }, + { + "answer_start": 897, + "text": "women born after 1949" + } + ] + } + ] +} \ No newline at end of file diff --git a/50b807bf-5cf4-4bd8-9d3e-7af036acfc73.json b/50b807bf-5cf4-4bd8-9d3e-7af036acfc73.json new file mode 100644 index 0000000000000000000000000000000000000000..8881fcdc4fa0a38039ed8ce1bc661fc6d7f53c69 --- /dev/null +++ b/50b807bf-5cf4-4bd8-9d3e-7af036acfc73.json @@ -0,0 +1,54 @@ +{ + "id": "50b807bf-5cf4-4bd8-9d3e-7af036acfc73", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "29617589", + "text": "BACKGROUND:\nChildhood overweight is associated with an increased risk of type 2 diabetes in adulthood. We investigated whether remission of overweight before early adulthood reduces this risk.\n\nMETHODS:\nWe conducted a study involving 62,565 Danish men whose weights and heights had been measured at 7 and 13 years of age and in early adulthood (17 to 26 years of age). Overweight was defined in accordance with Centers for Disease Control and Prevention criteria. Data on type 2 diabetes status (at age ≥30 years, 6710 persons) were obtained from a national health registry.\n\nRESULTS:\nOverweight at 7 years of age (3373 of 62,565 men; 5.4%), 13 years of age (3418 of 62,565; 5.5%), or early adulthood (5108 of 62,565; 8.2%) was positively associated with the risk of type 2 diabetes; associations were stronger at older ages at overweight and at younger ages at diagnosis of type 2 diabetes. Men who had had remission of overweight before the age of 13 years had a risk of having type 2 diabetes diagnosed at 30 to 60 years of age that was similar to that among men who had never been overweight (hazard ratio, 0.96; 95% confidence interval [CI], 0.75 to 1.21). As compared with men who had never been overweight, men who had been overweight at 7 and 13 years of age but not during early adulthood had a higher risk of type 2 diabetes (hazard ratio, 1.47; 95% CI, 1.10 to 1.98), but their risk was lower than that among men with persistent overweight (hazard ratio [persistently overweight vs. never overweight], 4.14; 95% CI, 3.57 to 4.79). An increase in body-mass index between 7 years of age and early adulthood was associated with an increased risk of type 2 diabetes, even among men whose weight had been normal at 7 years of age.\n\nCONCLUSIONS:\nChildhood overweight at 7 years of age was associated with increased risks of adult type 2 diabetes only if it continued until puberty or later ages. (Funded by the European Union.)." + }, + "questions": [ + { + "id": "d8162280-3d00-4faf-8493-f6ca3e0b6052", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 585, + "text": "Overweight at 7 years of age" + }, + { + "answer_start": 642, + "text": "13 years of age" + }, + { + "answer_start": 685, + "text": "early adulthood" + }, + { + "answer_start": 814, + "text": "older ages at overweight and at younger age" + }, + { + "answer_start": 1214, + "text": "men who had been overweight at 7 and 13 years of age but not during early adulthood" + }, + { + "answer_start": 1751, + "text": "Childhood overweight at 7 years of age" + } + ] + } + ] +} \ No newline at end of file diff --git a/511a39dc-81c2-4ff4-8441-8c1f8e4db701.json b/511a39dc-81c2-4ff4-8441-8c1f8e4db701.json new file mode 100644 index 0000000000000000000000000000000000000000..99df676d3c1e0c7c7246ebf875f94bbfdd5e5957 --- /dev/null +++ b/511a39dc-81c2-4ff4-8441-8c1f8e4db701.json @@ -0,0 +1,34 @@ +{ + "id": "511a39dc-81c2-4ff4-8441-8c1f8e4db701", + "disease": { + "id": "H00408", + "names": [ + "Type 1 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E10" + ], + "mesh": [ + "D003922" + ] + }, + "category": "Metabolic disease; Immune system disease; Endocrine disease" + }, + "article": { + "id": "8063039", + "text": "Associations of infant feeding patterns and milk consumption with cow's milk protein antibody titres were studied in 697 newly-diagnosed diabetic children, 415 sibling-control children and 86 birth-date- and sex-matched population-based control children in the nationwide \"Childhood Diabetes in Finland\" study. IgA and IgG antibody titres to the proteins of cow's milk formula, BLG and BSA, and IgM antibody titres to cow's milk formula proteins were measured by ELISA. Several inverse correlations were observed between the duration of breast-feeding or age at introduction of dairy products and antibody titres, and positive correlations were observed between milk consumption and antibody titres in all three populations studied. Multivariate analyses which included the infant feeding variables, milk consumption and current age simultaneously showed that the earlier the introduction of dairy products and the greater the consumption of milk was, the higher several antibody titres were. High IgA antibody titres to cow's milk formula were associated with a greater risk of IDDM both among diabetic-population-control and diabetic-sibling-control pairs when adjusted for other cow's milk antibody titres, dietary variables and in diabetic-sibling-control pairs also for ICA. The results suggest that young age at introduction of dairy products and high milk consumption during childhood increase the levels of cow's milk antibodies and that high IgA antibodies to cow's milk formula are independently associated with increased risk of IDDM." + }, + "questions": [ + { + "id": "35032852-9ae2-48a9-996a-cb8d27dfe52d", + "text": "What are the risk factors of Type 1 diabetes mellitus?", + "answers": [ + { + "answer_start": 1446, + "text": "high IgA antibodies to cow's milk formula " + } + ] + } + ] +} \ No newline at end of file diff --git a/51a4dc90-3eb5-465e-b08d-e650486a2b76.json b/51a4dc90-3eb5-465e-b08d-e650486a2b76.json new file mode 100644 index 0000000000000000000000000000000000000000..a145dbc0470888e3d4c38fd945090dd6a7957c0a --- /dev/null +++ b/51a4dc90-3eb5-465e-b08d-e650486a2b76.json @@ -0,0 +1,55 @@ +{ + "id": "51a4dc90-3eb5-465e-b08d-e650486a2b76", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "8810605", + "text": "To identify modifiable risk factors for wheezing illness in childhood, the associations between current asthma or wheezing and factors such as household smoking, damp and dietary salt preference were measured in a questionnaire-based prevalence study of schoolchildren 7 to 9 yr of age in Cape Town. In a random sample of 15 schools, questionnaires were completed by parents of 1,955 children, from which 368 cases and 294 controls were selected on the basis of reported asthma diagnosis or symptoms. Urinary cotinine concentrations were measured, and the parents were interviewed. An exposure-response relationship between the urinary cotinine creatinine ratio and asthma/wheeze was observed. In multivariate analysis, predictors of asthma/wheeze were hay fever (odds ratio [OR] - 5.30; 95% confidence interval [CI] = 3.16 to 8.89), eczema (OR = 2.19; 95% CI = 1.33-3.62), parental asthma (OR = 1.77; 95% CI = 1.11 to 2.84), absence of paternal contribution to income (OR = 1.72; 95% CI = 1.17 to 2.54), maternal smoking in pregnancy (OR = 1.87; 95% CI = 1.25 to 2.81), and each additional household smoker (OR = 1.15; 95% CI = 1.01 to 1.30). Findings were similar, with higher odds ratios for most variables, except number of household smokers, when the group was restricted to children with parent-reported asthma. The findings confirm that household smoking is an important modifiable risk factor in asthma/wheeze among young schoolchildren, and they suggest that maternal smoking in pregnancy and current household exposure are independent contributors to this effect." + }, + "questions": [ + { + "id": "38c5991f-8638-4565-9d67-96635105f6bf", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 753, + "text": "hay fever" + }, + { + "answer_start": 874, + "text": "parental asthma" + }, + { + "answer_start": 834, + "text": "eczema" + }, + { + "answer_start": 926, + "text": "absence of paternal contribution to income" + }, + { + "answer_start": 1005, + "text": "maternal smoking in pregnancy" + }, + { + "answer_start": 1075, + "text": "each additional household smoker" + } + ] + } + ] +} \ No newline at end of file diff --git a/520988c7-599d-4f59-940d-38594b6798c0.json b/520988c7-599d-4f59-940d-38594b6798c0.json new file mode 100644 index 0000000000000000000000000000000000000000..45bcab72c44aaace1fc96699ffa27a0e87d39056 --- /dev/null +++ b/520988c7-599d-4f59-940d-38594b6798c0.json @@ -0,0 +1,34 @@ +{ + "id": "520988c7-599d-4f59-940d-38594b6798c0", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "21470009", + "text": "BACKGROUND:\nThe association of body-mass index (BMI) from adolescence to adulthood with obesity-related diseases in young adults has not been completely delineated.\n\nMETHODS:\nWe conducted a prospective study in which we followed 37,674 apparently healthy young men for incident angiography-proven coronary heart disease and diabetes through the Staff Periodic Examination Center of the Israeli Army Medical Corps. The height and weight of participants were measured at regular intervals, with the first measurements taken when they were 17 years of age.\n\nRESULTS:\nDuring approximately 650,000 person-years of follow-up (mean follow-up, 17.4 years), we documented 1173 incident cases of type 2 diabetes and 327 of coronary heart disease. In multivariate models adjusted for age, family history, blood pressure, lifestyle factors, and biomarkers in blood, elevated adolescent BMI (the weight in kilograms divided by the square of the height in meters; mean range for the first through last deciles, 17.3 to 27.6) was a significant predictor of both diabetes (hazard ratio for the highest vs. the lowest decile, 2.76; 95% confidence interval [CI], 2.11 to 3.58) and angiography-proven coronary heart disease (hazard ratio, 5.43; 95% CI, 2.77 to 10.62). Further adjustment for BMI at adulthood completely ablated the association of adolescent BMI with diabetes (hazard ratio, 1.01; 95% CI, 0.75 to 1.37) but not the association with coronary heart disease (hazard ratio, 6.85; 95% CI, 3.30 to 14.21). After adjustment of the BMI values as continuous variables in multivariate models, only elevated BMI in adulthood was significantly associated with diabetes (β=1.115, P=0.003; P=0.89 for interaction). In contrast, elevated BMI in both adolescence (β=1.355, P=0.004) and adulthood (β=1.207, P=0.03) were independently associated with angiography-proven coronary heart disease (P=0.048 for interaction).\n\nCONCLUSIONS:\nAn elevated BMI in adolescence--one that is well within the range currently considered to be normal--constitutes a substantial risk factor for obesity-related disorders in midlife. Although the risk of diabetes is mainly associated with increased BMI close to the time of diagnosis, the risk of coronary heart disease is associated with an elevated BMI both in adolescence and in adulthood, supporting the hypothesis that the processes causing incident coronary heart disease, particularly atherosclerosis, are more gradual than those resulting in incident diabetes. (Funded by the Chaim Sheba Medical Center and the Israel Defense Forces Medical Corps.)." + }, + "questions": [ + { + "id": "007f52f6-5a36-444b-8f34-687689bf429e", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 2253, + "text": "elevated BMI both in adolescence and in adulthood" + } + ] + } + ] +} \ No newline at end of file diff --git a/52ca7397-4803-433c-af0a-92dac9cc1c22.json b/52ca7397-4803-433c-af0a-92dac9cc1c22.json new file mode 100644 index 0000000000000000000000000000000000000000..ce51768d13b6290c50cde27c1f48354d33e3ed70 --- /dev/null +++ b/52ca7397-4803-433c-af0a-92dac9cc1c22.json @@ -0,0 +1,35 @@ +{ + "id": "52ca7397-4803-433c-af0a-92dac9cc1c22", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "26416719", + "text": "INTRODUCTION:\nInfection with Epstein-Barr virus (EBV) has been suggested to contribute to the pathogenesis of autoimmune diseases, including rheumatoid arthritis (RA). We sought to determine whether prior infection with the virus occurs more frequently in patients with RA compared to controls.\n\nMETHODS:\nWe performed a systematic review and meta-analyses of studies that reported the prevalence of anti-EBV antibodies in the sera of cases with RA and controls by searching Medline and Embase databases from 1946 to 2014, with no language restriction. Mantel-Haenszel odds ratios for the detection of anti-EBV antibodies were calculated, and meta-analyses conducted. Quality assessments were performed using a modified version of the Newcastle-Ottawa scale.\n\nRESULTS:\nTwenty-three studies were included. Quality assessment found most studies reported acceptable selection criteria but poor descriptions of how cases and controls were recruited. When all studies were included, there was a statistically significant higher seroprevalence of anti-VCA IgG in patients with RA compared to controls with an odds ratio (OR) of 1.61 (95 % confidence interval (CI) 1.05-2.46, p = 0.03), which is a similar-sized summary OR to that reported for systemic lupus erythematosus (SLE). However, when studies were restricted to those reporting more plausible levels of exposure to EBV in the control groups, no significant association was apparent, OR 1.47 (95 % CI 0.88-2.46, p = 0.14). Using anti-EBNA 1 or anti-EA IgG as markers of previous infection also did not yield significant associations (OR 1.05, 95 % CI 0.68-1.61, p = 0.82; OR 2.2, 95 % CI 0.86-5.65, p = 0.10 respectively).\n\nCONCLUSIONS:\nOverall, these findings do not demonstrate an association between EBV seroprevalence and RA and therefore do not support the hypothesis that prior infection with EBV predisposes to the development of RA. This contrasts with meta-analyses that indicate EBV infection is associated with multiple sclerosis and SLE." + }, + "questions": [ + { + "id": "728de9b5-59ee-45a4-9d86-b44e3919899a", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 1022, + "text": "seroprevalence of anti-VCA IgG" + } + ] + } + ] +} \ No newline at end of file diff --git a/5312c3bb-4cfa-4239-a568-da28cff33ec9.json b/5312c3bb-4cfa-4239-a568-da28cff33ec9.json new file mode 100644 index 0000000000000000000000000000000000000000..acebc7a0122b17c4ce25608ebc5bc2153202233e --- /dev/null +++ b/5312c3bb-4cfa-4239-a568-da28cff33ec9.json @@ -0,0 +1,46 @@ +{ + "id": "5312c3bb-4cfa-4239-a568-da28cff33ec9", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "16112301", + "text": "BACKGROUND:\nMany reported associations between common genetic polymorphisms and complex diseases have not been confirmed in subsequent studies. An exception could be the association between NAT2 slow acetylation, GSTM1 null genotype, and bladder-cancer risk. However, current evidence is based on meta-analyses of relatively small studies (range 23-374 cases) with some evidence of publication bias and study heterogeneity. Associations between polymorphisms in other NAT and GST genes and bladder-cancer risk have been inconsistent.\n\nMETHODS:\nWe investigated polymorphisms in NAT2, GSTM1, NAT1, GSTT1, GSTM3, and GSTP1 in 1150 patients with transitional-cell carcinoma of the urinary bladder and 1149 controls in Spain; all the participants were white. We also carried out meta-analyses of NAT2, GSTM1, and bladder cancer that included more than twice as many cases as in previous reports.\n\nFINDINGS:\nIn our study, the odds ratios for bladder cancer for individuals with deletion of one or two copies of the GSTM1 gene were 1.2 (95% CI 0.8-1.7) and 1.9 (1.4-2.7) respectively (p for trend \u003c0.0001). Compared with NAT2 rapid or intermediate acetylators, NAT2 slow acetylators had an increased overall risk of bladder cancer (1.4 [1.2-1.7]) that was stronger for cigarette smokers than for never smokers (p for interaction 0.008). No significant associations were found with the other polymorphisms. Meta-analyses showed that the overall association for NAT2 was robust (p\u003c0.0001), and case-only meta-analyses provided support for an interaction between NAT2 and smoking (p for interaction 0.009). The overall association for GSTM1 was also robust (p\u003c0.0001) and was not modified by smoking status (p=0.86).\n\nINTERPRETATION:\nThe GSTM1 null genotype increases the overall risk of bladder cancer, and the NAT2 slow-acetylator genotype increases risk particularly among cigarette smokers. These findings provide compelling evidence for the role of common polymorphisms in the aetiology of cancer.\n\nRELEVANCE TO PRACTICE:\nAlthough the relative risks are modest, these polymorphisms could account for up to 31% of bladder cancers because of their high prevalence." + }, + "questions": [ + { + "id": "bce3ea80-9253-4184-a96b-86d15a38fa1a", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 955, + "text": "individuals with deletion of one or two copies of the GSTM1 gene" + }, + { + "answer_start": 1154, + "text": "NAT2 slow acetylators" + }, + { + "answer_start": 1724, + "text": "The GSTM1 null genotype" + }, + { + "answer_start": 1802, + "text": "NAT2 slow-acetylator genotype" + } + ] + } + ] +} \ No newline at end of file diff --git a/5323189b-84e4-453b-882f-e60eccb28e71.json b/5323189b-84e4-453b-882f-e60eccb28e71.json new file mode 100644 index 0000000000000000000000000000000000000000..13c3baf074c3845fcde518fee8a2cd287772d056 --- /dev/null +++ b/5323189b-84e4-453b-882f-e60eccb28e71.json @@ -0,0 +1,39 @@ +{ + "id": "5323189b-84e4-453b-882f-e60eccb28e71", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "23870058", + "text": "BACKGROUND:\nThe International Study on Asthma and Allergies in Childhood (ISAAC) reported a prevalence of asthma symptoms in 17 centers in nine Latin American countries that was similar to prevalence rates reported in non-tropical countries. It has been proposed that the continuous exposure to infectious diseases in rural populations residing in tropical areas leads to a relatively low prevalence of asthma symptoms. As almost a quarter of Latin American people live in rural tropical areas, the encountered high prevalence of asthma symptoms is remarkable. Wood smoke exposure and environmental tobacco smoke have been identified as possible risk factors for having asthma symptoms.\n\nMETHODS:\nWe performed a cross-sectional observational study from June 1, 2012 to September 30, 2012 in which we interviewed parents and guardians of Warao Amerindian children from Venezuela. Asthma symptoms were defined according to the ISAAC definition as self-reported wheezing in the last 12 months. The associations between wood smoke exposure and environmental tobacco smoke and the prevalence of asthma symptoms were calculated by means of univariate and multivariable logistic regression analyses.\n\nRESULTS:\nWe included 630 children between two and ten years of age. Asthma symptoms were recorded in 164 of these children (26%). The prevalence of asthma symptoms was associated with the cooking method. Children exposed to the smoke produced by cooking on open wood fires were at higher risk of having asthma symptoms compared to children exposed to cooking with gas (AOR 2.12, 95% CI 1.18 - 3.84). Four percent of the children lived in a household where more than ten cigarettes were smoked per day and they had a higher risk of having asthma symptoms compared to children who were not exposed to cigarette smoke (AOR 2.69, 95% CI 1.11 - 6.48).\n\nCONCLUSION:\nOur findings suggest that children living in rural settings in a household where wood is used for cooking or where more than ten cigarettes are smoked daily have a higher risk of having asthma symptoms." + }, + "questions": [ + { + "id": "f6847e89-aacb-4045-bb69-46133280a73a", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1398, + "text": "Children exposed to the smoke produced by cooking on open wood fires" + }, + { + "answer_start": 1880, + "text": "children living in rural settings in a household where wood is used for cooking or where more than ten cigarettes are smoked daily" + } + ] + } + ] +} \ No newline at end of file diff --git a/53b8d3c2-35ee-41b3-a899-f1e0ef0e787e.json b/53b8d3c2-35ee-41b3-a899-f1e0ef0e787e.json new file mode 100644 index 0000000000000000000000000000000000000000..df7c6e9db61b08054c53de2d305800be63a0843c --- /dev/null +++ b/53b8d3c2-35ee-41b3-a899-f1e0ef0e787e.json @@ -0,0 +1,34 @@ +{ + "id": "53b8d3c2-35ee-41b3-a899-f1e0ef0e787e", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "12466343", + "text": "A multicenter study of Turner syndrome (TS) patients was carried out to estimate the prevalence of celiac disease (CD) and to detect clinical characteristics and laboratory data of affected patients. Three hundred eighty-nine girls with TS were screened by IgA antigliadin antibodies and/or antiendomysial antibodies. Intestinal biopsy was offered to positive cases. CD was diagnosed in 25 patients. In celiac subjects, anemia, anorexia, and delayed growth (with respect to Italian TS curves) were frequently present; whereas distended abdomen, chronic diarrhea, constipation, and vomiting occurred more rarely. In addition, low serum iron levels, hemoglobinemia, and high values of aminotransferases were observed. Ten patients showed classic CD, 8 showed atypical symptoms, and 7 showed a silent CD. In 11 symptomatic patients, the diagnosis of CD was made at the onset of symptoms, whereas 7 of them showed a median delay of 79 months in diagnosis. Other autoimmune disorders were observed in 40% of the patients. Our study confirms the high prevalence (6.4%) of CD in a large series of TS patients. Moreover, the subclinical picture in 60% of the cases, the diagnostic delay, and the incidence of other autoimmune disorders suggest that routine screening of CD in TS is indicated." + }, + "questions": [ + { + "id": "1ee44846-1e73-4622-a9ce-746cce8776e2", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 23, + "text": "Turner syndrome (TS) patients" + } + ] + } + ] +} \ No newline at end of file diff --git a/5456a4b0-dcce-4fe2-a1ab-9fcba7dcf8d0.json b/5456a4b0-dcce-4fe2-a1ab-9fcba7dcf8d0.json new file mode 100644 index 0000000000000000000000000000000000000000..03f7565c11cc30ffd067f400888541c4d3544ce1 --- /dev/null +++ b/5456a4b0-dcce-4fe2-a1ab-9fcba7dcf8d0.json @@ -0,0 +1,35 @@ +{ + "id": "5456a4b0-dcce-4fe2-a1ab-9fcba7dcf8d0", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "15867846", + "text": "Both asthma and obesity are large and growing public health issues. Mounting evidence now implicates obesity as a major risk factor for asthma, thus linking these 2 major epidemics. Moreover, both in human subjects and in mice, obesity appears to predispose toward airway hyperresponsiveness. This review describes potential mechanisms whereby obesity might modify airway smooth muscle function to explain these observations. These mechanisms include both static and dynamic mechanical factors attributable to decreases in functional residual capacity and decreases in tidal volume that are observed in the obese. They include also obesity-related changes in lung development, chronic systemic inflammation (including increased serum levels of inflammatory cytokines and chemokines), and adipocyte-derived factors, including leptin, adiponectin, and plasminogen activator inhibitor." + }, + "questions": [ + { + "id": "fca9874d-ffc5-48ce-86bc-13a9fdc27e7d", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 101, + "text": "obesity" + } + ] + } + ] +} \ No newline at end of file diff --git a/54b39368-30ab-428f-894e-44affd375919.json b/54b39368-30ab-428f-894e-44affd375919.json new file mode 100644 index 0000000000000000000000000000000000000000..95d95708101e248f1a6efca4ff0031cd7c7b5e10 --- /dev/null +++ b/54b39368-30ab-428f-894e-44affd375919.json @@ -0,0 +1,37 @@ +{ + "id": "54b39368-30ab-428f-894e-44affd375919", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "29025130", + "text": "BACKGROUND:\nPhysical activity is associated with reduced risk of colorectal cancer, but most epidemiological studies have focused on occupational and recreational physical activity. The evidence for other domains of activity, and for sedentary behaviour, is limited.\n\nMETHODS:\nMedline, Embase and Web of Science were searched from inception to December 2015 for studies examining domain-specific physical activity or sedentary behaviour and the risk of colon and/or rectal cancer. We extracted maximally adjusted relative risks (RRs) except when RRs not adjusted for body mass index, were also presented. We used random-effects meta-analysis to compute pooled RRs comparing the highest versus the lowest level of exposure. We used meta-regression to assess sources of heterogeneity in estimates.\n\nRESULTS:\nWe identified 17 cohort and 21 case-control studies, of which 17 had occupational data, 23 had recreational data, three each had data on transport and household physical activity domains, and 6 studies had data on occupational sedentary behaviour. The pooled relative risks (RRs) for colon cancer were 0.74 (95% confidence interval (CI): 0.67, 0.82) for occupational activity, 0.80 (95% CI: 0.71, 0.89) for recreational activity, 0.66 (95% CI: 0.45, 0.98) for transport-related physical activity, 0.85 (95% CI: 0.71, 1.02) for household physical activity, and 1.44 (95% CI: 1.28, 1.62) for occupational sedentary behaviour. For rectal cancer, the pooled RRs were 0.88 (95% CI: 0.79, 0.98) for occupational activity, 0.87 (95% CI: 0.75, 1.01) for recreational activity, 0.88 (95% CI: 0.70, 1.12) for transport-related physical activity, 1.01 (95% CI: 0.80, 1.27) for household physical activity, and 1.02 (95% CI: 0.82, 1.28) for occupational sedentary behaviour.\n\nCONCLUSIONS:\nIn addition to increasing occupational and recreational physical activity, promoting physical activity during transport and reducing sedentary behaviour in the workplace may also be useful colorectal cancer prevention strategies." + }, + "questions": [ + { + "id": "b94efede-b628-4e8c-81cc-dcaf6dee772b", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1396, + "text": "occupational sedentary behaviour" + } + ] + } + ] +} \ No newline at end of file diff --git a/54c969f9-9813-4de0-96a7-b464bf826d7d.json b/54c969f9-9813-4de0-96a7-b464bf826d7d.json new file mode 100644 index 0000000000000000000000000000000000000000..a2d3369ef2cc04a7aca934f29f49819d3e7969e1 --- /dev/null +++ b/54c969f9-9813-4de0-96a7-b464bf826d7d.json @@ -0,0 +1,46 @@ +{ + "id": "54c969f9-9813-4de0-96a7-b464bf826d7d", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "26199070", + "text": "OBJECTIVES:\nTo examine the prospective associations between consumption of sugar sweetened beverages, artificially sweetened beverages, and fruit juice with type 2 diabetes before and after adjustment for adiposity, and to estimate the population attributable fraction for type 2 diabetes from consumption of sugar sweetened beverages in the United States and United Kingdom.\n\nDESIGN:\nSystematic review and meta-analysis.\n\nDATA SOURCES AND ELIGIBILITY:\nPubMed, Embase, Ovid, and Web of Knowledge for prospective studies of adults without diabetes, published until February 2014. The population attributable fraction was estimated in national surveys in the USA, 2009-10 (n = 4729 representing 189.1 million adults without diabetes) and the UK, 2008-12 (n = 1932 representing 44.7 million).\n\nSYNTHESIS METHODS:\nRandom effects meta-analysis and survey analysis for population attributable fraction associated with consumption of sugar sweetened beverages.\n\nRESULTS:\nPrespecified information was extracted from 17 cohorts (38,253 cases/10,126,754 person years). Higher consumption of sugar sweetened beverages was associated with a greater incidence of type 2 diabetes, by 18% per one serving/day (95% confidence interval 9% to 28%, I(2) for heterogeneity = 89%) and 13% (6% to 21%, I(2) = 79%) before and after adjustment for adiposity; for artificially sweetened beverages, 25% (18% to 33%, I(2) = 70%) and 8% (2% to 15%, I(2) = 64%); and for fruit juice, 5% (-1% to 11%, I(2) = 58%) and 7% (1% to 14%, I(2) = 51%). Potential sources of heterogeneity or bias were not evident for sugar sweetened beverages. For artificially sweetened beverages, publication bias and residual confounding were indicated. For fruit juice the finding was non-significant in studies ascertaining type 2 diabetes objectively (P for heterogeneity = 0.008). Under specified assumptions for population attributable fraction, of 20.9 million events of type 2 diabetes predicted to occur over 10 years in the USA (absolute event rate 11.0%), 1.8 million would be attributable to consumption of sugar sweetened beverages (population attributable fraction 8.7%, 95% confidence interval 3.9% to 12.9%); and of 2.6 million events in the UK (absolute event rate 5.8%), 79,000 would be attributable to consumption of sugar sweetened beverages (population attributable fraction 3.6%, 1.7% to 5.6%).\n\nCONCLUSIONS:\nHabitual consumption of sugar sweetened beverages was associated with a greater incidence of type 2 diabetes, independently of adiposity. Although artificially sweetened beverages and fruit juice also showed positive associations with incidence of type 2 diabetes, the findings were likely to involve bias. None the less, both artificially sweetened beverages and fruit juice were unlikely to be healthy alternatives to sugar sweetened beverages for the prevention of type 2 diabetes. Under assumption of causality, consumption of sugar sweetened beverages over years may be related to a substantial number of cases of new onset diabetes." + }, + "questions": [ + { + "id": "8d962a63-f849-46db-9547-9b02ae84227c", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 2378, + "text": "Habitual consumption of sugar sweetened beverages" + }, + { + "answer_start": 1059, + "text": "Higher consumption of sugar sweetened beverage" + }, + { + "answer_start": 1339, + "text": "artificially sweetened beverages" + }, + { + "answer_start": 1442, + "text": "fruit juice" + } + ] + } + ] +} \ No newline at end of file diff --git a/554e629f-f7db-44a7-ab78-5401ee70b70b.json b/554e629f-f7db-44a7-ab78-5401ee70b70b.json new file mode 100644 index 0000000000000000000000000000000000000000..b9993deea22dc4dd0aabe3cf6802218a1019ae8e --- /dev/null +++ b/554e629f-f7db-44a7-ab78-5401ee70b70b.json @@ -0,0 +1,37 @@ +{ + "id": "554e629f-f7db-44a7-ab78-5401ee70b70b", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "10720158", + "text": "Collectively, the evidence from epidemiologic, animal and human studies strongly suggests that folate status modulates the risk of developing cancers in selected tissues, the most notable of which is the colorectum. Folate depletion appears to enhance carcinogenesis whereas folate supplementation above what is presently considered to be the basal requirement appears to convey a protective effect. The means by which this modulation of cancer risk is mediated is not known with certainty, but there are several plausible mechanisms which have been described. Folate plays a major role in the formation of S-adenosylmethionine, the universal methyl donor, as well as in the formation of purine and thymidine synthesis for DNA and RNA. Therefore, most mechanistic studies performed to date have focused on alterations in DNA methylation, disruption of DNA integrity and disruption of DNA repair, all of which have been observed with folate depletion. These aberrations in DNA are believed to enhance carcinogenesis by altering the expression of critical tumor suppressor genes and proto-oncogenes. Recently, the role of a common polymorphism of the methylenetetrahydrofolate reductase gene has been highlighted as well. This review presents those mechanisms which are the most likely candidates to explain folate's effects and it proposes an integrated scheme to explain how these mechanisms might interact." + }, + "questions": [ + { + "id": "f8e984df-27b2-4df6-b204-cdff2f590c29", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 216, + "text": "Folate depletion" + } + ] + } + ] +} \ No newline at end of file diff --git a/55944abe-ed36-41a4-8b69-692fe943bd19.json b/55944abe-ed36-41a4-8b69-692fe943bd19.json new file mode 100644 index 0000000000000000000000000000000000000000..21089590fe249cd428308ffce13d5e34b295dbf5 --- /dev/null +++ b/55944abe-ed36-41a4-8b69-692fe943bd19.json @@ -0,0 +1,39 @@ +{ + "id": "55944abe-ed36-41a4-8b69-692fe943bd19", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "2314963", + "text": "According to a substantial literature, passive smoking by children is associated with an increased incidence of lower respiratory illness and diminished pulmonary function. The relationship between passive smoking and childhood asthma, however, is not clear. Data from the Child Health Supplement to the 1981 National Health Interview Survey were analyzed with information about 4331 children aged 0 to 5 years to study the relationship between maternal smoking and (1) the prevalence of childhood asthma, (1) the likelihood of taking asthma medication, (3) the age of onset of children's asthma, and (4) the number of hospitalizations among children with and without asthma. An odds ratio for asthma of 2.1 was shown by multivariate logistic regressions among children whose mothers smoke 0.5 packs of cigarettes or more per day compared with children of nonsmokers (P = .001). In similar analyses maternal smoking of 0.5 packs per day was identified as an independent risk for children's use of asthma medications (odds ratio 4.6, P = .0006) and for asthma developing in the first year of life (odds ratio 2.6, P = .0006). Maternal smoking is also associated with increased numbers of hospitalizations by its association with an increased risk of asthma as well as by contributing to hospitalizations independently of a child having asthma. Among children with asthma, however, maternal smoking is not associated with increased numbers of hospitalizations. It was concluded that maternal smoking is associated with higher rates of asthma, an increased likelihood of using asthma medications, and an earlier onset of the disease.(ABSTRACT TRUNCATED AT 250 WORDS)" + }, + "questions": [ + { + "id": "51512db3-4c39-4450-a8be-7def2544f3bc", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 899, + "text": "maternal smoking of 0.5 packs per day" + }, + { + "answer_start": 1481, + "text": "maternal smoking" + } + ] + } + ] +} \ No newline at end of file diff --git a/55de3eff-a7f8-45ae-b67b-d875ac1e9988.json b/55de3eff-a7f8-45ae-b67b-d875ac1e9988.json new file mode 100644 index 0000000000000000000000000000000000000000..820076b0bc065d42c9ea134d25bd4f10a963eb34 --- /dev/null +++ b/55de3eff-a7f8-45ae-b67b-d875ac1e9988.json @@ -0,0 +1,46 @@ +{ + "id": "55de3eff-a7f8-45ae-b67b-d875ac1e9988", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "18663160", + "text": "BACKGROUND:\nType 2 diabetes mellitus is an increasingly serious health problem among African American women. Consumption of sugar-sweetened drinks was associated with an increased risk of diabetes in 2 studies but not in a third; however, to our knowledge, no data are available on African Americans regarding this issue. Our objective was to examine the association between consumption of sugar-sweetened beverages, weight gain, and incidence of type 2 diabetes mellitus in African American women.\n\nMETHODS:\nA prospective follow-up study of 59,000 African American women has been in progress since 1995. Participants reported on food and beverage consumption in 1995 and 2001. Biennial follow-up questionnaires ascertained new diagnoses of type 2 diabetes. The present analyses included 43,960 women who gave complete dietary and weight information and were free from diabetes at baseline. We identified 2713 incident cases of type 2 diabetes mellitus during 338,884 person-years of follow-up. The main outcome measure was the incidence of type 2 diabetes mellitus.\n\nRESULTS:\nThe incidence of type 2 diabetes mellitus was higher with higher intake of both sugar-sweetened soft drinks and fruit drinks. After adjustment for confounding variables including other dietary factors, the incidence rate ratio for 2 or more soft drinks per day was 1.24 (95% confidence interval, 1.06-1.45). For fruit drinks, the comparable incidence rate ratio was 1.31 (95% confidence interval, 1.13-1.52). The association of diabetes with soft drink consumption was almost entirely mediated by body mass index, whereas the association with fruit drink consumption was independent of body mass index.\n\nCONCLUSIONS:\nRegular consumption of sugar-sweetened soft drinks and fruit drinks is associated with an increased risk of type 2 diabetes mellitus in African American women. While there has been increasing public awareness of the adverse health effects of soft drinks, little attention has been given to fruit drinks, which are often marketed as a healthier alternative to soft drinks." + }, + "questions": [ + { + "id": "87afca63-88d0-4264-b87b-28b44e31eccb", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1135, + "text": "higher intake of both sugar-sweetened soft drinks and fruit drinks" + }, + { + "answer_start": 1308, + "text": "2 or more soft drinks per day" + }, + { + "answer_start": 1389, + "text": "fruit drinks" + }, + { + "answer_start": 1694, + "text": "Regular consumption of sugar-sweetened soft drinks and fruit drinks" + } + ] + } + ] +} \ No newline at end of file diff --git a/55ed8512-707d-4d51-ad1d-7865ecd70285.json b/55ed8512-707d-4d51-ad1d-7865ecd70285.json new file mode 100644 index 0000000000000000000000000000000000000000..aedf526ea412f51b93f8cfef2ce3d5616a2a4262 --- /dev/null +++ b/55ed8512-707d-4d51-ad1d-7865ecd70285.json @@ -0,0 +1,38 @@ +{ + "id": "55ed8512-707d-4d51-ad1d-7865ecd70285", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "30760441", + "text": "OBJECTIVE:\nTo determine whether infection with human enterovirus or adenovirus, both common intestinal viruses, predicts development of coeliac disease.\n\nDESIGN:\nCase-control study nested within Norwegian birth cohort recruited between 2001 and 2007 and followed to September 2016.\n\nSETTING:\nNorwegian population.\n\nPARTICIPANTS:\nChildren carrying the HLA genotype DR4-DQ8/DR3-DQ2 conferring increased risk of coeliac disease.\n\nEXPOSURES:\nEnterovirus and adenovirus detected using real time polymerase chain reaction in monthly stool samples from age 3 to 36 months.\n\nMAIN OUTCOME MEASURE:\nCoeliac disease diagnosed according to standard criteria. Coeliac disease antibodies were tested in blood samples taken at age 3, 6, 9, and 12 months and then annually. Adjusted odds ratios from mixed effects logistic regression model were used to assess the relation between viral infections before development of coeliac disease antibodies and coeliac disease.\n\nRESULTS:\nAmong 220 children, and after a mean of 9.9 (SD 1.6) years, 25 children were diagnosed as having coeliac disease after screening and were matched to two controls each. Enterovirus was found in 370 (17%) of 2135 samples and was significantly more frequent in samples collected before development of coeliac disease antibodies in cases than in controls (adjusted odds ratio 1.49, 95% confidence interval 1.07 to 2.06; P=0.02). The association was restricted to infections after introduction of gluten. High quantity samples (\u003e100 000 copies/μL) (adjusted odds ratio 2.11, 1.24 to 3.60; P=0.01) and long lasting infections (\u003e2 months) (2.16, 1.16 to 4.04; P=0.02) gave higher risk estimates. Both the commonly detected enterovirus species and were significantly associated with coeliac disease. The association was not found for infections during or after development of coeliac disease antibodies. Adenovirus was not associated with coeliac disease.\n\nCONCLUSIONS:\nIn this longitudinal study, a higher frequency of enterovirus, but not adenovirus, during early childhood was associated with later coeliac disease. The finding adds new information on the role of viral infections in the aetiology of coeliac disease." + }, + "questions": [ + { + "id": "99fb53a5-a1ff-41ee-93f8-1e0e342dd279", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 1660, + "text": "commonly detected enterovirus" + }, + { + "answer_start": 1954, + "text": "higher frequency of enterovirus, but not adenovirus, during early childhood" + } + ] + } + ] +} \ No newline at end of file diff --git a/563df264-1a58-400c-839a-92f566bc8a66.json b/563df264-1a58-400c-839a-92f566bc8a66.json new file mode 100644 index 0000000000000000000000000000000000000000..1e15b87890d7ca3f18f0189455b617d313f9bbc2 --- /dev/null +++ b/563df264-1a58-400c-839a-92f566bc8a66.json @@ -0,0 +1,42 @@ +{ + "id": "563df264-1a58-400c-839a-92f566bc8a66", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "20505766", + "text": "BACKGROUND:\nType 2 Diabetes (T2D) and other chronic diseases are caused by a complex combination of many genetic and environmental factors. Few methods are available to comprehensively associate specific physical environmental factors with disease. We conducted a pilot Environmental-Wide Association Study (EWAS), in which epidemiological data are comprehensively and systematically interpreted in a manner analogous to a Genome Wide Association Study (GWAS).\n\nMETHODS AND FINDINGS:\nWe performed multiple cross-sectional analyses associating 266 unique environmental factors with clinical status for T2D defined by fasting blood sugar (FBG) concentration \u003e or =126 mg/dL. We utilized available Centers for Disease Control (CDC) National Health and Nutrition Examination Survey (NHANES) cohorts from years 1999 to 2006. Within cohort sample numbers ranged from 503 to 3,318. Logistic regression models were adjusted for age, sex, body mass index (BMI), ethnicity, and an estimate of socioeconomic status (SES). As in GWAS, multiple comparisons were controlled and significant findings were validated with other cohorts. We discovered significant associations for the pesticide-derivative heptachlor epoxide (adjusted OR in three combined cohorts of 1.7 for a 1 SD change in exposure amount; p\u003c0.001), and the vitamin gamma-tocopherol (adjusted OR 1.5; p\u003c0.001). Higher concentrations of polychlorinated biphenyls (PCBs) such as PCB170 (adjusted OR 2.2; p\u003c0.001) were also found. Protective factors associated with T2D included beta-carotenes (adjusted OR 0.6; p\u003c0.001).\n\nCONCLUSIONS AND SIGNIFICANCE:\nDespite difficulty in ascertaining causality, the potential for novel factors of large effect associated with T2D justify the use of EWAS to create hypotheses regarding the broad contribution of the environment to disease. Even in this study based on prior collected epidemiological measures, environmental factors can be found with effect sizes comparable to the best loci yet found by GWAS." + }, + "questions": [ + { + "id": "89c8067f-ede1-4aa7-9ef9-2faf502358ee", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1167, + "text": "pesticide-derivative heptachlor epoxide" + }, + { + "answer_start": 1309, + "text": "vitamin gamma-tocopherol" + }, + { + "answer_start": 1387, + "text": "polychlorinated biphenyls (PCBs) such as PCB170" + } + ] + } + ] +} \ No newline at end of file diff --git a/56429939-2b70-4c56-86ce-d3343f99d15f.json b/56429939-2b70-4c56-86ce-d3343f99d15f.json new file mode 100644 index 0000000000000000000000000000000000000000..76af27d6a213ed1654b74a5a89f6e28157a749fd --- /dev/null +++ b/56429939-2b70-4c56-86ce-d3343f99d15f.json @@ -0,0 +1,36 @@ +{ + "id": "56429939-2b70-4c56-86ce-d3343f99d15f", + "disease": { + "id": "M2023_04_26_16_49_01", + "names": [ + "Metabolic syndrome" + ], + "dbLinks": { + "mesh": [ + "C18.452.394.968.500.570", + "C18.452.625" + ] + }, + "description": "Metabolic syndrome is a complex constellation of metabolic derangements that increase the risk of atherosclerotic cardiovascular disease, type 2 diabetes, and all-cause mortality. The key features of metabolic syndrome include central obesity, insulin resistance, dyslipidemia, and hypertension. These abnormalities are believed to arise from a combination of genetic predisposition and environmental factors, such as sedentary behavior, poor dietary habits, and chronic stress. Diagnosis of metabolic syndrome requires meeting three or more established criteria, based on standardized guidelines. Management of metabolic syndrome involves a comprehensive approach, including lifestyle modifications such as weight loss, physical activity, and dietary changes, as well as pharmacotherapy to address underlying risk factors such as hypertension, dyslipidemia, and hyperglycemia. Early intervention and aggressive management of metabolic syndrome are critical to preventing or delaying the onset of complications and improving long-term health outcomes." + }, + "article": { + "id": "24550031", + "text": "OBJECTIVE:\nThe purpose of this study was to examine the relationship between usual sugar-sweetened beverage (SSB) consumption and prevalence of abnormal metabolic health across body mass index (BMI) categories.\n\nMETHODS:\nThe metabolic health of 6,842 non-diabetic adults was classified using cross-sectional data from the Framingham Heart Study Offspring (1998-2001) and Third Generation (2002-2005) cohorts. Adults were classified as normal weight, overweight or obese and, within these categories, metabolic health was defined based on five criteria-hypertension, elevated fasting glucose, elevated triglycerides, low HDL cholesterol, and insulin resistance. Individuals without metabolic abnormalities were considered metabolically healthy. Logistic regression was used to examine the associations between categories of SSB consumption and risk of metabolic health after stratification by BMI.\n\nRESULTS:\nComparing the highest category of SSB consumers (median of 7 SSB per week) to the lowest category (non-consumers), odds ratios (95% confidence intervals) for metabolically abnormal phenotypes, compared to the metabolically normal, were 1.9 (1.1-3.4) among the obese, 2.0 (1.4-2.9) among the overweight, and 1.9 (1.4-2.6) among the normal weight individuals.\n\nCONCLUSIONS:\nIn this cross-sectional analysis, it is observed that, irrespective of weight status, consumers of SSB were more likely to display metabolic abnormalities compared to non-consumers in a dose-dependent manner." + }, + "questions": [ + { + "id": "ffa65348-012a-4a84-ad4a-5a7429b165b6", + "text": "What is a risk factor for Metabolic Syndrome?", + "answers": [ + { + "answer_start": 83, + "text": "sugar-sweetened beverage (SSB)" + }, + { + "answer_start": 1365, + "text": "consumers of SSB" + } + ] + } + ] +} \ No newline at end of file diff --git a/5700dab9-4dc3-474e-af38-47d451451359.json b/5700dab9-4dc3-474e-af38-47d451451359.json new file mode 100644 index 0000000000000000000000000000000000000000..c2aa3f2456267aacf438a1f1c4d2fc34aa08759c --- /dev/null +++ b/5700dab9-4dc3-474e-af38-47d451451359.json @@ -0,0 +1,38 @@ +{ + "id": "5700dab9-4dc3-474e-af38-47d451451359", + "disease": { + "id": "H00408", + "names": [ + "Type 1 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E10" + ], + "mesh": [ + "D003922" + ] + }, + "category": "Metabolic disease; Immune system disease; Endocrine disease" + }, + "article": { + "id": "14519706", + "text": "CONTEXT:\nDietary factors modifying type 1 diabetes mellitus (DM) risk have been proposed, but little is known if they trigger the islet autoimmunity that precedes clinical disease.\n\nOBJECTIVE:\nTo determine whether breastfeeding duration, food supplementation, or age at introduction of gluten-containing foods influences the risk of developing islet autoantibodies.\n\nDESIGN AND SETTING:\nProspective natural history cohort study conducted from 1989 to 2003 in inpatient/outpatient clinics in Germany.\n\nPARTICIPANTS:\nThe BABYDIAB study follows newborn children of parents with type 1 DM. Eligibility requirements were met in 1610 children. Blood samples were obtained at birth, age 9 months, 2, 5, and 8 years. Dropout rate was 14.4% by age 5 years. Breastfeeding data were obtained by prospective questionnaires (91% complete), and food supplementation data were obtained by family interview (72% for food supplementation and 80% for age of gluten introduction).\n\nMAIN OUTCOME MEASURE:\nDevelopment of islet autoantibodies (insulin, glutamic acid decarboxylase, or IA-2 antibodies) in 2 consecutive blood samples.\n\nRESULTS:\nLife-table islet autoantibody frequency was 5.8% (SE, 0.6%) by age 5 years. Reduced total or exclusive breastfeeding duration did not significantly increase the risk of developing islet autoantibodies. Food supplementation with gluten-containing foods before age 3 months, however, was associated with significantly increased islet autoantibody risk (adjusted hazard ratio, 4.0; 95% confidence interval, 1.4-11.5; P =.01 vs children who received only breast milk until age 3 months). Four of 17 children who received gluten foods before age 3 months developed islet autoantibodies (life-table 5-year risk, 24%; SE, 10%). All 4 children had the high-risk DRB1*03/04,DQB1*0302 genotype. Early exposure to gluten did not significantly increase the risk of developing celiac disease-associated autoantibodies. Children who first received gluten foods after age 6 months did not have increased risks for islet or celiac disease autoantibodies.\n\nCONCLUSION:\nEnsuring compliance to infant feeding guidelines is a possible way to reduce the risk of development of type 1 DM autoantibodies." + }, + "questions": [ + { + "id": "c4133ba5-6dc5-4fc5-9d76-c84a25014fda", + "text": "What are the risk factors of Type 1 diabetes mellitus?", + "answers": [ + { + "answer_start": 1324, + "text": "Food supplementation with gluten-containing foods before age 3 months" + }, + { + "answer_start": 1766, + "text": "high-risk DRB1*03/04,DQB1*0302 genotype" + } + ] + } + ] +} \ No newline at end of file diff --git a/571c626d-98af-406e-b9d8-d19f2b5e8aed.json b/571c626d-98af-406e-b9d8-d19f2b5e8aed.json new file mode 100644 index 0000000000000000000000000000000000000000..abe79593e967b83c3405fb5f018e66fb87302ce1 --- /dev/null +++ b/571c626d-98af-406e-b9d8-d19f2b5e8aed.json @@ -0,0 +1,34 @@ +{ + "id": "571c626d-98af-406e-b9d8-d19f2b5e8aed", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "11268224", + "text": "OBJECTIVE:\nTo examine the relations of cardiorespiratory fitness, as measured by maximal oxygen uptake and exercise test duration at the initiation of the study, with overall, cardiovascular disease (CVD)-related, and non-CVD-related mortality.\n\nMETHODS:\nA population-based cohort study of 1294 men with no CVD, pulmonary disease, or cancer at baseline in Kuopio and surrounding communities in eastern Finland. During an average follow-up of 10.7 years, there were 124 overall, 42 CVD-related, and 82 non-CVD-related deaths.\n\nRESULTS:\nThe relative risk of overall death in unfit men (maximal oxygen uptake \u003c27.6 mL/kg per minute) was 2.76 (95% confidence interval, 1.43-5.33) (P =.002), and the relative risk of CVD-related death was 3.09 (95% confidence interval, 1.10-9.56) (P =.05), compared with fit men (maximal oxygen uptake \u003e37.1 mL/kg per minute) after adjusting for age, examination years, smoking, and alcohol consumption. The relative risk of non-CVD-related death in unfit men was almost the same magnitude as for overall death. Furthermore, adjustment for serum lipid levels, blood pressure, plasma fibrinogen level, diabetes, and fasting serum insulin level did not weaken these associations significantly. Exercise test duration also had a strong inverse relation to overall, CVD-related, and non-CVD-related mortality. Poor cardiorespiratory fitness was comparable with elevated systolic blood pressure, smoking, obesity, and diabetes in importance as a risk factor for mortality.\n\nCONCLUSIONS:\nCardiorespiratory fitness had a strong, graded, inverse association with overall, CVD-related, and non-CVD-related mortality. Maximal oxygen uptake and exercise test duration represent the strongest predictors of mortality." + }, + "questions": [ + { + "id": "714379b4-94f4-485e-a5bc-4683c503b7eb", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 573, + "text": "unfit men (maximal oxygen uptake \u003c27.6 mL/kg per minute)" + } + ] + } + ] +} \ No newline at end of file diff --git a/57f88159-023b-457f-9928-fa62cfd84b7a.json b/57f88159-023b-457f-9928-fa62cfd84b7a.json new file mode 100644 index 0000000000000000000000000000000000000000..925cf37660df7061edd8047e04210f0d4829d445 --- /dev/null +++ b/57f88159-023b-457f-9928-fa62cfd84b7a.json @@ -0,0 +1,42 @@ +{ + "id": "57f88159-023b-457f-9928-fa62cfd84b7a", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "26493265", + "text": "We prospectively examined the association between smoking and the risk of breast cancer in a racially/ethnically diverse population comprising mainly women who did not drink alcohol. From 1993 to 2010, we followed 83,300 women who were enrolled in the Multiethnic Cohort Study at 45-75 years of age. We identified cancer cases via linkage to the Surveillance, Epidemiology, and End Results Program cancer registries that covered the states of Hawaii and California through December 2010. We used Cox proportional hazards models to estimate hazard ratios and 95% confidence intervals while adjusting for confounders that were decided a priori. During a mean follow-up of 15 years, 4,484 women developed invasive breast cancer. Compared with parous never smokers, women who had smoked for more than 20 pack-years and initiated smoking more than 5 years before their first childbirth had an overall risk of breast cancer that was 35% higher (hazard ratio = 1.35, 95% confidence interval: 1.13, 1.63). Among women who did not drink alcohol, the risk was 40% higher (hazard ratio = 1.40, 95% confidence interval: 1.08, 1.81). This higher risk did not significantly differ among racial/ethnic groups (P(interaction) = 0.82). We found that various measures of smoking exposure were associated with a higher risk of breast cancer, especially smoking initiated many years before first childbirth, and that risk did not differ by alcohol consumption (yes vs. no) or racial/ethnic group." + }, + "questions": [ + { + "id": "3963f560-26fc-4158-9a11-8313522389b7", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1233, + "text": "various measures of smoking exposure" + }, + { + "answer_start": 1334, + "text": "smoking initiated many years before first childbirth" + }, + { + "answer_start": 762, + "text": "women who had smoked for more than 20 pack-years and initiated smoking more than 5 years before their first childbirth" + } + ] + } + ] +} \ No newline at end of file diff --git a/58ceb4a0-4a88-4f57-ab2b-a3cd3109cd1b.json b/58ceb4a0-4a88-4f57-ab2b-a3cd3109cd1b.json new file mode 100644 index 0000000000000000000000000000000000000000..cf3558ca284ac8fcbfd9686240bd4601a157e602 --- /dev/null +++ b/58ceb4a0-4a88-4f57-ab2b-a3cd3109cd1b.json @@ -0,0 +1,38 @@ +{ + "id": "58ceb4a0-4a88-4f57-ab2b-a3cd3109cd1b", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "15898094", + "text": "BACKGROUND:\nExposure to occupational hazards among firefighters may lead to increased mortality from cancer, lung, or heart disease.\n\nMETHODS:\nAge- and gender-adjusted mortality rates of 34,796 male and 2,017 female Florida professional firefighters between 1972 and 1999 were compared with the Florida general population.\n\nRESULTS:\nOne thousand four hundred eleven male and 38 female firefighter deaths with known causes were identified. In male firefighters, mortality due to all causes and most non-malignant diseases was significantly less than expected. There was no excess overall mortality from cancer, but excesses existed for male breast cancer [standardized mortality ratio (SMR = 7.41; 95% confidence interval (CI): 1.99-18.96) and thyroid cancer (SMR = 4.82; 95% CI: 1.30-12.34)]. Mortality from bladder cancer was increased and approached statistical significance (SMR = 1.79; 95% CI: 0.98-3.00). Firefighters certified between 1972 and 1976 had excess mortality from bladder cancer (SMR = 1.95; 95% CI: 1.04-3.33). Female firefighters had similar morality patterns to Florida women except for atherosclerotic heart disease (SMR = 3.85; 95% CI: 1.66-7.58).\n\nCONCLUSIONS:\nExcess mortality risk from bladder cancer may be related to occupational exposure during firefighting. The thyroid cancer and breast cancer risk in males, as well as the excess risk of cardiovascular disease mortality noted in females warrant further investigation." + }, + "questions": [ + { + "id": "abb301b9-fda7-4893-826b-549c2d610b33", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 1244, + "text": "occupational exposure during firefighting" + }, + { + "answer_start": 910, + "text": "Firefighters certified between 1972 and 1976" + } + ] + } + ] +} \ No newline at end of file diff --git a/58d35c27-2eb7-4658-bbf0-9add5a856359.json b/58d35c27-2eb7-4658-bbf0-9add5a856359.json new file mode 100644 index 0000000000000000000000000000000000000000..83d518974a771629588cf319592227a84c8c4817 --- /dev/null +++ b/58d35c27-2eb7-4658-bbf0-9add5a856359.json @@ -0,0 +1,37 @@ +{ + "id": "58d35c27-2eb7-4658-bbf0-9add5a856359", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "26376686", + "text": "Higher folate has been associated with a reduced colorectal cancer (CRC) risk, but excessive folate may promote tumor progression. The role of unmetabolized folic acid (UFA) from high folic acid consumption in carcinogenesis is largely unexplored. We evaluated prediagnostic plasma levels of UFA in relation to CRC risk in nested case-control studies (618 CRC case patients and 1207 matched control) with blood samples collected prior to folic acid fortification. UFA was detected in 21.4% of control UFA levels were not associated with CRC risk. Compared with undetectable levels, the multivariable relative risks (RRs) of CRC were 1.03 (95% confidence interval [CI] = 0.73 to 1.46) for less than 0.5 nmol/L and 1.12 (95% CI = 0.81 to 1.55) for 0.5 nmol/L or more (Ptrend = .32). A positive association between UFA levels and CRC risk was observed among men (RR = 1.57, 95% CI = 0.99 to 2.49 for ≥0.5 nmol/L vs undetectable, Pinteraction = .04), and a positive association was also observed among those with the methylene-tetrahydrofolate reductase (MTHFR) CT/TT genotype (RR = 2.20, 95% CI = 1.22 to 3.94 for ≥0.5 nmol/L vs undetectable, Pinteraction=0.02). In conclusion, prediagnostic plasma levels of UFA from the prefortification period were not associated with risk of CRC." + }, + "questions": [ + { + "id": "96568d3d-9d0c-4fcc-ae08-4c7cdb36c499", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 998, + "text": "those with the methylene-tetrahydrofolate reductase (MTHFR) CT/TT genotype" + } + ] + } + ] +} \ No newline at end of file diff --git a/58e1ed91-0729-49b1-a94c-0e244f5ba4ce.json b/58e1ed91-0729-49b1-a94c-0e244f5ba4ce.json new file mode 100644 index 0000000000000000000000000000000000000000..4dbb2054de1d490c964c018baf094d4c1f2dde50 --- /dev/null +++ b/58e1ed91-0729-49b1-a94c-0e244f5ba4ce.json @@ -0,0 +1,43 @@ +{ + "id": "58e1ed91-0729-49b1-a94c-0e244f5ba4ce", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "18805332", + "text": "BACKGROUND:\nExposure to paracetamol during intrauterine life, childhood, and adult life may increase the risk of developing asthma. We studied 6-7-year-old children from Phase Three of the International Study of Asthma and Allergies in Childhood (ISAAC) programme to investigate the association between paracetamol consumption and asthma.\n\nMETHODS:\nAs part of Phase Three of ISAAC, parents or guardians of children aged 6-7 years completed written questionnaires about symptoms of asthma, rhinoconjunctivitis, and eczema, and several risk factors, including the use of paracetamol for fever in the child's first year of life and the frequency of paracetamol use in the past 12 months. The primary outcome variable was the odds ratio (OR) of asthma symptoms in these children associated with the use of paracetamol for fever in the first year of life, as calculated by logistic regression.\n\nFINDINGS:\n205 487 children aged 6-7 years from 73 centres in 31 countries were included in the analysis. In the multivariate analyses, use of paracetamol for fever in the first year of life was associated with an increased risk of asthma symptoms when aged 6-7 years (OR 1.46 [95% CI 1.36-1.56]). Current use of paracetamol was associated with a dose-dependent increased risk of asthma symptoms (1.61 [1.46-1.77] and 3.23 [2.91-3.60] for medium and high use vs no use, respectively). Use of paracetamol was similarly associated with the risk of severe asthma symptoms, with population-attributable risks between 22% and 38%. Paracetamol use, both in the first year of life and in children aged 6-7 years, was also associated with an increased risk of symptoms of rhinoconjunctivitis and eczema.\n\nINTERPRETATION:\nUse of paracetamol in the first year of life and in later childhood, is associated with risk of asthma, rhinoconjunctivitis, and eczema at age 6 to 7 years. We suggest that exposure to paracetamol might be a risk factor for the development of asthma in childhood." + }, + "questions": [ + { + "id": "96ff3091-b1b1-4d2b-98cc-56beeb5aa976", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1025, + "text": "use of paracetamol for fever in the first year of life" + }, + { + "answer_start": 1187, + "text": "Current use of paracetamol" + }, + { + "answer_start": 1702, + "text": "Use of paracetamol in the first year of life and in later childhood" + } + ] + } + ] +} \ No newline at end of file diff --git a/59027f1e-26ac-4389-ae1e-fd2c9166497c.json b/59027f1e-26ac-4389-ae1e-fd2c9166497c.json new file mode 100644 index 0000000000000000000000000000000000000000..60d23ae939ba73d53c9379fef6b965f5bc9005d1 --- /dev/null +++ b/59027f1e-26ac-4389-ae1e-fd2c9166497c.json @@ -0,0 +1,43 @@ +{ + "id": "59027f1e-26ac-4389-ae1e-fd2c9166497c", + "disease": { + "id": "H00056", + "names": [ + "Alzheimer disease", + "Dementia due to Alzheimer disease" + ], + "dbLinks": { + "icd10": [ + "G30" + ], + "mesh": [ + "D000544" + ] + }, + "category": "Neurodegenerative disease" + }, + "article": { + "id": "11935076", + "text": "BACKGROUND:\nThe main stumbling block in the clinical management and in the search for a cure of Alzheimer disease (AD) is that the cause of this disorder has remained uncertain until now.\n\nSUMMARY OF REVIEW:\nEvidence that sporadic (nongenetic) AD is primarily a vascular rather than a neurodegenerative disorder is reviewed. This conclusion is based on the following evidence: (1) epidemiological studies showing that practically all risk factors for AD reported thus far have a vascular component that reduces cerebral perfusion; (2) risk factor association between AD and vascular dementia (VaD); (3) improvement of cerebral perfusion obtained from most pharmacotherapy used to reduce the symptoms or progression of AD; (4) detection of regional cerebral hypoperfusion with the use of neuroimaging techniques to preclinically identify AD candidates; (5) presence of regional brain microvascular abnormalities before cognitive and neurodegenerative changes; (6) common overlap of clinical AD and VaD cognitive symptoms; (7) similarity of cerebrovascular lesions present in most AD and VaD patients; (8) presence of cerebral hypoperfusion preceding hypometabolism, cognitive decline, and neurodegeneration in AD; and (9) confirmation of the heterogeneous and multifactorial nature of AD, likely resulting from the diverse presence of vascular risk factors or indicators of vascular disease.\n\nCONCLUSIONS:\nSince the value of scientific evidence generally revolves around probability and chance, it is concluded that the data presented here pose a powerful argument in support of the proposal that AD should be classified as a vascular disorder. According to elementary statistics, the probability or chance that all these findings are due to an indirect pathological effect or to coincidental circumstances related to the disease process of AD seems highly unlikely. The collective data presented in this review strongly support the concept that sporadic AD is a vascular disorder. It is recommended that current clinical management of patients, treatment targets, research designs, and disease prevention efforts need to be critically reassessed and placed in perspective in light of these important findings." + }, + "questions": [ + { + "id": "f1d59f75-cb73-4eff-8637-8f325c386d53", + "text": "What are the risk factors of Alzheimer disease?", + "answers": [ + { + "answer_start": 739, + "text": "regional cerebral hypoperfusion" + }, + { + "answer_start": 479, + "text": "vascular component that reduces cerebral perfusion" + }, + { + "answer_start": 1116, + "text": "cerebral hypoperfusion preceding hypometabolism, cognitive decline, and neurodegeneration in AD" + } + ] + } + ] +} \ No newline at end of file diff --git a/5956bab1-cdd4-4ab1-876e-792779c0436b.json b/5956bab1-cdd4-4ab1-876e-792779c0436b.json new file mode 100644 index 0000000000000000000000000000000000000000..55b0c744db5d2bfc36c864f56806eb91c4614451 --- /dev/null +++ b/5956bab1-cdd4-4ab1-876e-792779c0436b.json @@ -0,0 +1,34 @@ +{ + "id": "5956bab1-cdd4-4ab1-876e-792779c0436b", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "16380592", + "text": "CONTEXT:\nWhile parental cardiovascular disease (CVD) doubles the risk for CVD in offspring, the extent of increased risk associated with sibling CVD is unclear.\n\nOBJECTIVE:\nTo determine, using validated events, whether sibling CVD predicts outcome in middle-aged adults independent of other risk factors.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nThe Framingham Offspring Study, an inception cohort of the Framingham Heart Study, a prospective population-based cohort study initiated in 1948 with the offspring cohort initiated in 1971. Participants (n = 2475) were members of the offspring cohort aged 30 years or older, free of CVD, and with at least 1 sibling in the study; all were followed up for 8 years.\n\nMAIN OUTCOME MEASURES:\nAssociation of sibling CVD with 8-year personal risk for CVD using pooled logistic regression. A secondary analysis restricted to offspring with both parents in the study assessed the joint impact of parental and sibling CVD occurrence.\n\nRESULTS:\nAmong 973 person-examinations in the sibling CVD group (mean age, 57 years) and 4506 person-examinations in the no sibling CVD group (mean age, 47 years), 329 CVD events occurred during follow-up. Baseline risk factors were more prevalent in the sibling CVD group compared with the no sibling CVD group. Sibling CVD was associated with a significantly increased risk for incident CVD (age- and sex-adjusted odds ratio [OR], 1.55; 95% confidence interval [CI], 1.19-2.03). Adjustment for risk factors did not substantially attenuate the risk (adjusted OR, 1.45; 95% CI, 1.10-1.91). In the analysis restricted to persons with both parents in the study, in models adjusting for both sibling and parental CVD, the multivariable-adjusted OR for sibling CVD (1.99; 95% CI, 1.32-3.00) exceeded that for parental CVD (1.45; 95% CI, 1.02-2.05).\n\nCONCLUSION:\nUsing validated events, sibling CVD conferred increased risk of future CVD events above and beyond established risk factors and parental CVD in middle-aged adults." + }, + "questions": [ + { + "id": "dcbf5aa9-66d4-4abb-bb22-6399197ec744", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1849, + "text": "sibling CVD" + } + ] + } + ] +} \ No newline at end of file diff --git a/599ebee6-d8aa-42b4-a4fd-8a179b960d10.json b/599ebee6-d8aa-42b4-a4fd-8a179b960d10.json new file mode 100644 index 0000000000000000000000000000000000000000..9c8d5f8bbe0d60937df0b63c0b25ed830e9ab52c --- /dev/null +++ b/599ebee6-d8aa-42b4-a4fd-8a179b960d10.json @@ -0,0 +1,52 @@ +{ + "id": "599ebee6-d8aa-42b4-a4fd-8a179b960d10", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "8217855", + "text": "The prevalence of chronic bronchitis and of clinical farmer's lung was studied in 30 districts of the French Doubs province in relation to individual (age, sex, smoking) and geographical (altitude) factors. 5703 exclusively dairy farmers (response rate 83%) participated in the study by answering a medical questionnaire. Prevalences of chronic bronchitis and clinical farmer's lung were 9.3% and 1.4% respectively. A logistic regression model was used to evaluate risk factors for chronic bronchitis and clinical farmer's lung. A risk of chronic bronchitis was associated with male sex (p \u003c 10(-4)), age (p \u003c 10(-4)), smoker category (p \u003c 10(-4)), and altitude (p \u003c 10(-4)). A risk of clinical farmer's lung was associated with non-smokers (p \u003c 0.05), and linearly with altitude (p \u003c 10(-4)). Also there was a strong positive relation between chronic bronchitis and clinical farmer's lung (odds ratio 19.5 (95% confidence interval 12.1-31.4) after adjustment for confounding variables. The main finding of this study is the highly significant increase of prevalence of the diseases in relation to altitude." + }, + "questions": [ + { + "id": "f12a9a26-9495-48c2-81c1-41f7868f7e9c", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 578, + "text": "male sex" + }, + { + "answer_start": 600, + "text": " age" + }, + { + "answer_start": 619, + "text": "smoker category" + }, + { + "answer_start": 653, + "text": "altitude" + }, + { + "answer_start": 1098, + "text": "altitude" + } + ] + } + ] +} \ No newline at end of file diff --git a/5a486e4e-c878-4008-80a9-4181187e3b3c.json b/5a486e4e-c878-4008-80a9-4181187e3b3c.json new file mode 100644 index 0000000000000000000000000000000000000000..b7befe4f63885f1b2dc9ee854a2224c42df3b76e --- /dev/null +++ b/5a486e4e-c878-4008-80a9-4181187e3b3c.json @@ -0,0 +1,46 @@ +{ + "id": "5a486e4e-c878-4008-80a9-4181187e3b3c", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "18591432", + "text": "BACKGROUND:\nPrediction of coronary heart disease (CHD) and cerebrovascular disease (CeVD) can aid healthcare providers and prevention programs. Previous reports have focused on traditional cardiovascular risk factors; less information has been available on the role of overweight and obesity.\n\nMETHODS AND RESULTS:\nBaseline data from 4780 Framingham Offspring Study adults with up to 24 years of follow-up were used to assess risk for a first CHD event (angina pectoris, myocardial infarction, or cardiac death) alone, first CeVD event (acute brain infarction, transient ischemic attack, and stroke-related death) alone, and CHD and CeVD events combined. Accelerated failure time models were developed for the time of first event to age, sex, cholesterol, high-density lipoprotein cholesterol, diabetes mellitus (DM), systolic blood pressure, smoking status, and body mass index (BMI). Likelihood-ratio tests of statistical significance were used to identify the best-fitting predictive functions. Age, sex, smoking status, systolic blood pressure, ratio of cholesterol to high-density lipoprotein cholesterol, and presence of DM were highly related (P\u003c0.01 for all) to the development of first CHD events, and all of the above except sex and DM were highly related to the first CeVD event. BMI also significantly predicted the occurrence of CHD (P=0.05) and CeVD (P=0.03) in multivariable models adjusting for traditional risk factors. The magnitude of the BMI effect was reduced but remained statistically significant when traditional variables were included in the prediction models.\n\nCONCLUSIONS:\nGreater BMI, higher systolic blood pressure, higher ratio of cholesterol to high-density lipoprotein cholesterol, and presence of DM were all predictive of first CHD events, and all but the presence of DM were predictive of first CeVD events. These results suggest that common pathophysiological mechanisms underlie the roles of BMI, DM, and systolic blood pressure as predictors for first CHD and CeVD events." + }, + "questions": [ + { + "id": "3aaafe5c-8fed-4b2c-96e3-a6b1dcedd28c", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1601, + "text": "Greater BMI" + }, + { + "answer_start": 1614, + "text": "higher systolic blood pressure" + }, + { + "answer_start": 1646, + "text": "higher ratio of cholesterol to high-density lipoprotein cholesterol" + }, + { + "answer_start": 1719, + "text": "presence of DM" + } + ] + } + ] +} \ No newline at end of file diff --git a/5a5eac99-22d7-4118-a50f-394a4699debc.json b/5a5eac99-22d7-4118-a50f-394a4699debc.json new file mode 100644 index 0000000000000000000000000000000000000000..496ad6bd26be297547df774e2c3fce7412667b8c --- /dev/null +++ b/5a5eac99-22d7-4118-a50f-394a4699debc.json @@ -0,0 +1,42 @@ +{ + "id": "5a5eac99-22d7-4118-a50f-394a4699debc", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "15602020", + "text": "BACKGROUND:\nFew studies have simultaneously investigated the role of soluble tumor necrosis factor alpha (TNF-alpha) receptors types 1 and 2 (sTNF-R1 and sTNF-R2), C-reactive protein, and interleukin-6 as predictors of cardiovascular events. The value of these inflammatory markers as independent predictors remains controversial.\n\nMETHODS:\nWe examined plasma levels of sTNF-R1, sTNF-R2, interleukin-6, and C-reactive protein as markers of risk for coronary heart disease among women participating in the Nurses' Health Study and men participating in the Health Professionals Follow-up Study in nested case-control analyses. Among participants who provided a blood sample and who were free of cardiovascular disease at baseline, 239 women and 265 men had a nonfatal myocardial infarction or fatal coronary heart disease during eight years and six years of follow-up, respectively. Using risk-set sampling, we selected controls in a 2:1 ratio with matching for age, smoking status, and date of blood sampling.\n\nRESULTS:\nAfter adjustment for matching factors, high levels of interleukin-6 and C-reactive protein were significantly related to an increased risk of coronary heart disease in both sexes, whereas high levels of soluble TNF-alpha receptors were significant only among women. Further adjustment for lipid and nonlipid factors attenuated all associations; only C-reactive protein levels remained significant. The relative risk among all participants was 1.79 for those with C-reactive protein levels of at least 3.0 mg per liter, as compared with those with levels of less than 1.0 mg per liter (95 percent confidence interval, 1.27 to 2.51; P for trend \u003c0.001). Additional adjustment for the presence or absence of diabetes and hypertension moderately attenuated the relative risk to 1.68 (95 percent confidence interval, 1.18 to 2.38; P for trend = 0.008).\n\nCONCLUSIONS:\nElevated levels of inflammatory markers, particularly C-reactive protein, indicate an increased risk of coronary heart disease. Although plasma lipid levels were more strongly associated with an increased risk than were inflammatory markers, the level of C-reactive protein remained a significant contributor to the prediction of coronary heart disease." + }, + "questions": [ + { + "id": "c2e15fa1-fa1a-4f6f-884f-24db15fc5833", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1881, + "text": "Elevated levels of inflammatory markers, particularly C-reactive protein" + }, + { + "answer_start": 2127, + "text": "level of C-reactive protein" + }, + { + "answer_start": 1091, + "text": "C-reactive protein" + } + ] + } + ] +} \ No newline at end of file diff --git a/5a9e1090-530f-44d4-bf98-e3a0af6f3507.json b/5a9e1090-530f-44d4-bf98-e3a0af6f3507.json new file mode 100644 index 0000000000000000000000000000000000000000..543a395a6ff5e7220257a39f49e797ddc1168eab --- /dev/null +++ b/5a9e1090-530f-44d4-bf98-e3a0af6f3507.json @@ -0,0 +1,47 @@ +{ + "id": "5a9e1090-530f-44d4-bf98-e3a0af6f3507", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "23607815", + "text": "INTRODUCTION:\nWhereas the overall association between smoking and rheumatoid arthritis (RA) must be regarded as established, considerably less is known about how much smoking is needed to increase the risk of RA, that is, the effect of smoking intensity, duration and cessation.\n\nMETHODS:\nThe Swedish Mammography Cohort, including 34,101 women aged 54 to 89 years, was followed up from January 1, 2003 through December 31, 2010 (219 RA cases identified). Relative risks (RR) and their 95% confidence intervals (CI) were estimated as rate ratios using Cox proportional hazards model.\n\nRESULTS:\nThere was a statistically significant association between smoking intensity (RR comparing 1 to 7 cigarettes/day vs never smoking 2.31 (95% CI: 1.59, 3.36)) as well as duration of smoking (comparing 1 to 25 years vs never smoking RR = 1.60 (95% CI: 1.07, 2.38)) and risk of RA. Compared to never smokers, the risk was still significantly elevated 15 years after smoking cessation (RR = 1.99 (95% CI: 1.23, 3.20)). However, among former smokers, the risk of RA seemed to be decreasing over time since stopping smoking: women who stopped smoking 15 years before the start of the follow-up had 30% lower risk of RA compared to those who stopped only a year before start of the follow-up (RR = 0.70 (95% CI: 0.24,2.02)).\n\nCONCLUSIONS:\nThis prospective study highlights that even light cigarette smoking is associated with increased risk of RA in women and that smoking cessation may reduce, though not remove, this risk." + }, + "questions": [ + { + "id": "dd17300b-b37e-4cda-ba2d-aa6bfea38de2", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 651, + "text": "smoking intensity" + }, + { + "answer_start": 760, + "text": "duration of smoking" + }, + { + "answer_start": 939, + "text": "15 years after smoking cessation" + }, + { + "answer_start": 1367, + "text": "light cigarette smoking" + } + ] + } + ] +} \ No newline at end of file diff --git a/5c9d9d42-126a-4d25-9dee-9de6f08775b2.json b/5c9d9d42-126a-4d25-9dee-9de6f08775b2.json new file mode 100644 index 0000000000000000000000000000000000000000..de565463380bcbebeab6f3d4367e838aacf6305c --- /dev/null +++ b/5c9d9d42-126a-4d25-9dee-9de6f08775b2.json @@ -0,0 +1,34 @@ +{ + "id": "5c9d9d42-126a-4d25-9dee-9de6f08775b2", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "30384883", + "text": "BACKGROUND:\nThere is a well-established inverse relationship between cardiorespiratory fitness (CRF) and mortality. However, this relationship has almost exclusively been studied using estimated CRF.\n\nOBJECTIVES:\nThis study aimed to assess the association of directly measured CRF, obtained using cardiopulmonary exercise (CPX) testing with all-cause, cardiovascular disease (CVD), and cancer mortality in apparently healthy men and women.\n\nMETHODS:\nParticipants included 4,137 self-referred apparently healthy adults (2,326 men, 1,811 women; mean age: 42.8 ± 12.2 years) who underwent CPX testing to determine baseline CRF. Participants were followed for 24.2 ± 11.7 years (1.1 to 49.3 years) for mortality. Cox-proportional hazard models were performed to determine the relationship of CRF (ml·kg·min) and CRF level (low, moderate, and high) with mortality outcomes.\n\nRESULTS:\nDuring follow-up, 727 participants died (524 men, 203 women). CPX-derived CRF was inversely related to all-cause, CVD, and cancer mortality. Low CRF was associated with higher risk for all-cause (hazard ratio [HR]: 1.73; 95% confidence interval [CI]: 1.20 to 3.50), CVD (HR: 2.27; 95% CI: 1.20 to 3.49), and cancer (HR: 2.07; 95% CI: 1.18 to 3.36) mortality compared with high CRF. Further, each metabolic equivalent increment increase in CRF was associated with a 11.6%, 16.1%, and 14.0% reductions in all-cause, CVD, and cancer mortality, respectively.\n\nCONCLUSIONS:\nGiven the prognostic ability of CPX-derived CRF for all-cause and disease-specific mortality outcomes, its use should be highly considered for apparently healthy populations as it may help to improve the efficacy of the individualized patient risk assessment and guide clinical decisions." + }, + "questions": [ + { + "id": "076779d2-3777-4e5b-9e9e-76ea4bc98047", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1020, + "text": "Low CRF" + } + ] + } + ] +} \ No newline at end of file diff --git a/5cd98da4-a19f-4488-9eb6-507607b01a92.json b/5cd98da4-a19f-4488-9eb6-507607b01a92.json new file mode 100644 index 0000000000000000000000000000000000000000..fd0076619290ba1460f14103a7b47e5a7bf4a09e --- /dev/null +++ b/5cd98da4-a19f-4488-9eb6-507607b01a92.json @@ -0,0 +1,43 @@ +{ + "id": "5cd98da4-a19f-4488-9eb6-507607b01a92", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "15319232", + "text": "OBJECTIVE:\nTo study the association between silica exposure and rheumatoid arthritis and how it is modified by cigarette smoking.\n\nMETHODS:\nData were analysed from 276 male cases and 276 male controls aged 18 to 70 years, included in a Swedish population based study between May 1996 and June 2001. A case was defined as a person recently diagnosed with rheumatoid arthritis according to the ACR criteria. Controls were selected from the study base as a stratified random sample accounting for age, sex, and residency. Men with a self reported history of work with rock drilling, stone crushing, or exposure to stone dust in general were defined as silica exposed. Rheumatoid factor (RF) status among cases was recorded.\n\nRESULTS:\nSilica exposed men had increased risk of rheumatoid arthritis, with an odds ratio (OR), adjusted for age, residential area, and smoking, of 2.2 (95% confidence interval, 1.2 to 3.9) among men aged 18 to 70 years, and 2.7 (1.2 to 5.8) among those aged 50 to 70 years. Men who had worked with rock drilling or stone crushing (regarded as highly exposed) had a slightly greater increase in risk of rheumatoid arthritis than silica exposed men in general, with an OR of 3.0 (1.2 to 7.6). The joint effects of silica exposure and smoking were compatible with synergy between these two exposures in the development of rheumatoid arthritis but this was not conclusive.\n\nCONCLUSIONS:\nSilica exposure is associated with increased risk of developing rheumatoid arthritis. This association is not explained by smoking habits." + }, + "questions": [ + { + "id": "9423d4b9-843b-4033-a81c-b456f8d1b2b2", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 731, + "text": "Silica exposed men" + }, + { + "answer_start": 998, + "text": "Men who had worked with rock drilling or stone crushing" + }, + { + "answer_start": 1407, + "text": "Silica exposure" + } + ] + } + ] +} \ No newline at end of file diff --git a/5cdff808-24c3-4087-af02-1e0018fb50bf.json b/5cdff808-24c3-4087-af02-1e0018fb50bf.json new file mode 100644 index 0000000000000000000000000000000000000000..369496becfe95782c740e0927015a97b568132c4 --- /dev/null +++ b/5cdff808-24c3-4087-af02-1e0018fb50bf.json @@ -0,0 +1,34 @@ +{ + "id": "5cdff808-24c3-4087-af02-1e0018fb50bf", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "22905651", + "text": "BACKGROUND:\nPREVENTCD, Prevent Coeliac Disease, is an international project investigating the hypothesis of possible induction of tolerance to gluten in genetically predisposed children through introducing small quantities of gluten during the period of breastfeeding.\n\nAIM:\nTo summarise current knowledge on the possible relationship between early feeding practices and the risk of coeliac disease (CD).\n\nMETHODS:\nThe Cochrane Library, MEDLINE, and EMBASE databases were searched in May 2011, and the search was updated in January 2012, and again in July 2012.\n\nRESULTS:\nBreastfeeding (BF) and CD: some studies show a protective effect of BF, while others show no effect. No studies have shown a long-term preventive effect. BF at the time of gluten introduction and CD: Results from a meta-analysis of five observational case-control studies suggest that BF at gluten introduction is associated with a lower risk of CD compared with formula feeding. It is unclear whether BF provides a permanent protection or only delays the onset of CD. Timing of gluten introduction: The data suggest that both early (≤4 months) and late (≥7 months) introduction of gluten may increase the risk of CD. Amount of gluten at weaning (and later) and CD: One incident case-referent study documented that the introduction of gluten in large amounts compared with small or medium amounts increased the risk of CD.\n\nCONCLUSIONS:\nIn the absence of clear evidence, in order to decrease the risk of later coeliac disease, it is reasonable to avoid both early (\u003c4 months) and late (≥7 months) introduction of gluten, and to introduce gluten while the infant is still being breastfed. Future studies may clarify the remaining uncertainties." + }, + "questions": [ + { + "id": "f3a0cada-4852-4bc5-9340-66cc36f842c7", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 1099, + "text": "early (≤4 months) and late (≥7 months) introduction of gluten" + } + ] + } + ] +} \ No newline at end of file diff --git a/5d10be56-1c21-481d-a3c0-1f16a8c1bd32.json b/5d10be56-1c21-481d-a3c0-1f16a8c1bd32.json new file mode 100644 index 0000000000000000000000000000000000000000..ead9b0d72e82c33b087fed6d51f5949f9e789610 --- /dev/null +++ b/5d10be56-1c21-481d-a3c0-1f16a8c1bd32.json @@ -0,0 +1,38 @@ +{ + "id": "5d10be56-1c21-481d-a3c0-1f16a8c1bd32", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "10738048", + "text": "BACKGROUND:\nPrevious research has suggested that thiazide diuretics and beta-blockers may promote the development of type 2 diabetes mellitus. However, the results of previous studies have been inconsistent, and many studies have been limited by inadequate data on outcomes and by potential confounding.\n\nMETHODS:\nWe conducted a prospective study of 12,550 adults 45 to 64 years old who did not have diabetes. An extensive health evaluation conducted at base line included assessment of medication use and measurement of blood pressure with a random-zero sphygmomanometer. The incidence of new cases of diabetes was assessed after three years and after six years by measurement of serum glucose concentrations while the subjects were fasting.\n\nRESULTS:\nAfter simultaneous adjustment for age, sex, race, education, adiposity, family history with respect to diabetes, physical-activity level, other health-related behavior, and coexisting illnesses, subjects with hypertension who were taking thiazide diuretics were not at greater risk for the subsequent development of diabetes than were subjects with hypertension who were not receiving any antihypertensive therapy (relative hazard, 0.91; 95 percent confidence interval, 0.73 to 1.13). Likewise, subjects who were taking angiotensin-converting-enzyme inhibitors and calcium-channel antagonists were not at greater risk than those not taking any medication. In contrast, subjects with hypertension who were taking beta-blockers had a 28 percent higher risk of subsequent diabetes (relative hazard, 1.28; 95 percent confidence interval, 1.04 to 1.57).\n\nCONCLUSIONS:\nConcern about the risk of diabetes should not discourage physicians from prescribing thiazide diuretics to nondiabetic adults who have hypertension. The use of beta-blockers appears to increase the risk of diabetes, but this adverse effect must be weighed against the proven benefits of beta-blockers in reducing the risk of cardiovascular events." + }, + "questions": [ + { + "id": "9871907c-777b-47d5-8717-7aeeceb73bfb", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1422, + "text": "subjects with hypertension who were taking beta-blockers" + }, + { + "answer_start": 1769, + "text": "use of beta-blockers" + } + ] + } + ] +} \ No newline at end of file diff --git a/5d558be5-a351-48f7-a8ff-63ce91130540.json b/5d558be5-a351-48f7-a8ff-63ce91130540.json new file mode 100644 index 0000000000000000000000000000000000000000..cc1b46fb5c2c17e7a8a68d60bd250527f3aa6bfe --- /dev/null +++ b/5d558be5-a351-48f7-a8ff-63ce91130540.json @@ -0,0 +1,39 @@ +{ + "id": "5d558be5-a351-48f7-a8ff-63ce91130540", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "29326337", + "text": "CONTEXT:\nThe association between acid-suppressive drug exposure during pregnancy and childhood asthma has not been well established.\n\nOBJECTIVE:\nTo conduct a systematic review and meta-analysis on this association to provide further justification for the current studies.\n\nDATA SOURCES:\nWe searched PubMed, Medline, Embase, the Cochrane Database of Systematic Reviews, EBSCO Information Services, Web of Science, and Google Scholar from inception until June 2017.\n\nSTUDY SELECTION:\nObservational studies in which researchers assessed acid-suppressive drug use during pregnancy and the risk of childhood asthma were included.\n\nDATA EXTRACTION:\nOf 556 screened articles, 8 population-based studies were included in the final analyses.\n\nRESULTS:\nWhen all the studies were pooled, acid-suppressive drug use in pregnancy was associated with an increased risk of asthma in childhood (relative risk [RR] = 1.45; 95% confidence interval [CI] 1.35-1.56; I = 0%; \u003c .00001). The overall risk of asthma in childhood increased among proton pump inhibitor users (RR = 1.34; 95% CI 1.18-1.52; I = 46%; \u003c .00001) and histamine-2 receptor antagonist users (RR = 1.57; 95% CI 1.46-1.69; I = 0%; \u003c .00001).\n\nLIMITATIONS:\nNone of the researchers in the studies in this meta-analysis adjusted for the full panel of known confounders in these associations.\n\nCONCLUSIONS:\nThe evidence suggests that prenatal, maternal, acid-suppressive drug use is associated with an increased risk of childhood asthma. This information may help clinicians and parents to use caution when deciding whether to take acid-suppressing drugs during pregnancy because of the risk of asthma in offspring." + }, + "questions": [ + { + "id": "5441d254-32e8-4c46-abfa-11967bcf873d", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 777, + "text": "acid-suppressive drug use in pregnancy" + }, + { + "answer_start": 1376, + "text": "prenatal, maternal, acid-suppressive drug use" + } + ] + } + ] +} \ No newline at end of file diff --git a/5d5c3083-f55a-4cdd-be0d-f7c6c255d54c.json b/5d5c3083-f55a-4cdd-be0d-f7c6c255d54c.json new file mode 100644 index 0000000000000000000000000000000000000000..e018f8a77f7a50e52089beefed22b018c4cb484f --- /dev/null +++ b/5d5c3083-f55a-4cdd-be0d-f7c6c255d54c.json @@ -0,0 +1,43 @@ +{ + "id": "5d5c3083-f55a-4cdd-be0d-f7c6c255d54c", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "29678946", + "text": "Antibiotic use during infancy alters gut microbiota and immune development and is associated with an increased risk of childhood asthma. The impact of prenatal antibiotic exposure is unclear. We sought to characterise the association between prenatal antibiotic exposure and childhood asthma.We performed a population-based cohort study using prescription records, hospitalisation records and physician billing claims from 213 661 mother-child dyads born in Manitoba, Canada between 1996 and 2012. Associations were determined using Cox regression, adjusting for maternal asthma, postnatal antibiotics and other potential confounders. Sensitivity analyses evaluated maternal antibiotic use before and after pregnancy.36.8% of children were exposed prenatally to antibiotics and 10.1% developed asthma. Prenatal antibiotic exposure was associated with an increased risk of asthma (adjusted hazard ratio (aHR) 1.23, 95% CI 1.20-1.27). There was an apparent dose response (aHR 1.15, 95% CI 1.11-1.18 for one course; aHR 1.26, 95% CI 1.21-1.32 for two courses; and aHR 1.51, 95% CI 1.44-1.59 for three or more courses). Maternal antibiotic use during 9 months before pregnancy (aHR 1.27, 95% CI 1.24-1.31) and 9 months postpartum (aHR 1.32, 95% CI 1.28-1.36) were similarly associated with asthma.Prenatal antibiotic exposure was associated with a dose-dependent increase in asthma risk. However, similar associations were observed for maternal antibiotic use before and after pregnancy, suggesting the association is either not directly causal, or not specific to pregnancy." + }, + "questions": [ + { + "id": "3297ade1-2897-46bd-9311-761bb0d97937", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1116, + "text": "Maternal antibiotic use during 9 months before pregnancy" + }, + { + "answer_start": 1293, + "text": "Prenatal antibiotic exposure" + }, + { + "answer_start": 1432, + "text": "maternal antibiotic use before and after pregnancy" + } + ] + } + ] +} \ No newline at end of file diff --git a/5db4f55e-f11f-4cac-b8a6-c20c1baaad0b.json b/5db4f55e-f11f-4cac-b8a6-c20c1baaad0b.json new file mode 100644 index 0000000000000000000000000000000000000000..d9f50b8fc12d83e31351b9afdeecb63aa74cae7b --- /dev/null +++ b/5db4f55e-f11f-4cac-b8a6-c20c1baaad0b.json @@ -0,0 +1,35 @@ +{ + "id": "5db4f55e-f11f-4cac-b8a6-c20c1baaad0b", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "31391220", + "text": "BACKGROUND:\nEmerging evidence suggests that air pollution may contribute to childhood asthma development. We estimated the burden of incident childhood asthma that may be attributable to outdoor nitrogen dioxide (NO), particulate matter ≤2.5 µm in diameter (PM) and black carbon (BC) in Europe.\n\nMETHODS:\nWe combined country-level childhood incidence rates and pooled exposure-response functions with childhood (age 1-14 years) population counts, and exposure estimates at 1 540 386 1 km×1 km cells, across 18 European countries and 63 442 419 children. Annual average pollutant concentrations were obtained from a validated and harmonised European land-use regression model. We investigated two exposure reduction scenarios. For the first, we used recommended annual World Health Organization (WHO) air quality guideline values. For the second, we used the minimum air pollution levels recorded across 41 studies in the underlying meta-analysis.\n\nRESULTS:\nNO ranged from 1.4 to 70.0 µg·m, with a mean of 11.8 µg·m. PM ranged from 2.0 to 41.1 µg·m, with a mean of 11.6 µg·m. BC ranged from 0.003 to 3.7×10 m, with a mean of 1.0×10 m. Compliance with the NO and PM WHO guidelines was estimated to prevent 2434 (0.4%) and 66 567 (11%) incident cases, respectively. Meeting the minimum air pollution levels for NO (1.5 µg·m), PM (0.4 µg·m) and BC (0.4×10 m) was estimated to prevent 135 257 (23%), 191 883 (33%) and 89 191 (15%) incident cases, respectively.\n\nCONCLUSIONS:\nA significant proportion of childhood asthma cases may be attributable to outdoor air pollution and these cases could be prevented. Our estimates underline an urgent need to reduce children's exposure to air pollution." + }, + "questions": [ + { + "id": "438f9660-52b6-4963-8379-56db2bb151af", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1544, + "text": "outdoor air pollution" + } + ] + } + ] +} \ No newline at end of file diff --git a/5ed1272a-f746-433b-899b-39d7779c3e8f.json b/5ed1272a-f746-433b-899b-39d7779c3e8f.json new file mode 100644 index 0000000000000000000000000000000000000000..776cdd09820476ccbf9ec5d6251adfed50ba474c --- /dev/null +++ b/5ed1272a-f746-433b-899b-39d7779c3e8f.json @@ -0,0 +1,34 @@ +{ + "id": "5ed1272a-f746-433b-899b-39d7779c3e8f", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "28228423", + "text": "We previously found that the introduction of small quantities of gluten at 4-6 mo of age did not reduce the risk of celiac disease (CD) in a group of high-risk children. However, the consumption of high amounts of gluten early in life has been suggested to increase CD risk. The aim of this study was to evaluate this hypothesis by using data from the previous study of the PreventCD trial (www.preventcd.com). Gluten intake was prospectively quantified by using specific food records between 11 and 36 mo of age in 715 children positive for the human leukocyte antigen ()- and/or from 5 European countries. According to the PreventCD protocol, infants received 100 mg immunologically active gluten/d or placebo from 4 to 6 mo of age, with a stepwise and fixed gluten increase until age 10 mo and unrestricted intake thereafter. The primary outcome of the present study was the impact of the amount of gluten consumed from age 10 mo onward on CD development. Mean daily gluten intakes from 10 mo onward were significantly different between countries for children at all ages ( \u003c 0.001) but not between children who developed CD and those who did not within the same country ( \u003e 0.05). The variables country, sex, intervention group, and gluten consumption pattern did not show significant associations with CD development risk (HRs not significant). In addition, the interaction between risk group and gluten consumption pattern showed no significant risk on CD development, except for the DQ2.2/DQ7 haplotype (HR: 5.81; 95% CI: 1.18, 28.74; = 0.031). Gluten consumption patterns as well as the amount of gluten consumed at 11-36 mo of age do not influence CD development for most related genotypes in children with a genetic risk. This study reports the gluten consumption pattern in children at risk of CD from different European countries. This trial was registered at www.controlled-trials.com as ISRCTN74582487." + }, + "questions": [ + { + "id": "77c1dabc-f7fb-4439-b960-37c8ec29eaa5", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 1490, + "text": "DQ2.2/DQ7 haplotype" + } + ] + } + ] +} \ No newline at end of file diff --git a/5eef2632-2a4b-42b3-9d22-380e7db399b6.json b/5eef2632-2a4b-42b3-9d22-380e7db399b6.json new file mode 100644 index 0000000000000000000000000000000000000000..8acdc0170c5650084f76b222532aefffd7ca61db --- /dev/null +++ b/5eef2632-2a4b-42b3-9d22-380e7db399b6.json @@ -0,0 +1,42 @@ +{ + "id": "5eef2632-2a4b-42b3-9d22-380e7db399b6", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "31184362", + "text": "BACKGROUND:\nInsulin resistance has been proposed as a mediator of the increased cancer incidence and mortality associated with obesity. However, prior studies included limited cancer deaths and had inconsistent findings. Therefore, we evaluated insulin resistance and cancer-specific and all-cause mortality in postmenopausal women participating in the Women's Health Initiative (WHI).\n\nMETHODS:\nEligible were a subsample of 22 837 WHI participants aged 50-79 years enrolled at 40 US clinical centers from 1993 to 1998 who had baseline fasting glucose and insulin levels. Baseline insulin resistance was measured by the homeostasis model assessment of insulin resistance (HOMA-IR). Cancers were verified by central medical record review and deaths verified by medical record and death certificate review enhanced by National Death Index queries. Cox proportional hazards regression models were used to calculate adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for cancer-specific and all-cause mortality. All statistical tests were two-sided.\n\nRESULTS:\nDuring a median of 18.9 years of follow-up, 1820 cancer deaths and 7415 total deaths occurred. Higher HOMA-IR quartile was associated with higher cancer-specific mortality (Q4 vs Q1, HR = 1.26, 95% CI = 1.09 to 1.47; Ptrend = .003) and all-cause mortality (Q4 vs Q1, HR = 1.63, 95% CI = 1.51 to 1.76; Ptrend \u003c .001). A sensitivity analysis for diabetes status did not change findings. Among women with body mass index less than 25 kg/m2, higher HOMA-IR quartile was associated with higher cancer mortality (Fine and Gray, P = .004).\n\nCONCLUSIONS:\nHigh insulin resistance, as measured by HOMA-IR, identifies postmenopausal women at higher risk for cancer-specific and all-cause mortality who could potentially benefit from early intervention." + }, + "questions": [ + { + "id": "eb8b6c55-8a4e-4aac-b556-c9bddd3329ce", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1164, + "text": "Higher HOMA-IR" + }, + { + "answer_start": 620, + "text": "homeostasis model assessment of insulin resistance (HOMA-IR)" + }, + { + "answer_start": 1616, + "text": "High insulin resistance, as measured by HOMA-IR" + } + ] + } + ] +} \ No newline at end of file diff --git a/5f73ac5b-c85f-489b-aba5-b5be86c19752.json b/5f73ac5b-c85f-489b-aba5-b5be86c19752.json new file mode 100644 index 0000000000000000000000000000000000000000..e38166b0873201b0c98d62bad52025184fdfcb34 --- /dev/null +++ b/5f73ac5b-c85f-489b-aba5-b5be86c19752.json @@ -0,0 +1,34 @@ +{ + "id": "5f73ac5b-c85f-489b-aba5-b5be86c19752", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "20548009", + "text": "BACKGROUND:\nBecause of differences in processing and nutrients, brown rice and white rice may have different effects on risk of type 2 diabetes mellitus. We examined white and brown rice consumption in relation to type 2 diabetes risk prospectively in the Health Professionals Follow-up Study and the Nurses' Health Study I and II.\n\nMETHODS:\nWe prospectively ascertained and updated diet, lifestyle practices, and disease status among 39,765 men and 157,463 women in these cohorts.\n\nRESULTS:\nAfter multivariate adjustment for age and other lifestyle and dietary risk factors, higher intake of white rice (\u003e or =5 servings per week vs \u003c1 per month) was associated with a higher risk of type 2 diabetes: pooled relative risk (95% confidence interval [CI]), 1.17 (1.02-1.36). In contrast, high brown rice intake (\u003e or =2 servings per week vs \u003c1 per month) was associated with a lower risk of type 2 diabetes: pooled relative risk, 0.89 (95% CI, 0.81-0.97). We estimated that replacing 50 g/d (cooked,equivalent to one-third serving per day) intake of white rice with the same amount of brown rice was associated with a 16% (95% CI, 9%-21%) lower risk of type 2 diabetes,whereas the same replacement with whole grains as a group was associated with a 36% (30%-42%) lower diabetes risk [corrected].\n\nCONCLUSIONS:\nSubstitution of whole grains, including brown rice, for white rice may lower risk of type 2 diabetes. These data support the recommendation that most carbohydrate intake should come from whole grains rather than refined grains to help prevent type 2 diabetes." + }, + "questions": [ + { + "id": "60c12043-c65c-4520-9709-7f6ddfb6eb28", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 576, + "text": "higher intake of white rice (\u003e or =5 servings per week vs \u003c1 per month)" + } + ] + } + ] +} \ No newline at end of file diff --git a/60143c7c-060c-4d55-bd87-3987a260a936.json b/60143c7c-060c-4d55-bd87-3987a260a936.json new file mode 100644 index 0000000000000000000000000000000000000000..49a18ddb3373b67fd212e54c9747788ab064ba10 --- /dev/null +++ b/60143c7c-060c-4d55-bd87-3987a260a936.json @@ -0,0 +1,34 @@ +{ + "id": "60143c7c-060c-4d55-bd87-3987a260a936", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "25833979", + "text": "BACKGROUND:\nEvidence for a role of dietary risk factors in the cause of breast cancer has been inconsistent. The evaluation of overall dietary patterns instead of foods in isolation may better reflect the nature of true dietary exposure in a population.\n\nOBJECTIVE:\nWe used 2 cohort studies to identify and confirm associations between dietary patterns and breast cancer risk.\n\nDESIGN:\nDietary patterns were derived by using a principal components factor analysis in 1097 breast cancer cases and an age-stratified subcohort of 3320 women sampled from 39,532 female participants in the Canadian Study of Diet, Lifestyle and Health (CSDLH). We conducted a confirmatory factor analysis in 49,410 subjects in the National Breast Screening Study (NBSS) in whom 3659 cases of incident breast cancer developed. Cox regression models were used to estimate HRs for the association between derived dietary factors and risk of breast cancer in both cohorts.\n\nRESULTS:\nThe following 3 dietary factors were identified from the CSDLH: healthy, ethnic, and meat and potatoes. In the CSDLH, the healthy dietary pattern was associated with reduced risk of breast cancer (HR for high compared with low quintiles: 0.73; 95% CI: 0.58, 0.91; P-trend = 0.001), and the meat and potatoes dietary pattern was associated with increased risk in postmenopausal women only (HR for high compared with low quintiles: 1.26; 95% CI: 0.92, 1.73; P-trend = 0.043). In the NBSS, the association between the meat and potatoes pattern and postmenopausal breast cancer risk was confirmed (HR: 1.31; 95% CI: 0.98, 1.76; P-trend = 0.043), but there was no association between the healthy pattern and risk of breast cancer.\n\nCONCLUSION:\nAdherence to a plant-based diet that limits red meat intake may be associated with reduced risk of breast cancer, particularly in postmenopausal women." + }, + "questions": [ + { + "id": "dd7fc23a-c981-4ce5-8247-3b24f12bef22", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1247, + "text": "meat and potatoes dietary pattern" + } + ] + } + ] +} \ No newline at end of file diff --git a/60830f14-ce46-4e6f-b427-3d77d20d0460.json b/60830f14-ce46-4e6f-b427-3d77d20d0460.json new file mode 100644 index 0000000000000000000000000000000000000000..3550a06607b57fc6aa1c55c1ed86da3be3a7190d --- /dev/null +++ b/60830f14-ce46-4e6f-b427-3d77d20d0460.json @@ -0,0 +1,40 @@ +{ + "id": "60830f14-ce46-4e6f-b427-3d77d20d0460", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "2220830", + "text": "Several research projects on work-related respiratory diseases have been conducted in Finland. One of the largest, \"Farmers' Occupational Health Programme,\" was conducted by the Social Insurance Institution of Finland during 1973-1983 in cooperation with Kuopio Regional Institute of Occupational Health and the National Board of Health. The main objective of the program was to develop a model for occupational health services for farmers. As a part of the program, postal surveys were conducted in 1979 and 1982. The surveys allowed an analysis of both the prevalence and the mean annual incidence of asthma, farmer's lung, and chronic bronchitis as well as of background variables related to the diseases. More than every tenth farmer suffered from these respiratory diseases. The occurrence of chronic bronchitis (the most common disease) was, in general, related to farming types in which grain crops (including animal feeds) were handled. Chronic bronchitis was most prevalent among farmers who worked in piggeries, implying a combined effect of grain dusts, dusts of animal origin, and development of the disease. Atopy predisposed to and had an additive effect with smoking on chronic bronchitis." + }, + "questions": [ + { + "id": "e89fcad5-b448-4fa0-afd5-abdb2ea52c26", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 871, + "text": "farming types in which grain crops (including animal feeds) were handled" + }, + { + "answer_start": 989, + "text": "farmers who worked in piggeries" + } + ] + } + ] +} \ No newline at end of file diff --git a/609be1b6-57b2-4e91-817f-020a1278ae72.json b/609be1b6-57b2-4e91-817f-020a1278ae72.json new file mode 100644 index 0000000000000000000000000000000000000000..8143e10030e6f55394588b057d3803749703e1f9 --- /dev/null +++ b/609be1b6-57b2-4e91-817f-020a1278ae72.json @@ -0,0 +1,38 @@ +{ + "id": "609be1b6-57b2-4e91-817f-020a1278ae72", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "17634245", + "text": "OBJECTIVES:\nAir pollution has been associated with an increased risk for lung cancer. We examined whether long-term air pollution is associated with bladder cancer risk.\n\nMETHODS:\nInformation from a case-control study in Spain that included 1219 incident cases and 1271 hospital controls was used. Information on residential history including several indicators of exposure to air pollution and other potential risk factors was collected in a face-to-face computerised personal interview. Odds ratios (OR) and 95% confidence intervals (95% CI) were adjusted for age, gender, region, smoking, occupation, water contaminants and diet.\n\nRESULTS:\nLiving more than 40 years in a city with a population of more than 100 000 was associated with an increased risk for bladder cancer overall (OR 1.30, 95% CI 1.04 to 1.63). Emissions of polycyclic aromatic hydrocarbons and diesel from industries near the residence, as evaluated by experts, were associated with an increased risk (OR 1.29, 95% CI 0.85 to 1.98), while lower or no excess risks were observed for other pollution-related variables. Odds ratios among never smokers tended to be higher than among smokers.\n\nCONCLUSIONS:\nThe small to moderate positive associations found for several indices of air pollution and bladder cancer, while suggestive of excess risk, require further evaluation in other settings." + }, + "questions": [ + { + "id": "79020f31-f242-4220-9c8d-8bc75a4344c5", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 643, + "text": "Living more than 40 years in a city with a population of more than 100 000" + }, + { + "answer_start": 815, + "text": "Emissions of polycyclic aromatic hydrocarbons and diesel from industries near the residence" + } + ] + } + ] +} \ No newline at end of file diff --git a/60b816a2-2512-471d-a4d2-e6c72fb370fa.json b/60b816a2-2512-471d-a4d2-e6c72fb370fa.json new file mode 100644 index 0000000000000000000000000000000000000000..4a60f5cee81b984c5ecaa282bc3c1493642aa347 --- /dev/null +++ b/60b816a2-2512-471d-a4d2-e6c72fb370fa.json @@ -0,0 +1,43 @@ +{ + "id": "60b816a2-2512-471d-a4d2-e6c72fb370fa", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "24190118", + "text": "PURPOSE:\nSteroid hormones, particularly androgens, play a major role in prostatic carcinogenesis. Personal history of severe acne, a surrogate for higher androgen activity, has been associated with an increased risk of prostate cancer (PCa), and one recent study indicated that severe teenage acne was a novel risk factor for melanoma. These findings suggest a possible relationship between PCa and risk of melanoma. We prospectively evaluated this association among US men.\n\nMETHODS:\nA total of 42,372 participants in the Health Professionals' Follow-Up Study (HPFS; 1986 to 2010) were included. Biennially self-reported PCa diagnosis was confirmed using pathology reports. Diagnosis of melanoma and nonmelanoma skin cancer (NMSC) was self-reported biennially, and diagnosis of melanoma was pathologically confirmed. We sought to confirm the association in 18,603 participants from the Physicians' Health Study (PHS; 1982 to 1998).\n\nRESULTS:\nWe identified 539 melanomas in the HPFS. Personal history of PCa was associated with an increased risk of melanoma (multivariate-adjusted hazard ratio [HR], 1.83; 95% CI, 1.32 to 2.54). Although we also detected a marginally increased risk of NMSC associated with PCa (HR, 1.08; 95% CI, 0.995 to 1.16), the difference in the magnitude of the association between melanoma and NMSC was significant (P for heterogeneity = .002). We did not find an altered risk of melanoma associated with personal history of other cancers. The association between PCa and risk of incident melanoma was confirmed in the PHS (HR, 2.17; 95% CI, 1.12 to 4.21).\n\nCONCLUSION:\nPersonal history of PCa is associated with an increased risk of melanoma, which may not be entirely a result of greater medical scrutiny." + }, + "questions": [ + { + "id": "fbc5c9fd-f971-4783-9ad9-c9b449f2b58e", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 219, + "text": "prostate cancer (PCa)" + }, + { + "answer_start": 1594, + "text": "Personal history of PCa" + }, + { + "answer_start": 984, + "text": "Personal history of PCa" + } + ] + } + ] +} \ No newline at end of file diff --git a/61332fa1-a939-44c9-a8ad-5d88eb144bce.json b/61332fa1-a939-44c9-a8ad-5d88eb144bce.json new file mode 100644 index 0000000000000000000000000000000000000000..bcc4b70b479b18243f3ae97b1311271f63dea47a --- /dev/null +++ b/61332fa1-a939-44c9-a8ad-5d88eb144bce.json @@ -0,0 +1,37 @@ +{ + "id": "61332fa1-a939-44c9-a8ad-5d88eb144bce", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "29706374", + "text": "BACKGROUND:\nThe management and life expectancy of patients with cystic fibrosis have improved substantially in the past three decades, which has resulted in an increased number of these patients being diagnosed with malignancies. Our aim was to assess the risk of gastrointestinal cancers in patients with cystic fibrosis.\n\nMETHODS:\nIn this systematic review and meta-analysis, we searched PubMed, MEDLINE, Google Scholar, Scopus, Embase, and Cochrane databases with no language restrictions for studies published from inception of the databases to Aug 1, 2017, assessing the risk of gastrointestinal cancers in patients with cystic fibrosis. We also searched abstracts from scientific meetings and the bibliographies of identified articles for additional references. Studies were included if they reported the standardised incidence ratio (SIR) or incidence ratio per person-years. No exclusion criteria with regard to patient characteristics (age, sex, comorbidities, cystic fibrosis mutation type), study setting (location and time period), or method of reporting cancer diagnoses were applied. The primary outcome was risk of gastrointestinal cancer and site-specific gastrointestinal cancers in patients with cystic fibrosis compared with the general population. Pooled summary estimates were calculated using a random-effects model, and subgroup analyses were done to establish whether risk of gastrointestinal cancer varied according to patient lung transplant status. The study is registered with PROSPERO, number CRD42017075396.\n\nFINDINGS:\nOur search identified 95 681 records, of which six cohort studies including 99 925 patients (544 695 person-years) were eligible for the meta-analysis. The overall risk of gastrointestinal cancer was significantly higher in patients with cystic fibrosis than in the general population (pooled SIR 8·13, 95% CI 6·48-10·21; p\u003c0·0001; log SIR 2·10, 95% CI 1·87-2·32; p\u003c0·0001, I=93·93%). Subgroup analyses showed that the risk of gastrointestinal cancer among patients with cystic fibrosis who had a lung transplant was increased compared with that of patients who did not receive a transplant (pooled SIR 21·13, 95% CI 14·82-30·14; p\u003c0·0001; log SIR 3·05, 95% CI 2·70-3·41; p\u003c0·0001, I=28·52% vs pooled SIR 4·18, 3·10-5·62; p\u003c0·0001; log SIR 1·43, 1·13-1·73; p\u003c0·0001, I=22·66%). The risk for the following site-specific cancers was also significantly increased in patients with cystic fibrosis compared with the general population: small bowel cancer (pooled SIR 18·94, 95% CI 9·37-38·27; p\u003c0·0001; log SIR 2·94, 95% CI 2·24-3·64; p\u003c0·0001, I=38·61%), colon cancer (10·91, 8·42-14·11; p\u003c0·0001; log SIR 2·39, 2·13-2·65; p\u003c0·0001, I=88·09%), biliary tract cancer (17·87, 8·55-37·36; p\u003c0·0001; log SIR 2·88, 2·15-3·62; p\u003c0·0001, I=10·16%), and pancreatic cancer (6·18, 1·31-29·27; p=0·022; log SIR 1·82, 0·27-3·38; p\u003c0·0001, I=62·57%).\n\nINTERPRETATION:\nOur study suggests that patients with cystic fibrosis had a significantly increased risk of gastrointestinal cancer compared with the general population, including small bowel, colon, biliary tract, and pancreatic cancers. These findings highlight the need to develop individualised screening strategies for site-specific gastrointestinal cancers in patients with cystic fibrosis.\n\nFUNDING:\nNone." + }, + "questions": [ + { + "id": "8b2b0756-8289-4932-8fb9-8f0b4212b704", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 2412, + "text": "patients with cystic fibrosis" + } + ] + } + ] +} \ No newline at end of file diff --git a/61740f3f-830f-4c02-a201-df116b870148.json b/61740f3f-830f-4c02-a201-df116b870148.json new file mode 100644 index 0000000000000000000000000000000000000000..6bf29dd265e7093f5c4c1d17773e4a14a0836021 --- /dev/null +++ b/61740f3f-830f-4c02-a201-df116b870148.json @@ -0,0 +1,50 @@ +{ + "id": "61740f3f-830f-4c02-a201-df116b870148", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "17090613", + "text": "AIMS:\nObesity is a risk factor for an acute coronary syndrome (ACS). The association between elevated body mass index (BMI) and ACS is independent of most traditional risk factors, suggesting a possible contribution of other body fat-related mediators. This study evaluated the association between adiponectin and ACS.\n\nMETHODS AND RESULTS:\nFour hundred and ninety-nine patients undergoing coronary angiography were divided into a subgroup without (n = 331) and with ACS (n = 168). In multiple regression analysis, higher adiponectin levels were independently associated with a lower risk of ACS [odds ratio (OR) = 0.61; 95% CIs: 0.46-0.81; P \u003c 0.001]. In contrast, a higher BMI, a history of myocardial infarction, C-reactive protein, and angiographic coronary artery disease severity were all associated with a higher risk. The greatest increase in risk for ACS was seen at adiponectin levels \u003c or = 5.5 microg/mL.\n\nCONCLUSION:\nHigher plasma adiponectin levels are independently associated with a lower risk of ACS." + }, + "questions": [ + { + "id": "5fbd9f2b-2d57-4175-9278-32137a00b9b0", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 668, + "text": "higher BMI" + }, + { + "answer_start": 682, + "text": "history of myocardial infarction" + }, + { + "answer_start": 716, + "text": "C-reactive protein" + }, + { + "answer_start": 740, + "text": "angiographic coronary artery disease severity" + }, + { + "answer_start": 876, + "text": "adiponectin levels \u003c or = 5.5 microg/mL" + } + ] + } + ] +} \ No newline at end of file diff --git a/61e985cf-6ab4-47cf-887d-f97edf176db7.json b/61e985cf-6ab4-47cf-887d-f97edf176db7.json new file mode 100644 index 0000000000000000000000000000000000000000..9a493cfa5936d1c4d0207978949c858e2a554729 --- /dev/null +++ b/61e985cf-6ab4-47cf-887d-f97edf176db7.json @@ -0,0 +1,34 @@ +{ + "id": "61e985cf-6ab4-47cf-887d-f97edf176db7", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "23411105", + "text": "Although family history (FH) of coronary artery disease (CAD) is considered a risk factor for future cardiovascular events, the prevalence, extent, severity, and prognosis of young patients with FH of CAD have been inadequately studied. From 27,125 consecutive patients who underwent coronary computed tomographic angiography, 6,308 young patients (men aged \u003c55 years and women aged \u003c65 years) without known CAD were identified. Obstructive CAD was defined as \u003e50% stenosis in a coronary artery \u003e2 mm diameter. Risk-adjusted logistic regression, Kaplan-Meier, and Cox proportional-hazards models were used to compare patients with and without FH of CAD. Compared with subjects without FH of CAD, those with FH of CAD (FH+) had higher prevalences of any CAD (40% vs 30%, p \u003c0.001) and obstructive CAD (11% vs 7%, p \u003c0.001), with multivariate odds of FH+ increasing the likelihood of obstructive CAD by 71% (p \u003c0.001). After a mean follow-up period of 2 ± 1 years (42 myocardial infarctions and 39 all-cause deaths), FH+ patients experienced higher annual rates of myocardial infarction (0.5% vs 0.2%, log-rank p = 0.001), with a positive FH the strongest predictor of myocardial infarction (hazard ratio 2.6, 95% confidence interval 1.4 to 4.8, p = 0.002). In conclusion, young FH+ patients have higher presence, extent, and severity of CAD, which are associated with increased risk for myocardial infarction. Compared with other clinical CAD risk factors, positive FH in young patients is the strongest clinical predictor of future unheralded myocardial infarction." + }, + "questions": [ + { + "id": "297f48b3-712b-48df-965a-891dfa953879", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 9, + "text": "family history (FH) of coronary artery disease (CAD)" + } + ] + } + ] +} \ No newline at end of file diff --git a/6274cf5a-2ad1-4971-add1-2063a3648ba8.json b/6274cf5a-2ad1-4971-add1-2063a3648ba8.json new file mode 100644 index 0000000000000000000000000000000000000000..30bc5d4ff8e1f3f97b49a89a8be638596dd5e04f --- /dev/null +++ b/6274cf5a-2ad1-4971-add1-2063a3648ba8.json @@ -0,0 +1,38 @@ +{ + "id": "6274cf5a-2ad1-4971-add1-2063a3648ba8", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "11344202", + "text": "Polycystic ovary syndrome (PCOS), one of the most common endocrine disorders of reproductive age women, is associated with an increased risk of type 2 diabetes mellitus. Defects in both insulin action and insulin secretion contribute to this predisposition to diabetes, but the extent to which these defects are heritable among PCOS families has not been examined. In the present study we used the frequently sampled iv glucose tolerance test to quantitate insulin secretion (AIRg), insulin action (Si), and their product (AIRg x Si) among women with PCOS (n = 33) and their nondiabetic first degree relatives (n = 48). We then quantitated the heritability of these measures from familial correlations estimated within a genetic model. Familial (spousal, rhoMF; parent-offspring, rhoPO; and sibling, rhoSS) correlations were derived for log-transformed body mass index (BMI) as well as for AIRg, Si, and AIRg x Si, the latter three of which were adjusted for BMI. There was no evidence of significant heritability for either lnBMI or lnSi in these families. In contrast, the sibling correlation (rhoSS = 0.74) for lnAIRg was highly significant (chi(2) = 7.65; 1 df; P = 0.006). In addition, the parameter quantitating insulin secretion in relation to insulin sensitivity [i.e. ln(AIRg x Si)] was significant among siblings (rho(SS) = 0.74; chi(2) = 4.32; 1 df; P = 0.04). In summary, the results of the present study indicate that there is an heritable component to beta-cell dysfunction in families of women with PCOS. We conclude that heritability of beta-cell dysfunction is likely to be a significant factor in the predisposition to diabetes in PCOS." + }, + "questions": [ + { + "id": "06bd329b-10a6-40f2-9a8a-3affddd37345", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 0, + "text": "Polycystic ovary syndrome (PCOS)" + }, + { + "answer_start": 1649, + "text": "PCOS" + } + ] + } + ] +} \ No newline at end of file diff --git a/6282783f-33ce-4b12-8340-447da74fbd07.json b/6282783f-33ce-4b12-8340-447da74fbd07.json new file mode 100644 index 0000000000000000000000000000000000000000..cd4a36e194e74a42d774e37073b70201ad9de7fd --- /dev/null +++ b/6282783f-33ce-4b12-8340-447da74fbd07.json @@ -0,0 +1,35 @@ +{ + "id": "6282783f-33ce-4b12-8340-447da74fbd07", + "disease": { + "id": "H00056", + "names": [ + "Alzheimer disease", + "Dementia due to Alzheimer disease" + ], + "dbLinks": { + "icd10": [ + "G30" + ], + "mesh": [ + "D000544" + ] + }, + "category": "Neurodegenerative disease" + }, + "article": { + "id": "8609748", + "text": "BACKGROUND:\nVascular causes of dementia may be more common than supposed. Vascular factors may also have a role in late-onset Alzheimer's disease, but the role of hypertension in the development of dementia is unclear.\n\nMETHODS:\nAs part of the Longitudinal Population Study of 70-year-olds in Göteborg, Sweden, we analysed the relation between blood pressure and the development of dementia in the age intervals 70-75, 75-79, and 79-85 years in those non-demented at age 70 (n = 382). The sample was followed up for 15 years and examined repeatedly with a comprehensive investigation, including a psychiatric and physical examination. a\n\nFINDINGS:\nParticipants who developed dementia at age 79-85 had higher systolic blood pressure at age 70 (mean 178 vs 164 mm Hg, p = 0.034) and higher diastolic blood pressure at ages 70 (101 vs 92, p = 0.004) and 75 (97 vs 90, p = 0.022) than those who did not develop dementia. For subtypes of dementia, higher diastolic blood pressure was recorded at age 70 (101, p = 0.019) for those developing Alzheimer's disease and at age 75 (101, p = 0.015) for those developing vascular dementia than for those who did not develop dementia. Participants with white-matter lesions on computed tomography at age 85 had higher blood pressure at age 70 than those without such lesions. Blood pressure declined in the years before dementia onset and was then similar to or lower than that in non-demented individuals.\n\nINTERPRETATION:\nPreviously increased blood pressure may increase the risk for dementia by inducing small-vessel disease and white-matter lesions. To what extent the decline in blood pressure before dementia onset is a consequence or a cause of the brain disease remains to be elucidated." + }, + "questions": [ + { + "id": "bdd29d55-5b50-40ee-b83d-afb59bb81e36", + "text": "What are the risk factors of Alzheimer disease?", + "answers": [ + { + "answer_start": 943, + "text": "higher diastolic blood pressure was recorded at age 70" + } + ] + } + ] +} \ No newline at end of file diff --git a/62fe48e3-5fd8-4b10-8d43-c11bcbc93c29.json b/62fe48e3-5fd8-4b10-8d43-c11bcbc93c29.json new file mode 100644 index 0000000000000000000000000000000000000000..bb62b45a45812e523b4164c9f263f176edc72285 --- /dev/null +++ b/62fe48e3-5fd8-4b10-8d43-c11bcbc93c29.json @@ -0,0 +1,34 @@ +{ + "id": "62fe48e3-5fd8-4b10-8d43-c11bcbc93c29", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "18390796", + "text": "OBJECTIVE:\nThe purpose of this study was to examine the association between fruit, vegetable, and fruit juice intake and development of type 2 diabetes.\n\nRESEARCH DESIGN AND METHODS:\nA total of 71,346 female nurses aged 38-63 years who were free of cardiovascular disease, cancer, and diabetes in 1984 were followed for 18 years, and dietary information was collected using a semiquantitative food frequency questionnaire every 4 years. Diagnosis of diabetes was self-reported.\n\nRESULTS:\nDuring follow-up, 4,529 cases of diabetes were documented, and the cumulative incidence of diabetes was 7.4%. An increase of three servings/day in total fruit and vegetable consumption was not associated with development of diabetes (multivariate-adjusted hazard ratio 0.99 [95% CI 0.94-1.05]), whereas the same increase in whole fruit consumption was associated with a lower hazard of diabetes (0.82 [0.72-0.94]). An increase of 1 serving/day in green leafy vegetable consumption was associated with a modestly lower hazard of diabetes (0.91 [0.84-0.98]), whereas the same change in fruit juice intake was associated with an increased hazard of diabetes (1.18 [1.10-1.26]).\n\nCONCLUSIONS:\nConsumption of green leafy vegetables and fruit was associated with a lower hazard of diabetes, whereas consumption of fruit juices may be associated with an increased hazard among women." + }, + "questions": [ + { + "id": "9134f0be-136f-4276-a609-38e451f27de2", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1281, + "text": "consumption of fruit juices" + } + ] + } + ] +} \ No newline at end of file diff --git a/630be024-9356-4cfb-85bf-432fd624cf72.json b/630be024-9356-4cfb-85bf-432fd624cf72.json new file mode 100644 index 0000000000000000000000000000000000000000..c41d91c6e939282da85172650cd9e2d37e09e377 --- /dev/null +++ b/630be024-9356-4cfb-85bf-432fd624cf72.json @@ -0,0 +1,35 @@ +{ + "id": "630be024-9356-4cfb-85bf-432fd624cf72", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "26124488", + "text": "PURPOSE:\nCitrus products are widely consumed foods that are rich in psoralens and furocoumarins, a group of naturally occurring chemicals with potential photocarcinogenic properties. We prospectively evaluated the risk of cutaneous malignant melanoma associated with citrus consumption.\n\nMETHODS:\nA total of 63,810 women in the Nurses' Health Study (1984 to 2010) and 41,622 men in the Health Professionals Follow-Up Study (1986 to 2010) were included. Dietary information was repeatedly assessed every 2 to 4 years during follow-up. Incident melanoma cases were identified through self-report and confirmed by pathologic records.\n\nRESULTS:\nOver 24 to 26 years of follow-up, we documented 1,840 incident melanomas. After adjustment for other risk factors, the pooled multivariable hazard ratios for melanoma were 1.00 for overall citrus consumption \u003c twice per week (reference), 1.10 (95% CI, 0.94 to 1.30) for two to four times per week, 1.26 (95% CI, 1.08 to 1.47) for five to six times per week, 1.27 (95% CI, 1.09 to 1.49) for once to 1.5 times per day, and 1.36 (95% CI, 1.14 to 1.63) for ≥ 1.6 times per day (Ptrend \u003c .001). Among individual citrus products, grapefruit showed the most apparent association with risk of melanoma, which was independent of other lifestyle and dietary factors. The pooled multivariable hazard ratio for melanoma comparing the extreme consumption categories of grapefruit (≥ three times per week v never) was 1.41 (95% CI, 1.10 to 1.82; Ptrend \u003c .001).\n\nCONCLUSION:\nCitrus consumption was associated with an increased risk of malignant melanoma in two cohorts of women and men. Nevertheless, further investigation is needed to confirm our findings and explore related health implications." + }, + "questions": [ + { + "id": "3d9508de-5fe6-4e73-9737-3619ac0744f5", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 1502, + "text": "Citrus consumption" + } + ] + } + ] +} \ No newline at end of file diff --git a/6326fa39-6abf-4dfa-ab09-0403734cf858.json b/6326fa39-6abf-4dfa-ab09-0403734cf858.json new file mode 100644 index 0000000000000000000000000000000000000000..f2c9f764cf0b928878f8f803a562d734af35d49d --- /dev/null +++ b/6326fa39-6abf-4dfa-ab09-0403734cf858.json @@ -0,0 +1,46 @@ +{ + "id": "6326fa39-6abf-4dfa-ab09-0403734cf858", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "25304359", + "text": "Epidemiological studies have examined breast cancer risk in relation to sex hormone concentrations measured by different methods: \"extraction\" immunoassays (with prior purification by organic solvent extraction, with or without column chromatography), \"direct\" immunoassays (no prior extraction or column chromatography), and more recently with mass spectrometry-based assays. We describe the associations of estradiol, estrone and testosterone with both body mass index and breast cancer risk in postmenopausal women according to assay method, using data from a collaborative pooled analysis of 18 prospective studies. In general, hormone concentrations were highest in studies that used direct assays and lowest in studies that used mass spectrometry-based assays. Estradiol and estrone were strongly positively associated with body mass index, regardless of the assay method; testosterone was positively associated with body mass index for direct assays, but less clearly for extraction assays, and there were few data for mass spectrometry assays. The correlations of estradiol with body mass index, estrone and testosterone were lower for direct assays than for extraction and mass spectrometry assays, suggesting that the estimates from the direct assays were less precise. For breast cancer risk, all three hormones were strongly positively associated with risk regardless of assay method (except for testosterone by mass spectrometry where there were few data), with no statistically significant differences in the trends, but differences may emerge as new data accumulate. Future epidemiological and clinical research studies should continue to use the most accurate assays that are feasible within the design characteristics of each study." + }, + "questions": [ + { + "id": "c73e1187-0c8e-4732-9be8-af2b3ab81c73", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1304, + "text": "all three hormones" + }, + { + "answer_start": 409, + "text": "estradiol" + }, + { + "answer_start": 420, + "text": "estrone" + }, + { + "answer_start": 432, + "text": "testosterone" + } + ] + } + ] +} \ No newline at end of file diff --git a/63c78668-15ba-4939-814f-3f5613fda421.json b/63c78668-15ba-4939-814f-3f5613fda421.json new file mode 100644 index 0000000000000000000000000000000000000000..a8c23ce6b401f50209e56a74155cf3707791c75f --- /dev/null +++ b/63c78668-15ba-4939-814f-3f5613fda421.json @@ -0,0 +1,39 @@ +{ + "id": "63c78668-15ba-4939-814f-3f5613fda421", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "26586037", + "text": "BACKGROUND:\nPrevious studies investigating the relationship between Mycoplasma pneumoniae and incident asthma in the general population have been inconclusive.\n\nOBJECTIVE:\nWe conducted a nationwide cohort study to clarify this relationship.\n\nMETHODS:\nUsing the National Health Insurance Research Database of Taiwan, we identified 1591 patients with M pneumoniae infection (International Classification of Diseases, Ninth Revision, Clinical Modification code 4830) given diagnoses between 2000 and 2008. We then frequency matched 6364 patients without M pneumoniae infection from the general population according to age, sex, and index year. Cox proportional hazards regression analysis was performed to determine the adjusted hazard ratio (aHR) of the occurrence of asthma in the M pneumoniae cohort compared with that in the non-M pneumoniae cohort.\n\nRESULTS:\nRegardless of comorbidities and the use of antibiotic or steroid therapies, patients with M pneumonia infection had a higher risk of incident asthma than those without it. The aHR of asthma was 3.35 (95% CI, 2.71-4.15) for the M pneumoniae cohort, with a significantly higher risk when patients were stratified by age, sex, follow-up time, and comorbidities, including allergic rhinitis, atopic dermatitis, or allergic conjunctivitis. Patients with M pneumoniae infection had a higher risk of having early-onset (age, \u003c12 years; aHR, 2.87) and late-onset (age, ≥12 years; aHR, 3.95) asthma. The aHR was also higher within the less than 2-year follow-up in the M pneumoniae cohort (aHR, 4.41; 95% CI, 3.40-5.74) than in the cohort without the infection.\n\nCONCLUSION:\nThis study found that incident cases of early-onset and late-onset asthma are closely related to M pneumoniae infection, even in nonatopic patients." + }, + "questions": [ + { + "id": "06b0b212-0102-47e6-84b9-d84f3ed29b71", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 937, + "text": "patients with M pneumonia infection" + }, + { + "answer_start": 1724, + "text": "M pneumoniae infection" + } + ] + } + ] +} \ No newline at end of file diff --git a/63f827e4-b08e-470c-8e16-b8b0a4251d38.json b/63f827e4-b08e-470c-8e16-b8b0a4251d38.json new file mode 100644 index 0000000000000000000000000000000000000000..558c26d84e516e92eae879f282b4fc869cbe22ab --- /dev/null +++ b/63f827e4-b08e-470c-8e16-b8b0a4251d38.json @@ -0,0 +1,48 @@ +{ + "id": "63f827e4-b08e-470c-8e16-b8b0a4251d38", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "26453630", + "text": "There are conflicting data regarding the magnitude and determinants of chronic obstructive pulmonary disease (COPD) risk in farmers.In a cross-sectional study of 917 nonfarming working controls and 3787 farmers aged 40-75 years, we assessed respiratory symptoms, tobacco exposure, job history (without direct exposure measurement) and lung function. COPD was defined by the Global Initiative for Chronic Obstructive Lung Disease (GOLD) criterion (post-bronchodilator forced expiratory volume in 1 s (FEV1)/forced vital capacity (FVC) \u003c0.70) and by the Quanjer reference equation (post-bronchodilator FEV1/FVC \u003clower limit of normal (LLN)).The prevalence (95% CI) of COPD according to the GOLD criterion was 5.1% (4.4-5.8%) and 2.9% (1.8-4.0%) in farmers and controls, respectively (p=0.005), and 3.1% (2.5-3.6%) and 1.5% (0.7-2.3%), respectively, for the LLN criterion (p\u003c0.01). For both COPD criteria after adjustment for age, sex and smoking status, COPD prevalence was similar in controls and crop farmers. Compared to controls, four job categories had a higher prevalence of COPD according to the GOLD criterion, namely, cattle breeders, swine breeders, poultry breeders and breeders of two or more livestock types. Among cattle breeders, only those from Franche-Comté had higher prevalence of COPD according to both GOLD and LLN criteria.The prevalence of COPD in farmers is higher than in nonfarming working controls, and depends on the farming activity, the region and the criterion used to define COPD." + }, + "questions": [ + { + "id": "49d9e265-3b6e-41e2-870b-c3672408aaa8", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 1125, + "text": "cattle breeders" + }, + { + "answer_start": 1142, + "text": "swine breeders" + }, + { + "answer_start": 1158, + "text": "poultry breeders" + }, + { + "answer_start": 1179, + "text": "breeders of two or more livestock types" + } + ] + } + ] +} \ No newline at end of file diff --git a/640262c6-dd7a-43e0-8f02-bc378dc8bc91.json b/640262c6-dd7a-43e0-8f02-bc378dc8bc91.json new file mode 100644 index 0000000000000000000000000000000000000000..79583bac5bfdb880f9853e5d8d446c411c313553 --- /dev/null +++ b/640262c6-dd7a-43e0-8f02-bc378dc8bc91.json @@ -0,0 +1,42 @@ +{ + "id": "640262c6-dd7a-43e0-8f02-bc378dc8bc91", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "17374835", + "text": "BACKGROUND:\nAlthough ecologic association and animal studies support a direct effect of dietary fat on the development of breast cancer, results of epidemiologic studies have been inconclusive.\n\nMETHODS:\nWe prospectively analyzed the association between fat consumption and the incidence of postmenopausal invasive breast cancer in the National Institutes of Health-AARP Diet and Health Study, a US cohort comprising 188,736 postmenopausal women who completed a 124-item food-frequency questionnaire in 1995-1996. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated using Cox proportional hazards regression models with adjustment for energy and potential confounding factors. All statistical tests were two-sided.\n\nRESULTS:\nOver an average follow-up of 4.4 years, the cohort yielded 3501 cases of invasive breast cancer. The hazard ratio of breast cancer for the highest (median intake, 40.1% energy from total fat; 434 cases per 100,000 person-years) versus the lowest (median intake, 20.3% energy from total fat; 392 cases per 100,000 person-years) quintile of total fat intake was 1.11 (95% CI = 1.00 to 1.24; P(trend) = .017). The corresponding hazard ratio for a twofold increase in percent energy from total fat on the continuous scale was 1.15 (95% CI = 1.05 to 1.26). Positive associations were also found for subtypes of fat (hazard ratio for a twofold increase in percent energy from saturated fat = 1.13; 95% CI = 1.05 to 1.22; from monounsaturated fat, HR = 1.12; 95% CI = 1.03 to 1.21; from polyunsaturated fat, HR = 1.10, 95% CI = 1.01 to 1.20). Correction for measurement error in nutrient intakes, on the basis of a calibration substudy that used two 24-hour dietary recalls, strengthened the associations, yielding an estimated hazard ratio for total fat of 1.32 (95% CI = 1.11 to 1.58). Secondary analyses showed that associations between total, saturated, and monounsaturated fat intakes were confined to women who were not using menopausal hormone therapy at baseline.\n\nCONCLUSION:\nIn this large prospective cohort with a wide range of fat intake, dietary fat intake was directly associated with the risk of postmenopausal invasive breast cancer." + }, + "questions": [ + { + "id": "ac2f9f2a-644f-48a3-851b-781ebf6e351b", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 883, + "text": "highest (median intake, 40.1% energy from total fat; 434 cases per 100,000 person-years) versus the lowest (median intake, 20.3% energy from total fat; 392 cases per 100,000 person-years) quintile of total fat intake" + }, + { + "answer_start": 1188, + "text": "twofold increase in percent energy from total fat" + }, + { + "answer_start": 2088, + "text": "dietary fat intake" + } + ] + } + ] +} \ No newline at end of file diff --git a/6402afe0-73c2-4941-bbf8-bf5ede369c8f.json b/6402afe0-73c2-4941-bbf8-bf5ede369c8f.json new file mode 100644 index 0000000000000000000000000000000000000000..96f80d7498c39838ff3755a2c00bab19457b0ad4 --- /dev/null +++ b/6402afe0-73c2-4941-bbf8-bf5ede369c8f.json @@ -0,0 +1,37 @@ +{ + "id": "6402afe0-73c2-4941-bbf8-bf5ede369c8f", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "14760377", + "text": "In a matched case-control study using the General Practice Research Database, current statin use was not associated with a significantly altered risk of any of 13 studied cancers. Untreated hyperlipidaemia was associated with slightly increased risks of colon cancer (relative risk 1.8; 95% confidence interval 1.2-2.8), prostate cancer (1.5; 1.1-2.0), and bladder cancer (1.9; 1.2-3.1)." + }, + "questions": [ + { + "id": "dd719a39-db6e-474e-8ca7-7bd25af60494", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 180, + "text": "Untreated hyperlipidaemia" + } + ] + } + ] +} \ No newline at end of file diff --git a/6420aacd-714f-41f4-a47c-833fc08c0b40.json b/6420aacd-714f-41f4-a47c-833fc08c0b40.json new file mode 100644 index 0000000000000000000000000000000000000000..179968e383498115c3a591aed15049d36797afaa --- /dev/null +++ b/6420aacd-714f-41f4-a47c-833fc08c0b40.json @@ -0,0 +1,40 @@ +{ + "id": "6420aacd-714f-41f4-a47c-833fc08c0b40", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "20935112", + "text": "RATIONALE:\nFew studies have investigated the factors associated with the early inception of chronic obstructive pulmonary disease (COPD).\n\nOBJECTIVES:\nWe investigated COPD risk factors in an international cohort of young adults using different spirometric definitions of the disease.\n\nMETHODS:\nWe studied 4,636 subjects without asthma who had prebronchodilator FEV(1)/FVC measured in the European Community Respiratory Health Survey both in 1991 to 1993 (when they were 20-44 yr old) and in 1999 to 2002. COPD was defined according to the Global Initiative for Chronic Obstructive Lung Disease fixed cut-off criterion (FEV(1)/FVC \u003c 0.70), and two criteria based on the Quanjer and LuftiBus reference equations (FEV(1)/FVC less than lower limit of normal). COPD determinants were studied using two-level Poisson regression models.\n\nMEASUREMENTS AND MAIN RESULTS:\nCOPD incidence ranged from 1.85 (lower limit of normal [Quanjer]) to 2.88 (Global Initiative for Chronic Obstructive Lung Disease) cases/1,000/yr. Although about half of the cases had smoked less than 20 pack-years, smoking was the main risk factor for COPD, and it accounted for 29 to 39% of the new cases during the follow-up. Airway hyperresponsiveness was the second strongest risk factor (15-17% of new cases). Other determinants were respiratory infections in childhood and a family history of asthma, whereas the role of sex, age, and of being underweight largely depended on the definition of COPD used.\n\nCONCLUSIONS:\nCOPD may start early in life. Smoking prevention should be given the highest priority to reduce COPD occurrence. Airway hyperresponsiveness, a family history of asthma, and respiratory infections in childhood are other important determinants of COPD. We suggest the need for a definition of COPD that is not exclusively based on spirometry." + }, + "questions": [ + { + "id": "08777ccd-5783-4976-ab9f-758274d2f422", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 1078, + "text": "smoking" + }, + { + "answer_start": 1191, + "text": "Airway hyperresponsiveness" + } + ] + } + ] +} \ No newline at end of file diff --git a/6464159b-114a-4d4b-a6f5-ea2fb16661b3.json b/6464159b-114a-4d4b-a6f5-ea2fb16661b3.json new file mode 100644 index 0000000000000000000000000000000000000000..b8b17932cdeb03f38f3b83481ae246a57453825a --- /dev/null +++ b/6464159b-114a-4d4b-a6f5-ea2fb16661b3.json @@ -0,0 +1,39 @@ +{ + "id": "6464159b-114a-4d4b-a6f5-ea2fb16661b3", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "17825896", + "text": "BACKGROUND:\nThe association between allergic rhinitis and asthma is well documented, but the temporal sequence of this association has not been closely examined.\n\nOBJECTIVE:\nWe sought to assess the associations between childhood allergic rhinitis and (1) asthma incidence from preadolescence to middle age and (2) asthma persistence to middle age.\n\nMETHODS:\nData were gathered from the 1968, 1974, and 2004 surveys of the Tasmanian Asthma Study. Cox regression was used to examine the association between childhood allergic rhinitis and asthma incidence in preadolescence, adolescence, and adult life. Binomial regression was used to examine the association between childhood allergic rhinitis and asthma beginning before the age of 7 years and persisting at age 44 years.\n\nRESULTS:\nChildhood allergic rhinitis was associated with a significant 2- to 7-fold increased risk of incident asthma in preadolescence, adolescence, or adult life. Childhood allergic rhinitis was associated with a 3-fold increased risk of childhood asthma persisting compared with remitting by middle age.\n\nCONCLUSIONS:\nChildhood allergic rhinitis increased the likelihood of new-onset asthma after childhood and the likelihood of having persisting asthma from childhood into middle age.\n\nCLINICAL IMPLICATIONS:\nAsthma burden in later life might be reduced by more aggressive treatment of allergic rhinitis in early life." + }, + "questions": [ + { + "id": "e8c58243-adaf-4665-b76f-17bd33dcf467", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1095, + "text": "Childhood allergic rhinitis" + }, + { + "answer_start": 1364, + "text": "allergic rhinitis in early life" + } + ] + } + ] +} \ No newline at end of file diff --git a/64a5ff90-9cdc-4bee-a2b5-62187eb2d1c0.json b/64a5ff90-9cdc-4bee-a2b5-62187eb2d1c0.json new file mode 100644 index 0000000000000000000000000000000000000000..f9a5cc806e240f987a005d2f9c4282fa1a551e82 --- /dev/null +++ b/64a5ff90-9cdc-4bee-a2b5-62187eb2d1c0.json @@ -0,0 +1,42 @@ +{ + "id": "64a5ff90-9cdc-4bee-a2b5-62187eb2d1c0", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "7872581", + "text": "OBJECTIVE:\nTo examine the relation between adult weight change and the risk for clinical diabetes mellitus among middle-aged women.\n\nDESIGN:\nProspective cohort study with follow-up from 1976 to 1990.\n\nSETTING:\n11 U.S. states.\n\nPARTICIPANTS:\n114,281 female registered nurses aged 30 to 55 years who did not have diagnosed diabetes mellitus, coronary heart disease, stroke, or cancer in 1976.\n\nOUTCOME MEASURES:\nNon-insulin-dependent diabetes mellitus.\n\nRESULTS:\n2204 cases of diabetes were diagnosed during 1.49 million person-years of follow-up. After adjustment for age, body mass index was the dominant predictor of risk for diabetes mellitus. Risk increased with greater body mass index, and even women with average weight (body mass index, 24.0 kg/m2) had an elevated risk. Compared with women with stable weight (those who gained or lost less than 5 kg between age 18 years and 1976) and after adjustment for age and body mass index at age 18 years, the relative risk for diabetes mellitus among women who had a weight gain of 5.0 to 7.9 kg was 1.9 (95% CI, 1.5 to 2.3). The corresponding relative risk for women who gained 8.0 to 10.9 kg was 2.7 (CI, 2.1 to 3.3). In contrast, women who lost more than 5.0 kg reduced their risk for diabetes mellitus by 50% or more. These results were independent of family history of diabetes.\n\nCONCLUSION:\nThe excess risk for diabetes with even modest and typical adult weight gain is substantial. These findings support the importance of maintaining a constant body weight throughout adult life and suggest that the 1990 U.S. Department of Agriculture guidelines that allow a substantial weight gain after 35 years of age are misleading." + }, + "questions": [ + { + "id": "0e46d752-5d2c-46eb-94a1-b288182ec864", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1386, + "text": "modest and typical adult weight gain" + }, + { + "answer_start": 1001, + "text": "women who had a weight gain of 5.0 to 7.9 kg" + }, + { + "answer_start": 1111, + "text": " women who gained 8.0 to 10.9 kg" + } + ] + } + ] +} \ No newline at end of file diff --git a/64e3e554-cbca-4a4f-8b26-8fbdf0414d67.json b/64e3e554-cbca-4a4f-8b26-8fbdf0414d67.json new file mode 100644 index 0000000000000000000000000000000000000000..29999844e0ae290f10916fa11e738f88db058bb6 --- /dev/null +++ b/64e3e554-cbca-4a4f-8b26-8fbdf0414d67.json @@ -0,0 +1,41 @@ +{ + "id": "64e3e554-cbca-4a4f-8b26-8fbdf0414d67", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "11287446", + "text": "BACKGROUND:\nSeveral recent large prospective cohort studies have failed to demonstrate the presumed protective effect of fruit, vegetable, and dietary fiber consumption on colorectal cancer risk. To further explore this issue, we have examined these associations in a population that consumes relatively low amounts of fruit and vegetables and high amounts of cereals.\n\nMETHODS:\nWe examined data obtained from a food-frequency questionnaire used in a population-based prospective mammography screening study of women in central Sweden. Women with colorectal cancer diagnosed through December 31, 1998, were identified by linkage to regional cancer registries. Cox proportional hazards models were used to estimate relative risks. All statistical tests were two-sided.\n\nRESULTS:\nDuring an average 9.6 years of follow-up of 61 463 women, we observed 460 incident cases of colorectal cancer (291 colon cancers, 159 rectal cancers, and 10 cancers at both sites). In the entire study population, total fruit and vegetable consumption was inversely associated with colorectal cancer risk. Subanalyses showed that this association was due largely to fruit consumption. The association was stronger, however, and the dose-response effect was more evident among individuals who consumed the lowest amounts of fruit and vegetables. Individuals who consumed less than 1.5 servings of fruit and vegetables per day had a relative risk for developing colorectal cancer of 1.65 (95% confidence interval = 1.23 to 2.20; P(trend) =.001) compared with individuals who consumed more than 2.5 servings. We observed no association between colorectal cancer risk and the consumption of cereal fiber, even at amounts substantially greater than previously examined, or of non-cereal fiber.\n\nCONCLUSIONS:\nIndividuals who consume very low amounts of fruit and vegetables have the greatest risk of colorectal cancer. Relatively high consumption of cereal fiber does not appear to lower the risk of colorectal cancer." + }, + "questions": [ + { + "id": "7ff626c8-f661-403b-ae67-a46240933ed5", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1322, + "text": "Individuals who consumed less than 1.5 servings of fruit and vegetables per day" + }, + { + "answer_start": 1780, + "text": "Individuals who consume very low amounts of fruit and vegetables" + } + ] + } + ] +} \ No newline at end of file diff --git a/6513f261-3c89-4d92-a26e-2ceb1817dbdd.json b/6513f261-3c89-4d92-a26e-2ceb1817dbdd.json new file mode 100644 index 0000000000000000000000000000000000000000..29120946e1832dfc65d429f6e828e19635b8bbd7 --- /dev/null +++ b/6513f261-3c89-4d92-a26e-2ceb1817dbdd.json @@ -0,0 +1,38 @@ +{ + "id": "6513f261-3c89-4d92-a26e-2ceb1817dbdd", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "1733810", + "text": "We studied the cross-sectional relationship between HbA1c and cardiovascular disease (CVD) in the survivors of the original cohort of the Framingham Heart Study (n = 1045). HbA1c was significantly related to prevalent CVD among women but not men. HbA1c was also related to hypertension and to the ratio of total to high-density lipoprotein cholesterol levels. In regression analyses that controlled for these and other potential risk factors, HbA1c remained significantly related to CVD among women. The relative odds of CVD increased 1.39-fold (95% confidence interval 1.06-1.83) for increases in HbA1c of 1% (e.g., for HbA1c from 5 to 6%). The relationship was not weakened when known diabetic subjects or subjects taking beta-blocker or thiazide medications were excluded from analysis. In contrast, there was no significant relationship between \"casual\" blood glucose and prevalent CVD. Our results reveal a strong, significant, independent association between hyperglycemia, measured by HbA1c, and CVD among older women." + }, + "questions": [ + { + "id": "2bf68156-66a2-4177-b67d-708d95923f6c", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 965, + "text": "hyperglycemia" + }, + { + "answer_start": 585, + "text": "increases in HbA1c of 1%" + } + ] + } + ] +} \ No newline at end of file diff --git a/65f4a7b8-4749-49bb-89e7-2c7204000bed.json b/65f4a7b8-4749-49bb-89e7-2c7204000bed.json new file mode 100644 index 0000000000000000000000000000000000000000..9a02b89df1af9e1193c19568c37c753147d6d413 --- /dev/null +++ b/65f4a7b8-4749-49bb-89e7-2c7204000bed.json @@ -0,0 +1,34 @@ +{ + "id": "65f4a7b8-4749-49bb-89e7-2c7204000bed", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "14757686", + "text": "BACKGROUND:\nMeasuring C-reactive protein (CRP) has been recommended to identify patients at high risk for coronary heart disease (CHD) with low LDL cholesterol (LDL-C). Lipoprotein-associated phospholipase A2 (Lp-PLA2) is a proinflammatory enzyme associated primarily with LDL.\n\nMETHODS AND RESULTS:\nIn a prospective, case cohort study in 12 819 apparently healthy middle-aged men and women in the Atherosclerosis Risk in Communities study, the relation between Lp-PLA2, CRP, traditional risk factors, and risk for CHD events over a period of approximately 6 years was examined in a proportional hazards model, stratified by LDL-C. Lp-PLA2 and CRP levels were higher in the 608 cases than the 740 noncases. Both Lp-PLA2 and CRP were associated with incident CHD after adjustment for age, sex, and race with a hazard ratio of 1.78 for the highest tertile of Lp-PLA2 and 2.53 for the highest category of CRP versus the lowest categories. Lp-PLA2 correlated positively with LDL-C (r=0.36) and negatively with HDL-C (r=-0.33) but not with CRP (r=-0.05). In a model adjusted for traditional risk factors including LDL-C, the association of Lp-PLA2 with CHD was attenuated and not statistically significant. For individuals with LDL-C below the median (130 mg/dL), Lp-PLA2 and CRP were both significantly and independently associated with CHD in fully adjusted models. For individuals with LDL-C \u003c130 mg/dL, those with both Lp-PLA2 and CRP levels in the highest tertile were at the greatest risk for a CHD event.\n\nCONCLUSIONS:\nLp-PLA2 and CRP may be complementary in identifying individuals at high CHD risk who have low LDL-C." + }, + "questions": [ + { + "id": "02d14917-b6b0-4d07-ada1-dd299203d825", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1367, + "text": "individuals with LDL-C \u003c130 mg/dL, those with both Lp-PLA2 and CRP levels in the highest tertile" + } + ] + } + ] +} \ No newline at end of file diff --git a/65f71d08-bd70-4c86-b6b1-9d8741ff18f9.json b/65f71d08-bd70-4c86-b6b1-9d8741ff18f9.json new file mode 100644 index 0000000000000000000000000000000000000000..8a4745c443b46d4299bb65688c89c5182bf5e023 --- /dev/null +++ b/65f71d08-bd70-4c86-b6b1-9d8741ff18f9.json @@ -0,0 +1,38 @@ +{ + "id": "65f71d08-bd70-4c86-b6b1-9d8741ff18f9", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "11142527", + "text": "BACKGROUND:\nCoffee consumption has been associated with an excess bladder cancer risk, but results from epidemiological studies are inconsistent. This association has been long debated, in part due to the potential confounding by smoking. We examined the risk associated with coffee consumption in nonsmokers in a pooled analysis of ten European bladder cancer case-control studies.\n\nMETHODS:\nThe pooled data set comprises 564 cases and 2929 hospital or population controls who had never smoked. They were enrolled in ten studies conducted in Denmark, Germany, Greece, France, Italy and Spain. Information on coffee consumption and occupation was re-coded following standard criteria. Unconditional logistic regression was applied adjusting for age, study center, occupation and gender.\n\nRESULTS:\nSeventy-nine percent of the study population reported having drunk coffee, and 2.4% were heavy drinkers, reporting having drunk on average ten or more cups per day. There was no excess risk in ever coffee drinkers (OR = 1.0, 95% CI 0.8-1.3) compared to never drinkers. The risk did not increase monotonically with dose but a statistically significant excess risk was seen for subjects having drunk ten or more cups per day (OR = 1.8, 95% CI 1.0-3.3). This excess was seen in both men and women. There was no evidence of an association of the risk with duration or type of coffee consumption. The pooled results were not dependent on the findings of any specific study, but they depended on the type of controls with an overall excess risk observed only for studies using hospital controls.\n\nCONCLUSION:\nNonsmokers who are heavy coffee drinkers may have a small excess risk of bladder cancer. Although these results cannot be attributed to confounding by smoking, the possibility of bias in control selection cannot be discarded. On the basis of these results, only a very small proportion of cancers of the bladder among nonsmokers could be attributed to coffee drinking." + }, + "questions": [ + { + "id": "cdf70696-6532-48e4-bd79-5ccc49cf9a22", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 1182, + "text": "having drunk ten or more cups per day" + }, + { + "answer_start": 1600, + "text": "Nonsmokers who are heavy coffee drinkers" + } + ] + } + ] +} \ No newline at end of file diff --git a/66c67aa5-cd6f-4e6a-8595-cbf998181acf.json b/66c67aa5-cd6f-4e6a-8595-cbf998181acf.json new file mode 100644 index 0000000000000000000000000000000000000000..a23d5a6a61e8398e7dde24d75bab84fa7ed99c66 --- /dev/null +++ b/66c67aa5-cd6f-4e6a-8595-cbf998181acf.json @@ -0,0 +1,66 @@ +{ + "id": "66c67aa5-cd6f-4e6a-8595-cbf998181acf", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "18343878", + "text": "Exposure to certain environmental toxicants may be associated with increased risk of developing diabetes. The authors' aim was to investigate the relation between lifetime exposure to specific agricultural pesticides and diabetes incidence among pesticide applicators. The study included 33,457 licensed applicators, predominantly non-Hispanic White males, enrolled in the Agricultural Health Study. Incident diabetes was self-reported in a 5-year follow-up interview (1999-2003), giving 1,176 diabetics and 30,611 nondiabetics for analysis. Lifetime exposure to pesticides and covariate information were reported by participants at enrollment (1993-1997). Using logistic regression, the authors considered two primary measures of pesticide exposure: ever use and cumulative lifetime days of use. They found seven specific pesticides (aldrin, chlordane, heptachlor, dichlorvos, trichlorfon, alachlor, and cyanazine) for which the odds of diabetes incidence increased with both ever use and cumulative days of use. Applicators who had used the organochlorine insecticides aldrin, chlordane, and heptachlor more than 100 lifetime days had 51%, 63%, and 94% increased odds of diabetes, respectively. The observed association of organochlorine and organophosphate insecticides with diabetes is consistent with results from previous human and animal studies. Long-term exposure from handling certain pesticides, in particular, organochlorine and organophosphate insecticides, may be associated with increased risk of diabetes." + }, + "questions": [ + { + "id": "aa74ac71-65f5-4240-adbb-93bdc9cb14d2", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 808, + "text": "seven specific pesticides (aldrin, chlordane, heptachlor, dichlorvos, trichlorfon, alachlor, and cyanazine)" + }, + { + "answer_start": 835, + "text": "aldrin" + }, + { + "answer_start": 843, + "text": "chlordan" + }, + { + "answer_start": 854, + "text": "heptachlor" + }, + { + "answer_start": 866, + "text": "dichlorvos" + }, + { + "answer_start": 878, + "text": "trichlorfon" + }, + { + "answer_start": 891, + "text": "alachlor" + }, + { + "answer_start": 905, + "text": "cyanazine" + }, + { + "answer_start": 1225, + "text": "organochlorine and organophosphate insecticides" + } + ] + } + ] +} \ No newline at end of file diff --git a/66db6810-af1d-46a7-8235-24e875229bc1.json b/66db6810-af1d-46a7-8235-24e875229bc1.json new file mode 100644 index 0000000000000000000000000000000000000000..a139b9b5ff9e376d9c1611563bb09edc2df5db42 --- /dev/null +++ b/66db6810-af1d-46a7-8235-24e875229bc1.json @@ -0,0 +1,45 @@ +{ + "id": "66db6810-af1d-46a7-8235-24e875229bc1", + "disease": { + "id": "M2023_04_26_16_38_52", + "names": [ + "Migraine" + ], + "dbLinks": { + "icd10": [ + "G43" + ], + "icd11": [ + "8A80" + ], + "mesh": [ + "C10.228.140.546.399.750" + ] + }, + "description": "Migraine is a chronic neurological disorder characterized by recurrent episodes of unilateral, pulsatile headaches associated with autonomic symptoms such as nausea, vomiting, photophobia, and phonophobia. The pathophysiology of migraine is multifactorial and involves complex interactions between genetic, environmental, and neurochemical factors that modulate cerebral vascular tone and nociception. Migraine attacks can be triggered by a variety of factors, including stress, hormonal changes, sleep disturbances, and certain foods or medications. Treatment options for migraine include pharmacotherapy for acute attacks, preventive medications for frequent or severe headaches, and lifestyle modifications to avoid triggers. In refractory cases, interventional therapies such as nerve blocks or neuromodulation techniques may be considered." + }, + "article": { + "id": "20871611", + "text": "Migraine with aura is a common, debilitating, recurrent headache disorder associated with transient and reversible focal neurological symptoms. A role has been suggested for the two-pore domain (K2P) potassium channel, TWIK-related spinal cord potassium channel (TRESK, encoded by KCNK18), in pain pathways and general anaesthesia. We therefore examined whether TRESK is involved in migraine by screening the KCNK18 gene in subjects diagnosed with migraine. Here we report a frameshift mutation, F139WfsX24, which segregates perfectly with typical migraine with aura in a large pedigree. We also identified prominent TRESK expression in migraine-salient areas such as the trigeminal ganglion. Functional characterization of this mutation demonstrates that it causes a complete loss of TRESK function and that the mutant subunit suppresses wild-type channel function through a dominant-negative effect, thus explaining the dominant penetrance of this allele. These results therefore support a role for TRESK in the pathogenesis of typical migraine with aura and further support the role of this channel as a potential therapeutic target." + }, + "questions": [ + { + "id": "7c84bf94-5d74-4bb6-bae3-a47c78f1dfaf", + "text": "what are the risk factors of Migraine?", + "answers": [ + { + "answer_start": 219, + "text": "TWIK-related spinal cord potassium channel (TRESK, encoded by KCNK18)" + }, + { + "answer_start": 607, + "text": "prominent TRESK expression" + }, + { + "answer_start": 1001, + "text": "TRESK" + } + ] + } + ] +} \ No newline at end of file diff --git a/66e7346c-47ab-4189-8a67-62f48a6871b5.json b/66e7346c-47ab-4189-8a67-62f48a6871b5.json new file mode 100644 index 0000000000000000000000000000000000000000..d28bbaaf0a16775333eea1688121d5ff54ec6492 --- /dev/null +++ b/66e7346c-47ab-4189-8a67-62f48a6871b5.json @@ -0,0 +1,45 @@ +{ + "id": "66e7346c-47ab-4189-8a67-62f48a6871b5", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "17000944", + "text": "BACKGROUND:\nAn association between diabetes mellitus (DM) and cancer has long been speculated, but no conclusive evidence has been obtained.\n\nMETHODS:\nWe prospectively examined the association between a history of DM and subsequent risk of cancer in the Japan Public Health Center-Based Prospective Study. A total of 97 771 general Japanese persons (46 548 men and 51 223 women) aged 40 to 69 years who responded to the baseline questionnaire, from January 1990 to December 1994, were followed up for cancer incidence through December 31, 2003. At baseline, 6.7% of men and 3.1% of women had a history of DM.\n\nRESULTS:\nA total of 6462 cases of newly diagnosed cancer were identified. In men, a 27% increase in the risk of total cancer incidence was observed in those with a history of DM (n = 3907 [366 with DM]; hazard ratio [HR], 1.27; 95% confidence interval [CI], 1.14-1.42). The HR was especially high for those with cancer of the liver (n = 312 [52 with DM]; HR, 2.24; 95% CI, 1.64-3.04), pancreas (n = 118 [16 with DM]; HR, 1.85; 95% CI, 1.07-3.20), and kidney (n = 99 [13 with DM]; HR, 1.92; 95% CI, 1.06-3.46). We also observed a moderately increased risk of colon cancer (n = 491 [46 with DM]; HR, 1.36; 95% CI, 1.00-1.85) and of stomach cancer with borderline significance (n = 977 [87 with DM]; HR, 1.23; 95% CI, 0.98-1.54). In women, a borderline significant increase in risk was observed for the incidence of total cancer (n = 2555 [104 with DM]; HR, 1.21; 95% CI, 0.99-1.47), while statistical significance was observed for the incidence of stomach cancer (n = 362 [20 with DM]; HR, 1.61; 95% CI, 1.02-2.54) and liver cancer (n = 120 [10 with DM]; HR, 1.94; 95% CI, 1.00-3.73) and borderline significance was observed for the incidence of ovarian cancer (n = 74 [5 with DM]; HR, 2.42; 95% CI, 0.96-6.09).\n\nCONCLUSION:\nPatients with DM drawn from the general Japanese population may be at increased risk of total cancer and of cancer in specific sites." + }, + "questions": [ + { + "id": "6497329a-8d2f-4a11-94bc-afd51c224e60", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 35, + "text": "diabetes mellitus (DM)" + }, + { + "answer_start": 761, + "text": "those with a history of DM" + }, + { + "answer_start": 1833, + "text": "Patients with DM" + } + ] + } + ] +} \ No newline at end of file diff --git a/67b34399-ec41-4a5f-9f36-a92de09c0bb8.json b/67b34399-ec41-4a5f-9f36-a92de09c0bb8.json new file mode 100644 index 0000000000000000000000000000000000000000..11d60dc925bd2145e4e064c07d3df0868f26a53d --- /dev/null +++ b/67b34399-ec41-4a5f-9f36-a92de09c0bb8.json @@ -0,0 +1,37 @@ +{ + "id": "67b34399-ec41-4a5f-9f36-a92de09c0bb8", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "12237282", + "text": "BACKGROUND:\nIncreasing numbers of BRCA1 mutation carriers are being identified in cancer risk evaluation programs. However, no estimates of cancer risk specific to a clinic-based population of mutation carriers are available. These data are clinically relevant, because estimates based on families ascertained for linkage studies may overestimate cancer risk in mutation carriers, and population-based series may underestimate it. Wide variation in risk estimates from these disparate ascertainment groups makes counseling in risk evaluation programs difficult. The purpose of this study was to estimate BRCA1-related cancer risks for individuals ascertained in a breast cancer risk evaluation clinic.\n\nMETHODS:\nCumulative observed and age-adjusted cancer risk estimates were determined by analyzing 483 BRCA1 mutation carriers in 147 families identified in two academic breast and ovarian cancer risk evaluation clinics. Cancer risks were computed from the proportion of individuals diagnosed with cancer during a 10-year age interval from among the total number of individuals alive and cancer-free at the beginning of that interval. Age-of-diagnosis comparisons were made using two-sided Student's t tests.\n\nRESULTS:\nBy age 70, female breast cancer risk was 72.8% (95% confidence interval [CI] = 67.9% to 77.7%) and ovarian cancer risk was 40.7% (95% CI = 35.7% to 45.6%). The risk for a second primary breast cancer by age 70 was 40.5% (95% CI = 34.1% to 47.0%). We also identified an increased risk of cancer of the colon (twofold), pancreas (threefold), stomach (fourfold), and fallopian tube (120-fold) in BRCA1 mutation carriers as compared with Surveillance, Epidemiology, and End Results (SEER) Program population-based estimates.\n\nCONCLUSION:\nThe estimates for breast and ovarian cancer risk in BRCA1 mutation carriers is higher than population-based estimates but lower than estimates based on families ascertained for linkage studies. These cancer risk estimates may most closely approximate those faced by BRCA1 mutation carriers identified in risk evaluation clinics." + }, + "questions": [ + { + "id": "b019c54c-00d7-4ab7-b5d7-3aa3612802a2", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1791, + "text": "cancer risk in BRCA1 mutation carriers" + } + ] + } + ] +} \ No newline at end of file diff --git a/68062cf7-3096-4650-85f0-f755c0240edb.json b/68062cf7-3096-4650-85f0-f755c0240edb.json new file mode 100644 index 0000000000000000000000000000000000000000..d6ece00eb33826f1dc877b363b60fe7c2643e301 --- /dev/null +++ b/68062cf7-3096-4650-85f0-f755c0240edb.json @@ -0,0 +1,37 @@ +{ + "id": "68062cf7-3096-4650-85f0-f755c0240edb", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "23633003", + "text": "PURPOSE:\nDiabetes is associated with increased risk of developing colorectal cancer (CRC), but its effect on overall and cancer-specific mortality in CRC patients has been little investigated. The aim of this study was to assess the influence of diabetes on overall and cancer-specific mortality in Italian CRC patients.\n\nMETHODS:\nCases of adult (≥15 years) CRC, diagnosed in 2003-2005, most followed-up to the end of 2008, were randomly selected from the Italian Cancer Registries database. Diabetic status, sex, age, tumor stage, subsite, treatment, morphology, and grade were obtained by consultation of patient clinical records. Poisson multivariable regression models, adjusted for potential confounding variables, were used to estimate hazard ratios (HRs) for all-cause and CRC-specific mortality, according to diabetic status.\n\nRESULTS:\nA total of 1,039 CRC cases with known fasting glucose or diabetic status, archived in 7 cancer registries, was analyzed. Compared to non-diabetics, diabetics (specific diagnosis or glucose ≥126 mg/dl) were older and less likely to receive adjuvant therapy. Diabetics were at higher risk of all-cause death [HR 1.41; 95 % confidence interval (CI) 1.18-1.70] and CRC death (HR 1.36; 95 % CI 1.11-1.67), with no differences by sex or subsite.\n\nCONCLUSIONS:\nDiabetes was significantly associated with increased overall and CRC-specific mortality. Our findings indicate that diabetes is a negative prognostic factor for CRC and suggest that in patients with CRC, diabetes prevention and treatments that stabilize the condition and control its complications might reduce mortality. Further studies are required to ascertain the mechanisms linking diabetes to greater mortality in CRC patients." + }, + "questions": [ + { + "id": "e03a4fdf-5b63-4478-9b6e-70081be50fb0", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1298, + "text": "Diabetes" + } + ] + } + ] +} \ No newline at end of file diff --git a/694d4f8c-0a57-40f1-ac7a-d15535e065e7.json b/694d4f8c-0a57-40f1-ac7a-d15535e065e7.json new file mode 100644 index 0000000000000000000000000000000000000000..16100baf8ae21a215f599a60a1cdd00b7d1a76b8 --- /dev/null +++ b/694d4f8c-0a57-40f1-ac7a-d15535e065e7.json @@ -0,0 +1,46 @@ +{ + "id": "694d4f8c-0a57-40f1-ac7a-d15535e065e7", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "18073361", + "text": "CONTEXT:\nObservational studies have suggested an association between active smoking and the incidence of type 2 diabetes.\n\nOBJECTIVE:\nTo conduct a systematic review with meta-analysis of studies assessing the association between active smoking and incidence of type 2 diabetes.\n\nDATA SOURCES:\nA search of MEDLINE (1966 to May 2007) and EMBASE (1980 to May 2007) databases was supplemented by manual searches of bibliographies of key retrieved articles, reviews of abstracts from scientific meetings, and contact with experts.\n\nSTUDY SELECTION:\nStudies were included if they reported risk of impaired fasting glucose, impaired glucose tolerance, or type 2 diabetes in relationship to smoking status at baseline; had a cohort design; and excluded persons with diabetes at baseline.\n\nDATA EXTRACTION AND DATA SYNTHESIS:\nTwo authors independently extracted the data, including the presence or absence of active smoking at baseline, the risk of diabetes, methods used to detect diabetes, and key criteria of study quality. Relative risks (RRs) were pooled using a random-effects model. Associations were tested in subgroups representing different patient characteristics and study quality criteria.\n\nRESULTS:\nThe search yielded 25 prospective cohort studies (N = 1.2 million participants) that reported 45 844 incident cases of diabetes during a study follow-up period ranging from 5 to 30 years. Of the 25 studies, 24 reported adjusted RRs greater than 1 (range for all studies, 0.82-3.74). The pooled adjusted RR was 1.44 (95% confidence interval [CI], 1.31-1.58). Results were consistent and statistically significant in all subgroups. The risk of diabetes was greater for heavy smokers (\u003e or =20 cigarettes/day; RR, 1.61; 95% CI, 1.43-1.80) than for lighter smokers (RR,1.29; 95% CI, 1.13-1.48) and lower for former smokers (RR, 1.23; 95% CI, 1.14-1.33) compared with active smokers, consistent with a dose-response phenomenon.\n\nCONCLUSION:\nActive smoking is associated with an increased risk of type 2 diabetes. Future research should attempt to establish whether this association is causal and to clarify its mechanisms." + }, + "questions": [ + { + "id": "2064d371-8578-4295-8a44-1c6cb1cc1d45", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1671, + "text": "heavy smokers (\u003e or =20 cigarettes/day" + }, + { + "answer_start": 1749, + "text": "lighter smokers" + }, + { + "answer_start": 1808, + "text": "former smokers" + }, + { + "answer_start": 1940, + "text": "Active smoking" + } + ] + } + ] +} \ No newline at end of file diff --git a/697d2f5f-f262-4e13-9386-be63026af25e.json b/697d2f5f-f262-4e13-9386-be63026af25e.json new file mode 100644 index 0000000000000000000000000000000000000000..990d50f6c2356882ea77c8b8fa7116a819dfb7b1 --- /dev/null +++ b/697d2f5f-f262-4e13-9386-be63026af25e.json @@ -0,0 +1,54 @@ +{ + "id": "697d2f5f-f262-4e13-9386-be63026af25e", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "26348752", + "text": "IMPORTANCE:\nPrevious studies have shown increasing prevalence of diabetes in the United States. New US data are available to estimate prevalence of and trends in diabetes.\n\nOBJECTIVE:\nTo estimate the recent prevalence and update US trends in total diabetes, diagnosed diabetes, and undiagnosed diabetes using National Health and Nutrition Examination Survey (NHANES) data.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nCross-sectional surveys conducted between 1988-1994 and 1999-2012 of nationally representative samples of the civilian, noninstitutionalized US population; 2781 adults from 2011-2012 were used to estimate recent prevalence and an additional 23,634 adults from 1988-2010 were used to estimate trends.\n\nMAIN OUTCOMES AND MEASURES:\nThe prevalence of diabetes was defined using a previous diagnosis of diabetes or, if diabetes was not previously diagnosed, by (1) a hemoglobin A1c level of 6.5% or greater or a fasting plasma glucose (FPG) level of 126 mg/dL or greater (hemoglobin A1c or FPG definition) or (2) additionally including 2-hour plasma glucose (2-hour PG) level of 200 mg/dL or greater (hemoglobin A1c, FPG, or 2-hour PG definition). Prediabetes was defined as a hemoglobin A1c level of 5.7% to 6.4%, an FPG level of 100 mg/dL to 125 mg/dL, or a 2-hour PG level of 140 mg/dL to 199 mg/dL.\n\nRESULTS:\nIn the overall 2011-2012 population, the unadjusted prevalence (using the hemoglobin A1c, FPG, or 2-hour PG definitions for diabetes and prediabetes) was 14.3% (95% CI, 12.2%-16.8%) for total diabetes, 9.1% (95% CI, 7.8%-10.6%) for diagnosed diabetes, 5.2% (95% CI, 4.0%-6.9%) for undiagnosed diabetes, and 38.0% (95% CI, 34.7%-41.3%) for prediabetes; among those with diabetes, 36.4% (95% CI, 30.5%-42.7%) were undiagnosed. The unadjusted prevalence of total diabetes (using the hemoglobin A1c or FPG definition) was 12.3% (95% CI, 10.8%-14.1%); among those with diabetes, 25.2% (95% CI, 21.1%-29.8%) were undiagnosed. Compared with non-Hispanic white participants (11.3% [95% CI, 9.0%-14.1%]), the age-standardized prevalence of total diabetes (using the hemoglobin A1c, FPG, or 2-hour PG definition) was higher among non-Hispanic black participants (21.8% [95% CI, 17.7%-26.7%]; P \u003c .001), non-Hispanic Asian participants (20.6% [95% CI, 15.0%-27.6%]; P = .007), and Hispanic participants (22.6% [95% CI, 18.4%-27.5%]; P \u003c .001). The age-standardized percentage of cases that were undiagnosed was higher among non-Hispanic Asian participants (50.9% [95% CI, 38.3%-63.4%]; P = .004) and Hispanic participants (49.0% [95% CI, 40.8%-57.2%]; P = .02) than all other racial/ethnic groups. The age-standardized prevalence of total diabetes (using the hemoglobin A1c or FPG definition) increased from 9.8% (95% CI, 8.9%-10.6%) in 1988-1994 to 10.8% (95% CI, 9.5%-12.0%) in 2001-2002 to 12.4% (95% CI, 10.8%-14.2%) in 2011-2012 (P \u003c .001 for trend) and increased significantly in every age group, in both sexes, in every racial/ethnic group, by all education levels, and in all poverty income ratio tertiles.\n\nCONCLUSIONS AND RELEVANCE:\nIn 2011-2012, the estimated prevalence of diabetes was 12% to 14% among US adults, depending on the criteria used, with a higher prevalence among participants who were non-Hispanic black, non-Hispanic Asian, and Hispanic. Between 1988-1994 and 2011-2012, the prevalence of diabetes increased in the overall population and in all subgroups evaluated." + }, + "questions": [ + { + "id": "eff3b5d7-7d02-4648-bbab-98dfcb99b3dc", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 3217, + "text": "non-Hispanic black" + }, + { + "answer_start": 3237, + "text": "non-Hispanic Asian" + }, + { + "answer_start": 3261, + "text": "Hispanic" + }, + { + "answer_start": 2137, + "text": "non-Hispanic black" + }, + { + "answer_start": 2210, + "text": "non-Hispanic Asian" + }, + { + "answer_start": 2287, + "text": "Hispanic" + } + ] + } + ] +} \ No newline at end of file diff --git a/6981c682-18dc-4ca6-bb3a-873b0810a954.json b/6981c682-18dc-4ca6-bb3a-873b0810a954.json new file mode 100644 index 0000000000000000000000000000000000000000..5725e1eea83842b1bb6b0364aef88222d5ac8c90 --- /dev/null +++ b/6981c682-18dc-4ca6-bb3a-873b0810a954.json @@ -0,0 +1,54 @@ +{ + "id": "6981c682-18dc-4ca6-bb3a-873b0810a954", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "15801485", + "text": "OBJECTIVE:\nTo investigate occupational risk factors for bladder cancer in seven Canadian provinces.\n\nMETHODS:\nWe analysed a population-based case-control dataset of 887 individuals with incident, histologically confirmed bladder cancer between 1994 and 1997. Controls (2847) frequency matched for age and gender were surveyed in 1996. Questionnaires were returned by about 60% of subjects. Odds ratios (ORs) for occupations and self-reported exposures were adjusted for province, age, race, smoking, and several dietary factors, using unconditional logistic regression.\n\nRESULTS:\nStatistically significant increased risks were observed among men employed as hairdressers (OR = 3.42; 1.09-10.8), primary metal workers (OR = 2.40; 1.29-4.50), miners (OR = 1.94; 1.18-3.17), and automechanics (OR = 1.69; 1.02-2.82). Primary metal workers and automechanics showed evidence of an employment duration-response trend. Modest elevated risks that were not significant were also observed for male government inspectors, printers, firefighters, general labourers, and welders. A duration-response trend was evident for government inspectors and general labourers. For females, significant elevations were observed among lumber processors (OR = 8.78; 1.28-60.1), general labourers (OR = 2.18; 1.05-4.52), nurses (OR = 1.54; 1.03-2.31), and general clerks (OR = 1.48; 1.01-2.17). The latter showed a positive duration-response trend.\n\nCONCLUSIONS:\nThis study found a statistically significant excess risk of bladder cancer, with a duration-response trend, among male primary metal workers and automechanics, and female office workers engaged in general clerical duties." + }, + "questions": [ + { + "id": "4adbbc99-e74c-4add-9f72-e68001e2e3c8", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 636, + "text": "among men employed as hairdressers" + }, + { + "answer_start": 695, + "text": "primary metal workers" + }, + { + "answer_start": 741, + "text": "miners" + }, + { + "answer_start": 776, + "text": "automechanics" + }, + { + "answer_start": 1154, + "text": "For females, significant elevations were observed among lumber processors" + }, + { + "answer_start": 1252, + "text": "general labourers" + } + ] + } + ] +} \ No newline at end of file diff --git a/69ec047d-aa8b-484a-a4f1-c84e6ec02d88.json b/69ec047d-aa8b-484a-a4f1-c84e6ec02d88.json new file mode 100644 index 0000000000000000000000000000000000000000..f53c63f448797575544d69f76668e18c5ccb19f8 --- /dev/null +++ b/69ec047d-aa8b-484a-a4f1-c84e6ec02d88.json @@ -0,0 +1,38 @@ +{ + "id": "69ec047d-aa8b-484a-a4f1-c84e6ec02d88", + "disease": { + "id": "H00408", + "names": [ + "Type 1 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E10" + ], + "mesh": [ + "D003922" + ] + }, + "category": "Metabolic disease; Immune system disease; Endocrine disease" + }, + "article": { + "id": "21395679", + "text": "AIM:\nTo describe Type 1 diabetes incidence trends in the UK between 1991 and 2008 in children aged 0-14 years and in young adults aged 15-34 years.\n\nMETHODS:\nData from the UK General Practice Research Database were analysed, including 3002 individuals (1565 aged 0-14 years and 1437 aged 15-34 years) newly diagnosed with Type 1 diabetes. Poisson regression was used to model annual incidence increases and seasonality effects.\n\nRESULTS:\nType 1 diabetes incidence increased from 11 to 24/100,000 person-years in boys and from 15 to 20/100,000 person-years in girls. In adults, the incidence rate increased from 13 to 20/100,000 person-years (men) and from 7 to 10/100,000 person-years (women). Annual incidence increases tended to be greater in children (4.1%, 95% CI 3.0-5.2%) compared with 15- to 34-year-olds (2.8%, 95% CI 1.6-3.9%). There was evidence of higher incidence rates during autumn and winter in children, but not in adults.\n\nCONCLUSIONS:\nA continuing increase in Type 1 diabetes incidence was shown that was greater in children than in young adults. Seasonal variation was observed in children only." + }, + "questions": [ + { + "id": "a0868949-c721-458e-a4ce-36a0f11f08a5", + "text": "What are the risk factors of Type 1 diabetes mellitus?", + "answers": [ + { + "answer_start": 1034, + "text": "children" + }, + { + "answer_start": 745, + "text": "children" + } + ] + } + ] +} \ No newline at end of file diff --git a/6a52d1ed-5151-4218-a3df-0c0c06445690.json b/6a52d1ed-5151-4218-a3df-0c0c06445690.json new file mode 100644 index 0000000000000000000000000000000000000000..262ce917ef19db5e49c7450cb4ebcb4b786d72b5 --- /dev/null +++ b/6a52d1ed-5151-4218-a3df-0c0c06445690.json @@ -0,0 +1,35 @@ +{ + "id": "6a52d1ed-5151-4218-a3df-0c0c06445690", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "11295666", + "text": "This study evaluated the relationship of caesarean section to the risk of asthma in adulthood. The data were based on a prospective birth cohort born in northern Finland in 1966. In 1997, when the members of the cohort were 31 years old, information on current doctor-diagnosed asthma and other allergic disorders was obtained from 1953 subjects by a self-administered questionnaire and skin prick test. Caesarean section had a strong effect on current doctor-diagnosed asthma in adulthood with an adjusted odds ratio (OR) of 3.23 (95% CI 1.53, 6.80). However, no substantial effects were observed for atopy, hay fever, and atopic eczema." + }, + "questions": [ + { + "id": "21c0daac-c1c8-4a17-a785-fecbbb9227f6", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 404, + "text": "Caesarean section" + } + ] + } + ] +} \ No newline at end of file diff --git a/6b264666-2105-4cc6-88d7-8e13c191bfb3.json b/6b264666-2105-4cc6-88d7-8e13c191bfb3.json new file mode 100644 index 0000000000000000000000000000000000000000..a451c92ba83fe6734ba58fe56b7b3539e2516d4c --- /dev/null +++ b/6b264666-2105-4cc6-88d7-8e13c191bfb3.json @@ -0,0 +1,40 @@ +{ + "id": "6b264666-2105-4cc6-88d7-8e13c191bfb3", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "22837378", + "text": "RATIONALE:\nGenome-wide association studies (GWAS) have identified loci influencing lung function, but fewer genes influencing chronic obstructive pulmonary disease (COPD) are known.\n\nOBJECTIVES:\nPerform meta-analyses of GWAS for airflow obstruction, a key pathophysiologic characteristic of COPD assessed by spirometry, in population-based cohorts examining all participants, ever smokers, never smokers, asthma-free participants, and more severe cases.\n\nMETHODS:\nFifteen cohorts were studied for discovery (3,368 affected; 29,507 unaffected), and a population-based family study and a meta-analysis of case-control studies were used for replication and regional follow-up (3,837 cases; 4,479 control subjects). Airflow obstruction was defined as FEV(1) and its ratio to FVC (FEV(1)/FVC) both less than their respective lower limits of normal as determined by published reference equations.\n\nMEASUREMENTS AND MAIN RESULTS:\nThe discovery meta-analyses identified one region on chromosome 15q25.1 meeting genome-wide significance in ever smokers that includes AGPHD1, IREB2, and CHRNA5/CHRNA3 genes. The region was also modestly associated among never smokers. Gene expression studies confirmed the presence of CHRNA5/3 in lung, airway smooth muscle, and bronchial epithelial cells. A single-nucleotide polymorphism in HTR4, a gene previously related to FEV(1)/FVC, achieved genome-wide statistical significance in combined meta-analysis. Top single-nucleotide polymorphisms in ADAM19, RARB, PPAP2B, and ADAMTS19 were nominally replicated in the COPD meta-analysis.\n\nCONCLUSIONS:\nThese results suggest an important role for the CHRNA5/3 region as a genetic risk factor for airflow obstruction that may be independent of smoking and implicate the HTR4 gene in the etiology of airflow obstruction." + }, + "questions": [ + { + "id": "e379cf6c-df64-4da2-9832-a808df6a960f", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 1281, + "text": "A single-nucleotide polymorphism in HTR4" + }, + { + "answer_start": 1626, + "text": "CHRNA5/3 region" + } + ] + } + ] +} \ No newline at end of file diff --git a/6ba0ab78-0bbf-444d-aac6-e44363f77c56.json b/6ba0ab78-0bbf-444d-aac6-e44363f77c56.json new file mode 100644 index 0000000000000000000000000000000000000000..0c60bff1ceda9d9b648ac75b87a3835879a4d802 --- /dev/null +++ b/6ba0ab78-0bbf-444d-aac6-e44363f77c56.json @@ -0,0 +1,49 @@ +{ + "id": "6ba0ab78-0bbf-444d-aac6-e44363f77c56", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "30352079", + "text": "BACKGROUND:\nSedentary behavior is thought to pose different risks to those attributable to physical inactivity. However, few studies have examined the association between physical activity and sitting time with cancer incidence within the same population.\n\nMETHODS:\nWe followed 38,154 healthy Norwegian adults in the Nord-Trøndelag Health Study (HUNT) for cancer incidence from 1995-97 to 2014. Cox proportional hazards regression was used to estimate risk of site-specific and total cancer incidence by baseline sitting time and physical activity.\n\nRESULTS:\nDuring the 16-years follow-up, 4,196 (11%) persons were diagnosed with cancer. We found no evidence that people who had prolonged sitting per day or had low levels of physical activity had an increased risk of total cancer incidence, compared to those who had low sitting time and were physically active. In the multivariate model, sitting ≥8 h/day was associated with 22% (95% CI, 1.05-1.42) higher risk of prostate cancer compared to sitting \u003c8 h/day. Further, men with low physical activity (≤8.3 MET-h/week) had 31% (95% CI, 1.00-1.70) increased risk of colorectal cancer (CRC) and 45% (95% CI, 1.01-2.09) increased risk of lung cancer compared to participants with a high physical activity (\u003e16.6 MET-h/week). The joint effects of physical activity and sitting time the indicated that prolonged sitting time increased the risk of CRC independent of physical activity in men.\n\nCONCLUSIONS:\nOur findings suggest that prolonged sitting and low physical activity are positively associated with colorectal-, prostate- and lung cancer among men. Sitting time and physical activity were not associated with cancer incidence among women. The findings emphasizing the importance of reducing sitting time and increasing physical activity." + }, + "questions": [ + { + "id": "31a6f695-6ebd-48eb-ac8b-71e995b00783", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1479, + "text": "prolonged sitting" + }, + { + "answer_start": 1501, + "text": "low physical activity" + }, + { + "answer_start": 891, + "text": "sitting ≥8 h/day " + }, + { + "answer_start": 1022, + "text": "men with low physical activity (≤8.3 MET-h/week)" + } + ] + } + ] +} \ No newline at end of file diff --git a/6bc28096-1fc3-41fa-bd67-4f01162dbc8e.json b/6bc28096-1fc3-41fa-bd67-4f01162dbc8e.json new file mode 100644 index 0000000000000000000000000000000000000000..3b6eeee0108b3ccd8df660cd06b0f9cb34b82a8e --- /dev/null +++ b/6bc28096-1fc3-41fa-bd67-4f01162dbc8e.json @@ -0,0 +1,48 @@ +{ + "id": "6bc28096-1fc3-41fa-bd67-4f01162dbc8e", + "disease": { + "id": "M2023_04_26_16_49_01", + "names": [ + "Metabolic syndrome" + ], + "dbLinks": { + "mesh": [ + "C18.452.394.968.500.570", + "C18.452.625" + ] + }, + "description": "Metabolic syndrome is a complex constellation of metabolic derangements that increase the risk of atherosclerotic cardiovascular disease, type 2 diabetes, and all-cause mortality. The key features of metabolic syndrome include central obesity, insulin resistance, dyslipidemia, and hypertension. These abnormalities are believed to arise from a combination of genetic predisposition and environmental factors, such as sedentary behavior, poor dietary habits, and chronic stress. Diagnosis of metabolic syndrome requires meeting three or more established criteria, based on standardized guidelines. Management of metabolic syndrome involves a comprehensive approach, including lifestyle modifications such as weight loss, physical activity, and dietary changes, as well as pharmacotherapy to address underlying risk factors such as hypertension, dyslipidemia, and hyperglycemia. Early intervention and aggressive management of metabolic syndrome are critical to preventing or delaying the onset of complications and improving long-term health outcomes." + }, + "article": { + "id": "15642873", + "text": "BACKGROUND:\nAmong young adults, the metabolic syndrome is an increasingly frequent risk factor for cardiovascular disease. Its determinants are, however, incompletely understood. We investigated the time course, from adolescence (age, 13 years) to young adulthood (age, 36 years), of important potential determinants (body fatness and fat distribution, cardiopulmonary fitness, and lifestyle) in 364 individuals (189 women).\n\nMETHODS:\nData were derived from the Amsterdam Growth and Health Longitudinal Study and analyzed with the use of generalized estimating equations.\n\nRESULTS:\nThe prevalence of the metabolic syndrome at the age of 36 years, as identified with a modified National Cholesterol Education Program definition of the syndrome, was 10.4%. Subjects with the metabolic syndrome at the age of 36 years, compared with those without the syndrome, had (from adolescence to the age of 36 years) the following: (1) a more marked increase in total body fatness and in subcutaneous trunk fat; (2) a more marked decrease in cardiopulmonary fitness levels; (3) a more marked increase in physical activities of light-to-moderate intensity, but a more marked decrease in hard physical activities; (4) a trend toward a higher energy intake throughout the years; and (5) a decreased likelihood of drinking alcoholic beverages.\n\nCONCLUSIONS:\nFatness, fitness, and lifestyle are important determinants of the metabolic syndrome in young adults. More important, these associations were independent of each other and, therefore, represent separate potential targets for the prevention of the metabolic syndrome. Our study further suggests that intervening early in life (eg, in the period of transition from adolescence to adulthood) may be a fruitful area for prevention of the metabolic syndrome." + }, + "questions": [ + { + "id": "1e909522-d608-4afd-847e-d761774ebf1b", + "text": "What is a risk factor for Metabolic Syndrome?", + "answers": [ + { + "answer_start": 923, + "text": "a more marked increase in total body fatness and in subcutaneous trunk fat" + }, + { + "answer_start": 1003, + "text": "a more marked decrease in cardiopulmonary fitness levels" + }, + { + "answer_start": 1065, + "text": "a more marked increase in physical activities of light-to-moderate intensity, but a more marked decrease in hard physical activities" + }, + { + "answer_start": 1203, + "text": "a trend toward a higher energy intake throughout the years" + }, + { + "answer_start": 1271, + "text": "a decreased likelihood of drinking alcoholic beverages" + } + ] + } + ] +} \ No newline at end of file diff --git a/6cc9e6cf-d2bd-46ca-afa7-989fecf1e4f7.json b/6cc9e6cf-d2bd-46ca-afa7-989fecf1e4f7.json new file mode 100644 index 0000000000000000000000000000000000000000..b971ea1d112f63194e6c5d1ecd83f190542aea9f --- /dev/null +++ b/6cc9e6cf-d2bd-46ca-afa7-989fecf1e4f7.json @@ -0,0 +1,34 @@ +{ + "id": "6cc9e6cf-d2bd-46ca-afa7-989fecf1e4f7", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "11976167", + "text": "BACKGROUND:\nCeliac disease, or permanent gluten-sensitive enteropathy, is an immunologic disease strictly dependent on exposure to wheat gluten or related proteins in rye and barley.\n\nOBJECTIVE:\nThe aim of this study was to explore whether breast-feeding and the mode of introducing dietary gluten influence the risk of celiac disease in childhood.\n\nDESIGN:\nA population-based incident case-referent study of Swedish children, 627 cases with celiac disease and 1254 referents, was conducted; 78% of the matched sets were included in the final analyses. A questionnaire was used to assess patterns of food introduction to infants. Models were built, based on current epidemiologic and immunologic knowledge of celiac disease, to study the potential influence of dietary patterns on disease risk and were evaluated by conditional logistic regression in multivariate analyses.\n\nRESULTS:\nThe risk of celiac disease was reduced in children aged \u003c2 y if they were still being breast-fed when dietary gluten was introduced [adjusted odds ratio (OR): 0.59; 95% CI: 0.42, 0.83]. This effect was even more pronounced in infants who continued to be breast-fed after dietary gluten was introduced (OR: 0.36; 95% CI: 0.26, 0.51). The risk was greater when gluten was introduced in the diet in large amounts (OR: 1.5; 95% CI: 1.1, 2.1) than when introduced in small or medium amounts. In older children, these risk factors were of no or only minor importance.\n\nCONCLUSIONS:\nThe gradual introduction of gluten-containing foods into the diet of infants while they are still being breast-fed reduces the risk of celiac disease in early childhood and probably also during the subsequent childhood period." + }, + "questions": [ + { + "id": "da4df544-3522-4e15-bf8f-c5b09618864d", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 1243, + "text": "gluten was introduced in the diet in large amounts" + } + ] + } + ] +} \ No newline at end of file diff --git a/6d662098-b425-4edd-95bf-c8696268fcf1.json b/6d662098-b425-4edd-95bf-c8696268fcf1.json new file mode 100644 index 0000000000000000000000000000000000000000..6cd4665154b097170453fcf37a81e2b5f46492ad --- /dev/null +++ b/6d662098-b425-4edd-95bf-c8696268fcf1.json @@ -0,0 +1,34 @@ +{ + "id": "6d662098-b425-4edd-95bf-c8696268fcf1", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "29279935", + "text": "IMPORTANCE:\nIn the United States, black individuals are twice as likely to develop type 2 diabetes compared with white individuals, and these disparities are particularly pronounced in young and middle age. Prior studies have identified differences in traditional risk factors that may be associated with racial disparities in diabetes incidence but have not simultaneously adjusted for risk factors measured across multiple domains (eg, the individual and the environment) and updated over time.\n\nOBJECTIVE:\nTo determine the relative associations of modifiable biological, neighborhood, psychosocial, socioeconomic, and behavioral factors in young adulthood with the observed racial disparity in diabetes incidence between middle-aged black and white individuals.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nBlack and white men and women from the observational Coronary Artery Risk Development in Young Adults study, aged 18 to 30 years, without diabetes at baseline (1985-1986; N = 4251) were observed through 2015-2016. Sex-stratified multivariable-adjusted Cox proportional hazards modeling, with adjustment for time-updated covariates, was used to estimate risk for incident diabetes. Percent reduction in the β coefficient (the logarithm used to calculate the hazard ratio [HR]) was calculated to compare black to white participants.\n\nEXPOSURES:\nSelf-identified race and factors including biological (eg, fasting glucose, body mass index), neighborhood (racial segregation and tract-level poverty), psychosocial (depressive symptoms), socioeconomic (eg, personal and parental educational attainment, current employment), and behavioral (eg, regular alcohol consumption, smoking) domains.\n\nMAIN OUTCOMES AND MEASURES:\nIncident type 2 diabetes mellitus.\n\nRESULTS:\nThe mean (SD) age at baseline was 25 (3.6) years, 49% (n = 2066) of the sample was black, and 54% (n = 2304) were women. Over a mean follow-up of 24.5 years, 504 cases of incident diabetes were identified. Using sex-stratified multivariable-adjusted Cox proportional hazards models, black women and men were more likely to develop diabetes than white men and women (black women: HR, 2.86 [95% CI, 2.19-3.72] and risk difference [RD], 89 cases/1000 people [95% CI, 61-117]; black men: HR, 1.67 [95% CI, 1.28-2.17] and RD, 47 cases/1000 people [95% CI, 15-78]) after adjustment for age and center. Biological factors were most strongly associated with the disparity in diabetes risk between black and white individuals for women (percent reduction in β, 112%) and men (percent reduction in β, 86%). There was no longer disparity in diabetes risk between black and white middle-aged adults after adjustment for biological, neighborhood, psychosocial, socioeconomic, and behavioral factors measured over time (HR for women, 0.79 [95% CI, 0.55-1.14]; HR for men, 0.92 [95% CI, 0.62-1.38]).\n\nCONCLUSIONS AND RELEVANCE:\nIn this cohort study comparing black and white participants, there was a statistically significant increased risk of incident type 2 diabetes among black women and men. However, after adjustment for modifiable risk factors during young adulthood, the disparity was no longer statistically significant." + }, + "questions": [ + { + "id": "65cf9432-a8ca-4e5d-abbb-c66b50b417e0", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 2043, + "text": "black women and men" + } + ] + } + ] +} \ No newline at end of file diff --git a/6d67b335-4cdc-4a76-bea8-1bac1c70c085.json b/6d67b335-4cdc-4a76-bea8-1bac1c70c085.json new file mode 100644 index 0000000000000000000000000000000000000000..4d816461c8b4af48e099fd9ee735352680fa7d8b --- /dev/null +++ b/6d67b335-4cdc-4a76-bea8-1bac1c70c085.json @@ -0,0 +1,47 @@ +{ + "id": "6d67b335-4cdc-4a76-bea8-1bac1c70c085", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "34406709", + "text": "OBJECTIVE:\nTo investigate passive smoking throughout the life course and the risk of rheumatoid arthritis (RA), while accounting for personal smoking.\n\nMETHODS:\nWe analyzed the Nurses' Health Study II prospective cohort, using information collected via biennial questionnaires. We assessed the influence of 1) maternal smoking during pregnancy (in utero exposure), 2) childhood parental smoking, and 3) years lived with smokers since age 18. Incident RA and serostatus were determined by medical record review. Using the marginal structural model framework, we estimated the controlled direct effect of each passive smoking exposure on adult incident RA risk by serologic phenotype, controlling for early-life factors and time-updated adulthood factors including personal smoking.\n\nRESULTS:\nAmong 90,923 women, we identified 532 incident RA cases (66% seropositive) during a median of 27.7 years of follow-up. Maternal smoking during pregnancy was associated with RA after adjustment for confounders, with a hazard ratio (HR) of 1.25 (95% confidence interval [95% CI] 1.03-1.52), but not after accounting for subsequent smoking exposures. Childhood parental smoking was associated with seropositive RA after adjustment for confounders (HR 1.41 [95% CI 1.08-1.83]). In the controlled direct effect analyses, childhood parental smoking was associated with seropositive RA (HR 1.75 [95% CI 1.03-2.98]) after controlling for adulthood personal smoking, and the association was accentuated among ever smokers (HR 2.18 [95% CI 1.23-3.88]). There was no significant association of adulthood passive smoking with RA (HR 1.30 for ≥20 years of living with a smoker versus none [95% CI 0.97-1.74]).\n\nCONCLUSION:\nWe found a potential direct influence of childhood parental smoking on adult-onset incident seropositive RA even after controlling for adulthood personal smoking." + }, + "questions": [ + { + "id": "7a97ccb8-e8f9-4842-8220-f87c374573c5", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 910, + "text": "Maternal smoking during pregnancy" + }, + { + "answer_start": 1139, + "text": "Childhood parental smoking" + }, + { + "answer_start": 1307, + "text": "childhood parental smoking" + }, + { + "answer_start": 1742, + "text": "childhood parental smoking" + } + ] + } + ] +} \ No newline at end of file diff --git a/6d7a3b29-8aab-41ed-b09d-2b4f3dd06c30.json b/6d7a3b29-8aab-41ed-b09d-2b4f3dd06c30.json new file mode 100644 index 0000000000000000000000000000000000000000..6c43c1b9abcf904019640083e3c8467db646926b --- /dev/null +++ b/6d7a3b29-8aab-41ed-b09d-2b4f3dd06c30.json @@ -0,0 +1,50 @@ +{ + "id": "6d7a3b29-8aab-41ed-b09d-2b4f3dd06c30", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "11092437", + "text": "Because of the temporal relations between reproductive risk factors and incidence of breast cancer, the authors developed a nonlinear Poisson regression that accounts for time and summarizes risk to age 70 years. Reproductive risk factors, benign breast disease, use of postmenopausal hormones, weight, and alcohol intake were evaluated as risk factors. Among 58,520 women aged 30-55 years in 1980, followed through June 1, 1994, 1,761 incident invasive breast cancer cases were identified. All risks are multivariate adjusted. History of benign breast disease is associated with a 57% increase (95% confidence interval (CI): 43%, 73%) in cumulative risk of breast cancer by age 70 years. Use of unopposed postmenopausal estrogen from ages 50-60 years increases risk of breast cancer to age 70 by 23% (95% CI: 6%, 42%) compared with a woman who never uses hormones. Ten years of use of estrogen plus progestin increases risk to age 70 years by 67% (95% CI: 18%, 136%). Compared with never drinking alcohol, one drink per day from age 18 years increases risk to age 70 by 7% (95% CI: 0%, 13%). Use of unopposed postmenopausal hormones for 10 years significantly increases the risk of breast cancer, and the addition of progestin further increases the risk." + }, + "questions": [ + { + "id": "08848c02-9d7f-4b0a-9a98-fff1706b70ec", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 528, + "text": "History of benign breast disease" + }, + { + "answer_start": 689, + "text": "Use of unopposed postmenopausal estrogen from ages 50-60 years" + }, + { + "answer_start": 866, + "text": "Ten years of use of estrogen plus progestin increases risk to age 70 years" + }, + { + "answer_start": 1007, + "text": "one drink per day from age 18 years" + }, + { + "answer_start": 1093, + "text": "Use of unopposed postmenopausal hormones for 10 years" + } + ] + } + ] +} \ No newline at end of file diff --git a/6deb6d0e-9fb9-4bf5-ac69-b269e5d58970.json b/6deb6d0e-9fb9-4bf5-ac69-b269e5d58970.json new file mode 100644 index 0000000000000000000000000000000000000000..b4d22634754cd593bcd1957e48d12bedbd68ebe5 --- /dev/null +++ b/6deb6d0e-9fb9-4bf5-ac69-b269e5d58970.json @@ -0,0 +1,39 @@ +{ + "id": "6deb6d0e-9fb9-4bf5-ac69-b269e5d58970", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "22443179", + "text": "BACKGROUND:\nProton pump inhibitors (PPIs) may activate the immune system and cause asthma.\n\nAIM:\nTo investigate the association of prenatal exposure to PPIs and histamine 2-receptor antagonists (H2RAs) with risk of asthma.\n\nMETHODS:\nIn this cohort study, 197,060 singletons born between 1996 and 2008 in northern Denmark were followed until the end of 2009. Data were obtained through Danish medical registries. Asthma in offspring was defined as at least two prescriptions of both a β-agonist and an inhaled glucocorticoid and/or a hospital diagnosis of asthma during the follow-up. Cox proportional-hazard regression was used to compute incidence rate ratios, adjusting for covariates.\n\nRESULTS:\nA total of 2238 (1.1%) children were prenatally exposed to PPIs and 24,506 (12.4%) children developed asthma during follow-up (median follow-up = 6.8 years). The adjusted IRR (aIRR) of asthma associated with prenatal exposure to PPIs was 1.41 (95% confidence interval (CI): 1.27-1.56), compared with those unexposed. The association did not vary by trimester of exposure, and prenatal exposure to H2RAs was associated with similar increase in risk. The aIRR for maternal PPI and H2RA use in the year after, but not during pregnancy was 1.32 (95% CI: 1.20-1.46) and 1.13 (0.93-1.36), respectively, compared with non-use during and in the year after pregnancy.\n\nCONCLUSIONS:\nPrenatal exposure to both PPIs and H2RAs was associated with an increased risk of asthma in our study. Because the observed association is not drug specific and also observed for maternal postnatal use it may be explained by a 'class effect' or maternal underlying condition." + }, + "questions": [ + { + "id": "9822758a-36ae-4360-86f0-ac4c2b21d153", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 906, + "text": "prenatal exposure to PPIs" + }, + { + "answer_start": 1371, + "text": "Prenatal exposure to both PPIs and H2RAs" + } + ] + } + ] +} \ No newline at end of file diff --git a/6eabdce5-541c-4e80-a268-cf6124bcaf3a.json b/6eabdce5-541c-4e80-a268-cf6124bcaf3a.json new file mode 100644 index 0000000000000000000000000000000000000000..27d6411f63bfaa7b57a3445c6308e4e1433f0ed9 --- /dev/null +++ b/6eabdce5-541c-4e80-a268-cf6124bcaf3a.json @@ -0,0 +1,41 @@ +{ + "id": "6eabdce5-541c-4e80-a268-cf6124bcaf3a", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "32968205", + "text": "BACKGROUND:\nIt is understudied whether the posed association of oral antibiotics with colorectal cancer (CRC) varies between antibiotic spectrums, colorectal continuum, and if a non-linear dose-dependent relationship is present.\n\nDESIGN:\nThree electronic databases and a trial platform were searched for all relevant studies, from inception until February 2020, without restrictions. Random-effects meta-analyses provided pooled effect-sizes (ES) with 95% confidence intervals (CI). Dose-response analyses modelling the relationship between number of days exposed to antibiotics and CRC risk were extended to non-linear multivariable random-effects models.\n\nRESULTS:\nOf 6483 identified publications ten were eligible, including 4.1 million individuals and over 73,550 CRC cases. The pooled CRC risk was increased among individuals who ever-used antibiotics (ES = 1.17, 95%CI 1.05-1.30), particularly for broad-spectrum antibiotics (ES = 1.70, 95%CI 1.26-2.30), but not for narrow-spectrum antibiotic (ES = 1.11, 95% 0.93-1.32). The dose-response analysis did not provide strong evidence of any particular dose-response association, and the risk patterns were rather similar for colon and rectal cancer.\n\nDISCUSSION:\nThe antibiotic use associated CRC risk seemingly differs between broad- and narrow-spectrum antibiotics, and possibly within the colorectal continuum. It remains unclear whether this association is causal, requiring more mechanistic studies and further clarification of drug-microbiome interactions." + }, + "questions": [ + { + "id": "b6b1fec1-c64d-48d5-b2bd-9c68a5037b44", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 819, + "text": "individuals who ever-used antibiotics" + }, + { + "answer_start": 904, + "text": "broad-spectrum antibiotics" + } + ] + } + ] +} \ No newline at end of file diff --git a/6f013f15-fb7f-4a42-8d90-c6844df2f937.json b/6f013f15-fb7f-4a42-8d90-c6844df2f937.json new file mode 100644 index 0000000000000000000000000000000000000000..13a29f2f0119fbae6d595d147ecfaff1c9b3c00c --- /dev/null +++ b/6f013f15-fb7f-4a42-8d90-c6844df2f937.json @@ -0,0 +1,38 @@ +{ + "id": "6f013f15-fb7f-4a42-8d90-c6844df2f937", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "16198986", + "text": "The amount of radiologically dense breast-tissue appearing on a mammogram varies between women because of differences in the composition of breast tissue, and is referred to here as mammographic density. This review presents evidence that mammographic density is a strong risk factor for breast cancer, and that risk of breast cancer is four to five times greater in women with density in more than 75% of the breast than in women with little or no density in the breast. Density in more than 50% of the breast could account for about a third of breast cancers. The epidemiology of mammographic density is consistent with its being a marker of susceptibility to breast cancer. Twin studies have shown that the proportion of the breast occupied by density, at a given age, is highly heritable, and inherited factors explain 63% of the variance. Mammographic breast density has the characteristics of a quantitative trait and might be determined by genes that are easier to identify than those for breast cancer itself. The genes that determine breast density might also be associated with risk of breast cancer, and their identification is also likely to provide insights into the biology of the breast and identify potential targets for preventive strategies." + }, + "questions": [ + { + "id": "5229574e-5e74-4f51-845f-af193cac7cc9", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 239, + "text": "mammographic density" + }, + { + "answer_start": 367, + "text": "women with density in more than 75% of the breast" + } + ] + } + ] +} \ No newline at end of file diff --git a/6f17278f-3031-4c56-981b-c0e9b840724a.json b/6f17278f-3031-4c56-981b-c0e9b840724a.json new file mode 100644 index 0000000000000000000000000000000000000000..2963507616286691aaa2f6fa9f28664ef70e3412 --- /dev/null +++ b/6f17278f-3031-4c56-981b-c0e9b840724a.json @@ -0,0 +1,36 @@ +{ + "id": "6f17278f-3031-4c56-981b-c0e9b840724a", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "21248322", + "text": "BACKGROUND:\nNumerous studies with varying associations between domestic use of solid biomass fuels (wood, dung, crop residue, charcoal) and respiratory diseases have been reported.\n\nOBJECTIVE:\nTo present the current data systematically associating use of biomass fuels with respiratory outcomes in rural women and children.\n\nMETHODS:\nSystematic searches were conducted in 13 electronic databases. Data were abstracted from original articles that satisfied selection criteria for meta-analyses. Publication bias and heterogeneity of samples were tested. Studies with common diagnoses were analysed using random-effect models.\n\nRESULTS:\nA total of 2717 studies were identified. Fifty-one studies were selected for data extraction and 25 studies were suitable for meta-analysis. The overall pooled ORs indicate significant associations with acute respiratory infection in children (OR 3.53, 95% CI 1.94 to 6.43), chronic bronchitis in women (OR 2.52, 95% CI 1.88 to 3.38) and chronic obstructive pulmonary disease in women (OR 2.40, 95% CI 1.47 to 3.93). In contrast, no significant association with asthma in children or women was noted.\n\nCONCLUSION:\nBiomass fuel exposure is associated with diverse respiratory diseases in rural populations. Concerted efforts in improving stove design and lowering exposure to smoke emission may reduce respiratory disease associated with biomass fuel exposure." + }, + "questions": [ + { + "id": "84a95fd9-27a0-4949-b66a-5da5fc4ecc08", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 1149, + "text": "Biomass fuel exposure" + } + ] + } + ] +} \ No newline at end of file diff --git a/6f719f73-5265-44e7-826c-caff2b0f7c46.json b/6f719f73-5265-44e7-826c-caff2b0f7c46.json new file mode 100644 index 0000000000000000000000000000000000000000..98faf7f16678dfd696a1b35a147f44e667cc9e87 --- /dev/null +++ b/6f719f73-5265-44e7-826c-caff2b0f7c46.json @@ -0,0 +1,38 @@ +{ + "id": "6f719f73-5265-44e7-826c-caff2b0f7c46", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "9259281", + "text": "A strong HLA association is seen in coeliac disease [specifically to the DQ(alpha1*0501,beta1*0201 heterodimer], but this cannot entirely account for the increased risk seen in relatives of affected cases. One or more genes at HLA-unlinked loci also predispose to coeliac disease and are probably stronger determinants of disease susceptibility than HLA. A recent study has proposed a number of candidate regions on chromosomes 6p23 (distinct from HLA), 6p12, 3q27, 5q33.3, 7q31.3, 11p11, 15q26, 19p13.3, 19q13.1, 19q13.4 and 22cen for the location of a non-HLA linked susceptibility gene. We have examined these regions in 28 coeliac disease families by linkage analysis. There was excess sharing of chromosome 6p markers, but no support for a predisposition locus telomeric to HLA. No significant evidence in favour of linkage to coeliac disease was obtained for chromosomes 3q27, 5q33.3, 7q31.3, 11p11, 19p13.3, 19q13.1, 19q13.4 or 22cen. There was, however, excess sharing close to D15S642. The maximum non-parametric linkage score was 1.99 (P = 0.03). Although the evidence for linkage of coeliac disease to chromosome 15q26 is not strong, the well established association between coeliac disease and insulin dependent diabetes mellitus, together with the mapping of an IDDM susceptibility locus (IDDM3) to chromosome 15q26, provide indirect support for this as a candidate locus conferring susceptibility to coeliac disease in some families." + }, + "questions": [ + { + "id": "b203f13c-611d-4433-a807-b50898ce0fd1", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 9, + "text": "HLA" + }, + { + "answer_start": 73, + "text": "DQ(alpha1*0501,beta1*0201 heterodimer" + } + ] + } + ] +} \ No newline at end of file diff --git a/6fe473ac-96cc-425d-93d4-49f9b9ddb37a.json b/6fe473ac-96cc-425d-93d4-49f9b9ddb37a.json new file mode 100644 index 0000000000000000000000000000000000000000..c117f8819a8dc87df9534097cee4a59bf9175061 --- /dev/null +++ b/6fe473ac-96cc-425d-93d4-49f9b9ddb37a.json @@ -0,0 +1,45 @@ +{ + "id": "6fe473ac-96cc-425d-93d4-49f9b9ddb37a", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "24444654", + "text": "We studied 2332 individuals with monoallelic mutations in MUTYH among 9504 relatives of 264 colorectal cancer (CRC) cases with a MUTYH mutation. We estimated CRC risks through 70 years of age of 7.2% for male carriers of monoallelic mutations (95% confidence interval [CI], 4.6%-11.3%) and 5.6% for female carriers of monoallelic mutations (95% CI, 3.6%-8.8%), irrespective of family history. For monoallelic MUTYH mutation carriers with a first-degree relative with CRC diagnosed by 50 years of age who does not have the MUTYH mutation, risks of CRC were 12.5% for men (95% CI, 8.6%-17.7%) and 10% for women (95% CI, 6.7%-14.4%). Risks of CRC for carriers of monoallelic mutations in MUTYH with a first-degree relative with CRC are sufficiently high to warrant more intensive screening than for the general population." + }, + "questions": [ + { + "id": "088b43f0-6a20-456d-aa87-c670ce206313", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 204, + "text": "male carriers of monoallelic mutations" + }, + { + "answer_start": 299, + "text": "female carriers of monoallelic mutations" + }, + { + "answer_start": 397, + "text": "monoallelic MUTYH mutation carriers with a first-degree relative with CRC diagnosed by 50 years of age who does not have the MUTYH mutation" + } + ] + } + ] +} \ No newline at end of file diff --git a/704466d0-3183-4da0-813b-ae2ade5b3dce.json b/704466d0-3183-4da0-813b-ae2ade5b3dce.json new file mode 100644 index 0000000000000000000000000000000000000000..fc752e8315c193191afbe9a7384521898192c485 --- /dev/null +++ b/704466d0-3183-4da0-813b-ae2ade5b3dce.json @@ -0,0 +1,54 @@ +{ + "id": "704466d0-3183-4da0-813b-ae2ade5b3dce", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "26182172", + "text": "IMPORTANCE:\nMore than two-thirds of US women are overweight or obese, placing them at increased risk for postmenopausal breast cancer.\n\nOBJECTIVE:\nTo investigate in this secondary analysis the associations of overweight and obesity with risk of postmenopausal invasive breast cancer after extended follow-up in the Women's Health Initiative (WHI) clinical trials.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nThe WHI clinical trial protocol incorporated measured height and weight, baseline and annual or biennial mammography, and adjudicated breast cancer end points in 67 142 postmenopausal women ages 50 to 79 years at 40 US clinical centers. The women were enrolled from 1993 to 1998 with a median of 13 years of follow-up through 2010; 3388 invasive breast cancers were observed.\n\nMAIN OUTCOMES AND MEASURES:\nHeight and weight were measured at baseline, and weight was measured annually thereafter. Data were collected on demographic characteristics, personal and family medical history, and personal habits (smoking, physical activity). Women underwent annual or biennial mammograms. Breast cancers were verified by medical records reviewed by physician adjudicators.\n\nRESULTS:\nWomen who were overweight and obese had an increased invasive breast cancer risk vs women of normal weight. Risk was greatest for obesity grade 2 plus 3 (body mass index [BMI], calculated as weight in kilograms divided by height in meters squared, \u003e35.0) (hazard ratio [HR] for invasive breast cancer, 1.58; 95% CI, 1.40-1.79). A BMI of 35.0 or higher was strongly associated with risk for estrogen receptor-positive and progesterone receptor-positive breast cancers (HR, 1.86; 95% CI, 1.60-2.17) but was not associated with estrogen receptor-negative cancers. Obesity grade 2 plus 3 was also associated with advanced disease, including larger tumor size (HR, 2.12; 95% CI, 1.67-2.69; P = .02), positive lymph nodes (HR, 1.89; 95% CI, 1.46-2.45; P = .06), regional and/or distant stage (HR, 1.94; 95% CI, 1.52-2.47; P = .05), and deaths after breast cancer (HR, 2.11; 95% CI, 1.57-2.84; P \u003c .001). Women with a baseline BMI of less than 25.0 who gained more than 5% of body weight over the follow-up period had an increased breast cancer risk (HR, 1.36; 95% CI, 1.1-1.65), but among women already overweight or obese we found no association of weight change (gain or loss) with breast cancer during follow-up. There was no effect modification of the BMI-breast cancer relationship by postmenopausal hormone therapy, and the direction of association across BMI categories was similar for never, past, and current hormone therapy use.\n\nCONCLUSIONS AND RELEVANCE:\nObesity is associated with increased invasive breast cancer risk in postmenopausal women. These clinically meaningful findings should motivate programs for obesity prevention.\n\nTRIAL REGISTRATION:\nclinicaltrials.gov Identifier: NCT00000611." + }, + "questions": [ + { + "id": "04dda747-e8a7-4360-aa39-8a20a5b7fe2d", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1175, + "text": "Women who were overweight and obese" + }, + { + "answer_start": 1305, + "text": "obesity grade 2 plus 3 (body mass index [BMI]" + }, + { + "answer_start": 1503, + "text": "A BMI of 35.0 or higher was" + }, + { + "answer_start": 1736, + "text": "Obesity grade 2 plus 3" + }, + { + "answer_start": 2073, + "text": "Women with a baseline BMI of less than 25.0 who gained more than 5% of body weight" + }, + { + "answer_start": 2636, + "text": "Obesity" + } + ] + } + ] +} \ No newline at end of file diff --git a/7127d095-d7f5-4286-86f2-562f79afc24d.json b/7127d095-d7f5-4286-86f2-562f79afc24d.json new file mode 100644 index 0000000000000000000000000000000000000000..5560c2a69f40dfe07aef8306bbc8009819d02ee4 --- /dev/null +++ b/7127d095-d7f5-4286-86f2-562f79afc24d.json @@ -0,0 +1,42 @@ +{ + "id": "7127d095-d7f5-4286-86f2-562f79afc24d", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "18557598", + "text": "The contribution of exposure to persistent organic pollutants (POPs) to the incidence of diabetes has received little attention until recently. A number of reports have emerged, however, concerning elevated diabetes in persons occupationally exposed to dioxin. United States (US) Air Force personnel in Vietnam who sprayed Agent Orange containing dioxin as a contaminant had elevated rates of diabetes, leading to US government compensation for diabetes in these veterans. Recent studies in populations exposed to polychlorinated biphenyls (PCBs) and chlorinated pesticides found a dose-dependent elevated risk of diabetes. An elevation in risk of diabetes in relation to levels of several POPs has been demonstrated by two different groups using the National Health and Nutrition Examination Survey (NHANES), a random sampling of US citizens. The strong associations seen in quite different studies suggest the possibility that exposure to POPs could cause diabetes. One striking observation is that obese persons that do not have elevated POPs are not at elevated risk of diabetes, suggesting that the POPs rather than the obesity per se is responsible for the association. Although a specific mechanism is not known, most POPs induce a great number and variety of genes, including several that alter insulin action. Because diabetes is a dangerous disease that is increasing in frequency throughout the world, further study of the possibility that exposure to POPs contributes to the etiology of diabetes is critical." + }, + "questions": [ + { + "id": "dbcf6eb8-40c8-48f0-b6ee-c807a56ddfa9", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 551, + "text": "chlorinated pesticides" + }, + { + "answer_start": 491, + "text": "populations exposed to polychlorinated biphenyls (PCBs)" + }, + { + "answer_start": 672, + "text": "levels of several POPs" + } + ] + } + ] +} \ No newline at end of file diff --git a/712d9842-2a3b-4be1-9efa-7c4a0d86753b.json b/712d9842-2a3b-4be1-9efa-7c4a0d86753b.json new file mode 100644 index 0000000000000000000000000000000000000000..ed01f623cfdf305827e774af7b139717a44c4d05 --- /dev/null +++ b/712d9842-2a3b-4be1-9efa-7c4a0d86753b.json @@ -0,0 +1,43 @@ +{ + "id": "712d9842-2a3b-4be1-9efa-7c4a0d86753b", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "16973983", + "text": "RATIONALE:\nAlthough involuntary exposure to maternal smoking during the in utero period and to secondhand smoke are associated with occurrence of childhood asthma, few studies have investigated the role of active cigarette smoking on asthma onset during adolescence.\n\nOBJECTIVES:\nTo determine whether regular smoking is associated with the new onset of asthma during adolescence.\n\nMETHODS:\nWe conducted a prospective cohort study among 2,609 children with no lifetime history of asthma or wheezing who were recruited from fourth- and seventh-grade classrooms and followed annually in schools in 12 southern California communities. Regular smoking was defined as smoking at least seven cigarettes per day on average over the week before and 300 cigarettes in the year before each annual interview. Incident asthma was defined using new cases of physician-diagnosed asthma.\n\nMEASUREMENTS AND MAIN RESULTS:\nRegular smoking was associated with increased risk of new-onset asthma. Children who reported smoking 300 or more cigarettes per year had a relative risk (RR) of 3.9 (95% confidence interval [95% CI], 1.7-8.5) for new-onset asthma compared with nonsmokers. The increased risk from regular smoking was greater in nonallergic than in allergic children. Regular smokers who were exposed to maternal smoking during gestation had the largest risk from active smoking (RR, 8.8; 95% CI, 3.2-24.0).\n\nCONCLUSIONS:\nRegular smoking increased risk for asthma among adolescents, especially for nonallergic adolescents and those exposed to maternal smoking during the in utero period." + }, + "questions": [ + { + "id": "078688f1-68bf-42b7-96b9-47d85c1050b2", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 904, + "text": "Regular smoking" + }, + { + "answer_start": 976, + "text": "Children who reported smoking 300 or more cigarettes per year" + }, + { + "answer_start": 1255, + "text": "Regular smokers who were exposed to maternal smoking during gestation" + } + ] + } + ] +} \ No newline at end of file diff --git a/719c2182-75f3-488f-b7fc-4f204e2a56b1.json b/719c2182-75f3-488f-b7fc-4f204e2a56b1.json new file mode 100644 index 0000000000000000000000000000000000000000..79492ad4bf0be4e701c9e044dbd13b5d2864a3ef --- /dev/null +++ b/719c2182-75f3-488f-b7fc-4f204e2a56b1.json @@ -0,0 +1,34 @@ +{ + "id": "719c2182-75f3-488f-b7fc-4f204e2a56b1", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "10511607", + "text": "BACKGROUND:\nBody-mass index (the weight in kilograms divided by the square of the height in meters) is known to be associated with overall mortality. We investigated the effects of age, race, sex, smoking status, and history of disease on the relation between body-mass index and mortality.\n\nMETHODS:\nIn a prospective study of more than 1 million adults in the United States (457,785 men and 588,369 women), 201,622 deaths occurred during 14 years of follow-up. We examined the relation between body-mass index and the risk of death from all causes in four subgroups categorized according to smoking status and history of disease. In healthy people who had never smoked, we further examined whether the relation varied according to race, cause of death, or age. The relative risk was used to assess the relation between mortality and body-mass index.\n\nRESULTS:\nThe association between body-mass index and the risk of death was substantially modified by smoking status and the presence of disease. In healthy people who had never smoked, the nadir of the curve for body-mass index and mortality was found at a body-mass index of 23.5 to 24.9 in men and 22.0 to 23.4 in women. Among subjects with the highest body-mass indexes, white men and women had a relative risk of death of 2.58 and 2.00, respectively, as compared with those with a body-mass index of 23.5 to 24.9. Black men and women with the highest body-mass indexes had much lower risks of death (1.35 and 1.21), which did not differ significantly from 1.00. A high body-mass index was most predictive of death from cardiovascular disease, especially in men (relative risk, 2.90; 95 percent confidence interval, 2.37 to 3.56). Heavier men and women in all age groups had an increased risk of death.\n\nCONCLUSIONS:\nThe risk of death from all causes, cardiovascular disease, cancer, or other diseases increases throughout the range of moderate and severe overweight for both men and women in all age groups. The risk associated with a high body-mass index is greater for whites than for blacks." + }, + "questions": [ + { + "id": "02ad7800-8cc2-44aa-80aa-5f1bcebc2c67", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1891, + "text": "moderate and severe overweight for both men and women in all age groups" + } + ] + } + ] +} \ No newline at end of file diff --git a/7225931e-1a26-40fb-b97a-c800e49a2845.json b/7225931e-1a26-40fb-b97a-c800e49a2845.json new file mode 100644 index 0000000000000000000000000000000000000000..5189b1ee06a8c09797efe550736956a8799e7285 --- /dev/null +++ b/7225931e-1a26-40fb-b97a-c800e49a2845.json @@ -0,0 +1,34 @@ +{ + "id": "7225931e-1a26-40fb-b97a-c800e49a2845", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "12093765", + "text": "BACKGROUND:\nInterleukin (IL)-18 plays a central role in orchestrating the cytokine cascade and accelerates atherosclerosis and plaque vulnerability in animal models. However, epidemiological data evaluating the role of IL-18 levels in atherosclerosis are lacking.\n\nMETHODS AND RESULTS:\nIn a prospective study of 1229 patients with documented coronary artery disease, we measured baseline serum concentrations of IL-18 and other markers of inflammation. During the follow-up period (median, 3.9 years), 95 patients died of cardiovascular causes. Median serum concentrations of IL-18 were significantly higher among patients who had a fatal cardiovascular event than among those who did not (68.4 versus 58.7 pg/mL; P\u003c0.0001). The hazard risk ratio of future cardiovascular death increased with increasing quartiles of IL-18 (hazard risk ratio, 1.46; 95% CI 1.21 to 1.76; P for trend \u003c0.0001). After adjustment for most potential confounders, including the strong predictor ejection fraction as well as the inflammatory variables IL-6, high-sensitive C-reactive protein, and fibrinogen, this relation remained almost unchanged, such that patients within the highest quartile of IL-18 had a 3.3-fold increase in hazard risk compared with those in the first quartile (95% CI, 1.3 to 8.4, P=0.01). This relation was observed in patients with stable angina and patients with unstable angina at baseline.\n\nCONCLUSIONS:\nSerum IL-18 level was identified as a strong independent predictor of death from cardiovascular causes in patients with coronary artery disease regardless of the clinical status at admission. This result strongly supports recent experimental evidence of IL-18-mediated inflammation leading to acceleration and vulnerability of atherosclerotic plaques." + }, + "questions": [ + { + "id": "9afb7fb1-8b77-405a-9a86-1936a886da7c", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1412, + "text": "Serum IL-18 level" + } + ] + } + ] +} \ No newline at end of file diff --git a/7243e024-9634-4f79-8cb8-7bd7eb64aca9.json b/7243e024-9634-4f79-8cb8-7bd7eb64aca9.json new file mode 100644 index 0000000000000000000000000000000000000000..e57a3135095ebb84ff2b3c181318f18e1437bb10 --- /dev/null +++ b/7243e024-9634-4f79-8cb8-7bd7eb64aca9.json @@ -0,0 +1,47 @@ +{ + "id": "7243e024-9634-4f79-8cb8-7bd7eb64aca9", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "23870058", + "text": "BACKGROUND:\nThe International Study on Asthma and Allergies in Childhood (ISAAC) reported a prevalence of asthma symptoms in 17 centers in nine Latin American countries that was similar to prevalence rates reported in non-tropical countries. It has been proposed that the continuous exposure to infectious diseases in rural populations residing in tropical areas leads to a relatively low prevalence of asthma symptoms. As almost a quarter of Latin American people live in rural tropical areas, the encountered high prevalence of asthma symptoms is remarkable. Wood smoke exposure and environmental tobacco smoke have been identified as possible risk factors for having asthma symptoms.\n\nMETHODS:\nWe performed a cross-sectional observational study from June 1, 2012 to September 30, 2012 in which we interviewed parents and guardians of Warao Amerindian children from Venezuela. Asthma symptoms were defined according to the ISAAC definition as self-reported wheezing in the last 12 months. The associations between wood smoke exposure and environmental tobacco smoke and the prevalence of asthma symptoms were calculated by means of univariate and multivariable logistic regression analyses.\n\nRESULTS:\nWe included 630 children between two and ten years of age. Asthma symptoms were recorded in 164 of these children (26%). The prevalence of asthma symptoms was associated with the cooking method. Children exposed to the smoke produced by cooking on open wood fires were at higher risk of having asthma symptoms compared to children exposed to cooking with gas (AOR 2.12, 95% CI 1.18 - 3.84). Four percent of the children lived in a household where more than ten cigarettes were smoked per day and they had a higher risk of having asthma symptoms compared to children who were not exposed to cigarette smoke (AOR 2.69, 95% CI 1.11 - 6.48).\n\nCONCLUSION:\nOur findings suggest that children living in rural settings in a household where wood is used for cooking or where more than ten cigarettes are smoked daily have a higher risk of having asthma symptoms." + }, + "questions": [ + { + "id": "53390569-7d16-4bab-8cbf-904424d7e4ef", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1398, + "text": "Children exposed to the smoke produced by cooking on open wood fires" + }, + { + "answer_start": 1614, + "text": "children lived in a household where more than ten cigarettes were smoked per day" + }, + { + "answer_start": 1880, + "text": "children living in rural settings in a household where wood is used for cooking" + }, + { + "answer_start": 1963, + "text": "where more than ten cigarettes are smoked daily" + } + ] + } + ] +} \ No newline at end of file diff --git a/724599c9-2a78-4c71-a2e0-81bf3a66c97d.json b/724599c9-2a78-4c71-a2e0-81bf3a66c97d.json new file mode 100644 index 0000000000000000000000000000000000000000..035135424023ea62faca61f2f60b6a45f6739737 --- /dev/null +++ b/724599c9-2a78-4c71-a2e0-81bf3a66c97d.json @@ -0,0 +1,39 @@ +{ + "id": "724599c9-2a78-4c71-a2e0-81bf3a66c97d", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "24905961", + "text": "BACKGROUND:\nThe risk of rheumatoid arthritis (RA) has been associated with living near traffic; however, there is evidence suggesting that air pollution may not be responsible for this association. Noise, another traffic-generated exposure, has not been studied as a risk factor for RA.\n\nOBJECTIVES:\nWe investigated proximity to traffic, ambient air pollution, and community noise in relation to RA in the Vancouver and Victoria regions of British Columbia, Canada.\n\nMETHODS:\nCases and controls were identified in a cohort of adults that was assembled using health insurance registration records. Incident RA cases from 1999 through 2002 were identified by diagnostic codes in combination with prescriptions and type of physician (e.g., rheumatologist). Controls were matched to RA cases by age and sex. Environmental exposures were assigned to each member of the study population by their residential postal code(s). We estimated relative risks using conditional logistic regression, with additional adjustment for median income at the postal code.\n\nRESULTS:\nRA incidence was increased with proximity to traffic, with an odds ratio (OR) of 1.37 (95% CI: 1.11, 1.68) for residence ≤ 50 m from a highway compared with residence \u003e 150 m away. We found no association with traffic-related exposures such as PM2.5, nitrogen oxides, or noise. Ground-level ozone, which was highest in suburban areas, was associated with an increased risk of RA (OR = 1.26; 95% CI: 1.18, 1.36 per interquartile range increase).\n\nCONCLUSIONS:\nOur study confirms a previously observed association of RA risk with proximity to traffic and suggests that neither noise levels nor traffic-related air pollutants are responsible for this relationship. Additional investigation of neighborhood and individual correlates of residence near roadways may provide new insight into risk factors for RA." + }, + "questions": [ + { + "id": "5c7c08cb-86ec-400f-af68-88c532115684", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 1092, + "text": "proximity to traffic" + }, + { + "answer_start": 1338, + "text": "Ground-level ozone, which was highest in suburban areas" + } + ] + } + ] +} \ No newline at end of file diff --git a/724785f2-fea4-40a6-b6a8-736dcf609b7f.json b/724785f2-fea4-40a6-b6a8-736dcf609b7f.json new file mode 100644 index 0000000000000000000000000000000000000000..9e9cc41cf3c9109af4cf0e37641f3f0b1a66d789 --- /dev/null +++ b/724785f2-fea4-40a6-b6a8-736dcf609b7f.json @@ -0,0 +1,43 @@ +{ + "id": "724785f2-fea4-40a6-b6a8-736dcf609b7f", + "disease": { + "id": "H00056", + "names": [ + "Alzheimer disease", + "Dementia due to Alzheimer disease" + ], + "dbLinks": { + "icd10": [ + "G30" + ], + "mesh": [ + "D000544" + ] + }, + "category": "Neurodegenerative disease" + }, + "article": { + "id": "1833349", + "text": "Case-control studies of Alzheimer's disease were re-analysed to examine the association of Alzheimer's disease with family history in first degree relatives of dementia, Down's syndrome and Parkinson's disease. Overall, the relative risk of Alzheimer's disease for those with at least one first degree relative with dementia was 3.5 (95% confidence interval 2.6-4.6). Stratification according to age of onset of Alzheimer's disease showed that the relative risk decreased with increasing onset age. However, among patients with an onset of disease after 80 years, there were still significantly more subjects with one or more first degree relatives with dementia as compared to controls (relative risk 2.6; 95% confidence interval 1.3-5.2). The relative risk of Alzheimer's disease was significantly lower in patients who had one first degree relative with dementia (relative risk 2.6; 95% confidence interval 2.0-3.5) as compared to those who had two or more affected relatives (relative risk 7.5; 95% confidence interval 3.3-16.7). Furthermore, the re-analysis showed a significant association between Alzheimer's disease and family history of Down's syndrome (relative risk 2.7; 95% confidence interval 1.2-5.7), which was strongest in those patients who had a positive family history of dementia. The relative risk of Alzheimer's disease for those with a positive family history of Parkinson's disease was 2.4 (95% confidence interval 1.0-5.8)." + }, + "questions": [ + { + "id": "7a8945dc-2ba8-4dd5-8198-542dbfdab4f5", + "text": "What are the risk factors of Alzheimer disease?", + "answers": [ + { + "answer_start": 1128, + "text": "family history of Down's syndrome" + }, + { + "answer_start": 1359, + "text": "positive family history of Parkinson's disease" + }, + { + "answer_start": 276, + "text": "at least one first degree relative with dementia" + } + ] + } + ] +} \ No newline at end of file diff --git a/727f5338-e7e1-438c-90bf-f733ec95b2f3.json b/727f5338-e7e1-438c-90bf-f733ec95b2f3.json new file mode 100644 index 0000000000000000000000000000000000000000..467837a84a9c32580ac4187fc6d918d6c483dd2f --- /dev/null +++ b/727f5338-e7e1-438c-90bf-f733ec95b2f3.json @@ -0,0 +1,35 @@ +{ + "id": "727f5338-e7e1-438c-90bf-f733ec95b2f3", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "14872479", + "text": "OBJECTIVE:\nAutoantibodies have been demonstrated in single serum samples from healthy subjects up to 10 years before they developed rheumatoid arthritis (RA). However, the time course for the development of antibodies before onset of clinical RA is unknown, nor is it known which antibody, or combinations of antibodies, might be most sensitive or specific for predicting future development of the disease. The present study was undertaken to investigate this.\n\nMETHODS:\nPatients with RA who had been blood donors before the onset of disease symptoms were enrolled. Frozen serum samples from each donor were retrieved, together with 2 serum samples from controls matched for age, sex, and date of donation. All samples were tested for IgM rheumatoid factor (IgM-RF) and anti-cyclic citrullinated peptide (anti-CCP) antibodies.\n\nRESULTS:\nSeventy-nine patients with RA (62% female; mean age at onset of symptoms 51 years) were included. A median of 13 samples (range 1-51) per patient were available; the earliest samples had been collected a median of 7.5 years (range 0.1-14.5) before the onset of symptoms. Thirty-nine patients (49%) were positive for IgM-RF and/or anti-CCP on at least one occasion before the development of RA symptoms, a median of 4.5 years (range 0.1-13.8) before symptom onset. Of the 2,138 control samples, 1.1% were positive for IgM-RF, and 0.6% were positive for anti-CCP.\n\nCONCLUSION:\nApproximately half of patients with RA have specific serologic abnormalities several years before the onset of symptoms. A finding of an elevated serum level of IgM-RF or anti-CCP in a healthy individual implies a high risk for the development of RA. We conclude that IgM-RF and anti-CCP testing with appropriately high specificity may assist in the early detection of RA in high-risk populations." + }, + "questions": [ + { + "id": "6d2769d8-c4e6-44b9-bc1d-7f77e18d4185", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 1533, + "text": "A finding of an elevated serum level of IgM-RF or anti-CCP in a healthy individual" + } + ] + } + ] +} \ No newline at end of file diff --git a/7349e3a6-5899-45a2-8456-14865a15432e.json b/7349e3a6-5899-45a2-8456-14865a15432e.json new file mode 100644 index 0000000000000000000000000000000000000000..3eeedda979509910e5f9e01cc6603efd0fd6ba30 --- /dev/null +++ b/7349e3a6-5899-45a2-8456-14865a15432e.json @@ -0,0 +1,59 @@ +{ + "id": "7349e3a6-5899-45a2-8456-14865a15432e", + "disease": { + "id": "H00056", + "names": [ + "Alzheimer disease", + "Dementia due to Alzheimer disease" + ], + "dbLinks": { + "icd10": [ + "G30" + ], + "mesh": [ + "D000544" + ] + }, + "category": "Neurodegenerative disease" + }, + "article": { + "id": "25030513", + "text": "BACKGROUND:\nRecent estimates suggesting that over half of Alzheimer's disease burden worldwide might be attributed to potentially modifiable risk factors do not take into account risk-factor non-independence. We aimed to provide specific estimates of preventive potential by accounting for the association between risk factors.\n\nMETHODS:\nUsing relative risks from existing meta-analyses, we estimated the population-attributable risk (PAR) of Alzheimer's disease worldwide and in the USA, Europe, and the UK for seven potentially modifiable risk factors that have consistent evidence of an association with the disease (diabetes, midlife hypertension, midlife obesity, physical inactivity, depression, smoking, and low educational attainment). The combined PAR associated with the risk factors was calculated using data from the Health Survey for England 2006 to estimate and adjust for the association between risk factors. The potential of risk factor reduction was assessed by examining the combined effect of relative reductions of 10% and 20% per decade for each of the seven risk factors on projections for Alzheimer's disease cases to 2050.\n\nFINDINGS:\nWorldwide, the highest estimated PAR was for low educational attainment (19·1%, 95% CI 12·3-25·6). The highest estimated PAR was for physical inactivity in the USA (21·0%, 95% CI 5·8-36·6), Europe (20·3%, 5·6-35·6), and the UK (21·8%, 6·1-37·7). Assuming independence, the combined worldwide PAR for the seven risk factors was 49·4% (95% CI 25·7-68·4), which equates to 16·8 million attributable cases (95% CI 8·7-23·2 million) of 33·9 million cases. However, after adjustment for the association between the risk factors, the estimate reduced to 28·2% (95% CI 14·2-41·5), which equates to 9·6 million attributable cases (95% CI 4·8-14·1 million) of 33·9 million cases. Combined PAR estimates were about 30% for the USA, Europe, and the UK. Assuming a causal relation and intervention at the correct age for prevention, relative reductions of 10% per decade in the prevalence of each of the seven risk factors could reduce the prevalence of Alzheimer's disease in 2050 by 8·3% worldwide.\n\nINTERPRETATION:\nAfter accounting for non-independence between risk factors, around a third of Alzheimer's diseases cases worldwide might be attributable to potentially modifiable risk factors. Alzheimer's disease incidence might be reduced through improved access to education and use of effective methods targeted at reducing the prevalence of vascular risk factors (eg, physical inactivity, smoking, midlife hypertension, midlife obesity, and diabetes) and depression.\n\nFUNDING:\nNational Institute for Health Research Collaboration for Leadership in Applied Health Research and Care for Cambridgeshire and Peterborough." + }, + "questions": [ + { + "id": "0cc22100-c3d9-4417-8b17-ba4184490d46", + "text": "What are the risk factors of Alzheimer disease?", + "answers": [ + { + "answer_start": 2493, + "text": "vascular risk factors (eg, physical inactivity, smoking, midlife hypertension, midlife obesity, and diabetes)" + }, + { + "answer_start": 2607, + "text": "depression" + }, + { + "answer_start": 2520, + "text": "physical inactivity" + }, + { + "answer_start": 2541, + "text": "smoking" + }, + { + "answer_start": 2550, + "text": "midlife hypertension" + }, + { + "answer_start": 2572, + "text": "midlife obesity" + }, + { + "answer_start": 2593, + "text": "diabetes" + } + ] + } + ] +} \ No newline at end of file diff --git a/73940376-8f87-4815-9e7c-0548ee985568.json b/73940376-8f87-4815-9e7c-0548ee985568.json new file mode 100644 index 0000000000000000000000000000000000000000..25af6daefd8d75e357a158626577420ff95475f7 --- /dev/null +++ b/73940376-8f87-4815-9e7c-0548ee985568.json @@ -0,0 +1,34 @@ +{ + "id": "73940376-8f87-4815-9e7c-0548ee985568", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "27629559", + "text": "OBJECTIVES:\nTo evaluate the risk of BlCa developing after radiation for PCa, stratified by ethnicity and follow-up duration.\n\nMETHODS:\nThe 1973-2011 surveillance, epidemiology and end results database was used to determine the observed and expected number of BlCa after PCa radiation. The adjusted relative risks (RRs) of developing BlCa were calculated for the various radiation modalities relative to no radiation, stratified by ethnicity and follow-up duration. BlCa characteristics were compared between patients with a history of prostate radiation and those without PCa.\n\nRESULTS:\nPCa was radiated in 346,429 men, 6401 of whom developed BlCa versus 2464 expected cases [SIR (95 % CI) of 2.60 (2.53-2.66)]. All radiation modalities were found to have an increased RR of developing BlCa after 10 years, with brachytherapy having a significantly higher RR than external beam radiation (EBRT) or combined EBRT and brachytherapy in Caucasian men and a significantly higher RR than EBRT in men of other/unknown ethnicity. Post-radiation BlCa, in particular that after brachytherapy, had higher grade (P = 0.0001) and lower stage (P = 0.0001) versus the general population.\n\nCONCLUSIONS:\nThe increased risk of BlCa after prostate radiation occurs predominantly after 10 years, regardless of ethnicity. The RR of developing BlCa after 10 years is significantly higher following brachytherapy than after EBRT or EBRT and brachytherapy. Bladder cancers after prostate radiation, especially after brachytherapy, are generally lower stage but higher grade than those in patients without PCa." + }, + "questions": [ + { + "id": "9a331efb-f3c9-46c3-9239-cb93a23f0025", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 1455, + "text": "prostate radiation, especially after brachytherapy" + } + ] + } + ] +} \ No newline at end of file diff --git a/73ba7f23-456e-4ed0-b9e9-bbb3aa097359.json b/73ba7f23-456e-4ed0-b9e9-bbb3aa097359.json new file mode 100644 index 0000000000000000000000000000000000000000..01e7c9cf5e8a1e5e23338a1bb06c1355fc811b38 --- /dev/null +++ b/73ba7f23-456e-4ed0-b9e9-bbb3aa097359.json @@ -0,0 +1,34 @@ +{ + "id": "73ba7f23-456e-4ed0-b9e9-bbb3aa097359", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "10769275", + "text": "BACKGROUND:\nInterleukin-6 (IL-6) plays a central role in inflammation and tissue injury. However, epidemiological data evaluating the role of IL-6 in atherogenesis are sparse.\n\nMETHODS AND RESULTS:\nIn a prospective study involving 14 916 apparently healthy men, we measured baseline plasma concentration of IL-6 in 202 participants who subsequently developed myocardial infarction (MI) and in 202 study participants matched for age and smoking status who did not report vascular disease during a 6-year follow-up. Median concentrations of IL-6 at baseline were higher among men who subsequently had an MI than among those who did not (1.81 versus 1. 46 pg/mL; P=0.002). The risk of future MI increased with increasing quartiles of baseline IL-6 concentration (P for trend \u003c0.001) such that men in the highest quartile at entry had a relative risk 2.3 times higher than those in the lowest quartile (95% CI 1.3 to 4.3, P=0.005); for each quartile increase in IL-6, there was a 38% increase in risk (P=0.001).This relationship remained significant after adjustment for other cardiovascular risk factors, was stable over long periods of follow-up, and was present in all low-risk subgroups, including nonsmokers. Although the strongest correlate of IL-6 in these data was C-reactive protein (r=0.43, P\u003c0.001), the relationship of IL-6 with subsequent risk remained after control for this factor (P\u003c0.001).\n\nCONCLUSIONS:\nIn apparently healthy men, elevated levels of IL-6 are associated with increased risk of future MI. These data thus support a role for cytokine-mediated inflammation in the early stages of atherogenesis." + }, + "questions": [ + { + "id": "f8cd7bf4-8515-4cfd-9afc-a31be297c23b", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1444, + "text": "elevated levels of IL-6" + } + ] + } + ] +} \ No newline at end of file diff --git a/74764a48-d531-446c-8e10-e7c23f1bd184.json b/74764a48-d531-446c-8e10-e7c23f1bd184.json new file mode 100644 index 0000000000000000000000000000000000000000..0af0d9a25f9f0f344e00bb0820533c61df6f4341 --- /dev/null +++ b/74764a48-d531-446c-8e10-e7c23f1bd184.json @@ -0,0 +1,59 @@ +{ + "id": "74764a48-d531-446c-8e10-e7c23f1bd184", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "28746700", + "text": "IMPORTANCE:\nMelanoma risk factors and incidence in renal transplant recipients can inform decision making for both patients and clinicians.\n\nOBJECTIVE:\nTo determine risk factors and characteristics of renal transplant recipients who develop melanoma.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nThis cohort study of a large national data registry used a cohort of renal transplant recipients from the United States Renal Data System (USRDS) database from the years 2004 through 2012. Differences in baseline characteristics between those who did and did not develop melanoma were examined, and a survival analysis was performed. Patients with renal transplants who received a diagnosis of melanoma according to any inpatient or outpatient claim associated with a billing code for melanoma were included. A history of pretransplant melanoma, previous kidney transplantation, or transplantation after 2012 or before 2004 were exclusion criteria. The data analysis was conducted from 2015 to 2016.\n\nEXPOSURE:\nReceipt of a renal transplant.\n\nMAIN OUTCOMES AND MEASURES:\nIncidence and risk factors for melanoma.\n\nRESULTS:\nOf 105 174 patients (64 151 [60.7%] male; mean [SD] age, 49.6 [15.3] years) who received kidney transplants between 2004 and 2012, 488 (0.4%) had a record of melanoma after transplantation. Significant risk factors for developing melanoma vs not developing melanoma included older age among recipients (mean [SD] age, 60.5 [10.2] vs 49.7 [15.3] years; P \u003c .001) and donors (42.6 [15.0] vs 39.2 [15.1] years; P \u003c .001), male sex (71.5% vs 60.7%; P \u003c .001), recipient (96.1% vs 66.5%; P \u003c .001) and donor (92.4% vs 82.9%; P \u003c .001) white race, less than 4 HLA mismatches (44.9% vs 37.1%; P = .001), living donors (44.7% vs 33.7%; P \u003c .001), and sirolimus (22.3% vs 13.2%; P \u003c .001) and cyclosporine (4.9% vs 3.2%; P = .04) therapy. Risk factors significant on survival analysis included older recipient age (hazard ratio [HR] per year, 1.06; 95% CI, 1.05-1.06; P \u003c .001), recipient male sex (HR, 1.53; 95% CI, 1.25-1.88; P \u003c .001), recipient white race, living donors (HR, 1.35; 95% CI, 1.11-1.64; P = .002), and sirolimus (HR, 1.54; 95% CI, 1.22-1.94; P \u003c .001) and cyclosporine (HR, 1.93; 95% CI, 1.24-2.99; P = .004) therapy. The age-standardized relative rate of melanoma in USRDS patients compared with Surveillance, Epidemiology, and End Results patients across all years was 4.9. A Kaplan-Meier estimate of the median time to melanoma among those patients who did develop melanoma was 1.45 years (95% CI, 1.31-1.70 years).\n\nCONCLUSIONS AND RELEVANCE:\nRenal transplant recipients had greater risk of developing melanoma than the general population. We believe that the risk factors we identified can guide clinicians in providing adequate care for patients in this vulnerable group." + }, + "questions": [ + { + "id": "475905f4-11fd-4600-864a-b5ac261b7ccf", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 1384, + "text": "older age among recipients" + }, + { + "answer_start": 1528, + "text": "male sex" + }, + { + "answer_start": 1565, + "text": "recipient" + }, + { + "answer_start": 1606, + "text": "donor" + }, + { + "answer_start": 1639, + "text": "white race, less than 4 HLA mismatches" + }, + { + "answer_start": 1706, + "text": "living donors" + }, + { + "answer_start": 2565, + "text": "Renal transplant recipients" + } + ] + } + ] +} \ No newline at end of file diff --git a/75169cdb-a457-4bd3-ada7-ab83b8222c25.json b/75169cdb-a457-4bd3-ada7-ab83b8222c25.json new file mode 100644 index 0000000000000000000000000000000000000000..40cba0bd543153a1af4a4987ef89bcd3920982bf --- /dev/null +++ b/75169cdb-a457-4bd3-ada7-ab83b8222c25.json @@ -0,0 +1,34 @@ +{ + "id": "75169cdb-a457-4bd3-ada7-ab83b8222c25", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "22917005", + "text": "OBJECTIVES:\nThe purpose of this study was to examine the effect of a family history of premature death, cardiovascular death in particular, on the risk of early cardiovascular disease.\n\nBACKGROUND:\nStudies suggest that fatal cardiovascular events and less severe cardiovascular diseases may co-occur in families. Consequently, a family history of premature death may indicate a familial cardiac frailty that predisposes to early cardiovascular disease.\n\nMETHODS:\nWe ascertained family history of premature death (age \u003c60 years) in all individuals born in Denmark from 1950 to 2008 and followed this cohort for early cardiovascular disease (age \u003c50 years). Using Poisson regression, we estimated incidence rate ratios (IRRs) reflecting the effect of premature death in the family on early cardiovascular disease risk.\n\nRESULTS:\nAmong 3,985,301 persons followed up for 89,294,258 person-years, 129,825, 31,172, and 5,214 were diagnosed with any early cardiovascular disease, ischemic heart disease, and ventricular arrhythmia, respectively. IRRs for these conditions given a history of premature cardiovascular death in first-degree relatives were 1.72 (95% confidence interval [CI]: 1.68 to 1.77), 2.21 (95% CI: 2.11 to 2.31), and 1.94 (95% CI: 1.70 to 2.20), respectively. With ≥2 cardiovascular deaths in a family, corresponding IRRs were 3.30 (95% CI: 2.77 to 3.94), 5.00 (95% CI: 3.87 to 6.45), and 6.18 (95% CI: 3.32 to 11.50). The IRR for any early cardiovascular disease given a family history of premature noncardiovascular death was significantly lower, 1.12 (95% CI: 1.10 to 1.14) (p(cardiac vs. noncardiac) \u003c 0.0001).\n\nCONCLUSIONS:\nFamily history of premature cardiovascular death was consistently and significantly associated with a risk of early cardiovascular disease, suggesting an inherited cardiac vulnerability. These results should be kept in mind when assessing cardiovascular disease risk in persons with a family history of premature cardiovascular death." + }, + "questions": [ + { + "id": "6504b633-0e5e-4b36-975b-4f72e30d025c", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1642, + "text": "Family history of premature cardiovascular death" + } + ] + } + ] +} \ No newline at end of file diff --git a/7550ac1a-f077-41ff-ae34-e4627629e411.json b/7550ac1a-f077-41ff-ae34-e4627629e411.json new file mode 100644 index 0000000000000000000000000000000000000000..d11352ddc0ba8996fde3d925577a7d4266b4bea7 --- /dev/null +++ b/7550ac1a-f077-41ff-ae34-e4627629e411.json @@ -0,0 +1,47 @@ +{ + "id": "7550ac1a-f077-41ff-ae34-e4627629e411", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "9145715", + "text": "OBJECTIVE:\nTo investigate the relationship of number and type of nevi to the development of melanoma.\n\nDESIGN:\nCase-control study.\n\nSETTING:\nOutpatient clinics in referral hospitals.\n\nPATIENTS:\nCases were 716 consecutive patients with newly diagnosed melanoma identified at 2 melanoma centers between January 1, 1991, and December 31, 1992. Stratified random sampling of patients from outpatient clinics was used to identify 1014 participating controls of the same age, sex, race, and geographic distribution as the melanoma cases. All study subjects underwent an interview, a complete skin examination, photography of the most atypical nevi, and, if the patient was willing, a biopsy of the most atypical nevus.\n\nMAIN OUTCOME MEASURES:\nNumber and type of nevi on the entire body were systematically reported. All diagnoses of clinically dysplastic nevi were confirmed by expert examiners.\n\nRESULTS:\nRisk for melanoma was strongly related to number of small nevi, large nondysplastic nevi, and clinically dysplastic nevi. In the absence of dysplastic nevi, increased numbers of small nevi were associated with an approximately 2-fold risk, and increased numbers of both small and large nondysplastic nevi were associated with a 4-fold risk. One clinically dysplastic nevus was associated with a 2-fold risk (95% confidence interval, 1.4-3.6), while 10 or more conferred a 12-fold increased risk (95% confidence interval, 4.4-31). Congenital nevi were not associated with increased risk of melanoma.\n\nCONCLUSIONS:\nAlthough nondysplastic nevi confer a small risk, clinically dysplastic nevi confer substantial risk for melanoma. On the basis of nevus number and type, clinicians can identify a population at high risk of this epidemic cancer for screening and intervention." + }, + "questions": [ + { + "id": "814b6d4d-9abc-42ad-8c4d-4a6b5215125e", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 942, + "text": "number of small nevi" + }, + { + "answer_start": 964, + "text": "large nondysplastic nevi" + }, + { + "answer_start": 994, + "text": "clinically dysplastic nevi" + }, + { + "answer_start": 1562, + "text": "clinically dysplastic nevi" + } + ] + } + ] +} \ No newline at end of file diff --git a/75da7724-17e7-4b11-adfc-5cc2563ced50.json b/75da7724-17e7-4b11-adfc-5cc2563ced50.json new file mode 100644 index 0000000000000000000000000000000000000000..608f5eee1898d3af3dbd112903863d30e8e194f2 --- /dev/null +++ b/75da7724-17e7-4b11-adfc-5cc2563ced50.json @@ -0,0 +1,34 @@ +{ + "id": "75da7724-17e7-4b11-adfc-5cc2563ced50", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "677576", + "text": "A rise in coronary heart disease incidence after menopause and a dramatic increase in the severity of the presenting diseases are noted in a cohort of 2873 Framingham women who were followed up for 24 years. No premenopausal woman developed a myocardial infarction or died of coronary heart disease. Such events were common in postmenopausal women. Even in women under 55, 40% of the postmenopausal coronary heart disease presented in these more serious forms, whether menopause was natural or surgical. The contrast was especially marked in the age group 40 to 44 years. In the age groups 45 to 49 and 50 to 54 years, incidence rates in menopausal and postmenopausal intervals were more than double those in premenopausal intervals, whether menopause was natural or surgical. In surgical menopause there was excess incidence whether the ovaries were removed or not. Postmenopausal women on hormones had a doubled risk of coronary heart disease." + }, + "questions": [ + { + "id": "acf3083e-502e-4154-ac69-cb0f79b0be94", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 867, + "text": "Postmenopausal women on hormones" + } + ] + } + ] +} \ No newline at end of file diff --git a/75f7ef16-4d92-4a6a-80df-d4328346e427.json b/75f7ef16-4d92-4a6a-80df-d4328346e427.json new file mode 100644 index 0000000000000000000000000000000000000000..33aa78fcca311fc62f068d4647248b46f6d21313 --- /dev/null +++ b/75f7ef16-4d92-4a6a-80df-d4328346e427.json @@ -0,0 +1,38 @@ +{ + "id": "75f7ef16-4d92-4a6a-80df-d4328346e427", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "19244173", + "text": "BACKGROUND:\nWith the exception of breast cancer, little is known about the effect of moderate intakes of alcohol, or of particular types of alcohol, on cancer risk in women.\n\nMETHODS:\nA total of 1,280,296 middle-aged women in the United Kingdom enrolled in the Million Women Study were routinely followed for incident cancer. Cox regression models were used to calculate adjusted relative risks and 95% confidence intervals (CIs) for 21 site-specific cancers according to amount and type of alcoholic beverage consumed. All statistical tests were two-sided.\n\nRESULTS:\nA quarter of the cohort reported drinking no alcohol; 98% of drinkers consumed fewer than 21 drinks per week, with drinkers consuming an average of 10 g alcohol (1 drink) per day. During an average 7.2 years of follow-up per woman 68,775 invasive cancers occurred. Increasing alcohol consumption was associated with increased risks of cancers of the oral cavity and pharynx (increase per 10 g/d = 29%, 95% CI = 14% to 45%, Ptrend \u003c .001), esophagus (22%, 95% CI = 8% to 38%, Ptrend = .002), larynx (44%, 95% CI = 10% to 88%, Ptrend = .008), rectum (10%, 95% CI = 2% to 18%, Ptrend = .02), liver (24%, 95% CI = 2% to 51%, Ptrend = .03), breast (12%, 95% CI = 9% to 14%, Ptrend \u003c .001), and total cancer (6%, 95% CI = 4% to 7%, Ptrend \u003c .001). The trends were similar in women who drank wine exclusively and other consumers of alcohol. For cancers of the upper aerodigestive tract, the alcohol-associated risk was confined to current smokers, with little or no effect of alcohol among never and past smokers (P(heterogeneity) \u003c .001). Increasing levels of alcohol consumption were associated with a decreased risk of thyroid cancer (Ptrend = .005), non-Hodgkin lymphoma (Ptrend = .001), and renal cell carcinoma (Ptrend = .03).\n\nCONCLUSIONS:\nLow to moderate alcohol consumption in women increases the risk of certain cancers. For every additional drink regularly consumed per day, the increase in incidence up to age 75 years per 1000 for women in developed countries is estimated to be about 11 for breast cancer, 1 for cancers of the oral cavity and pharynx, 1 for cancer of the rectum, and 0.7 each for cancers of the esophagus, larynx and liver, giving a total excess of about 15 cancers per 1000 women up to age 75." + }, + "questions": [ + { + "id": "93f22d16-9b70-487f-9ab7-370ce611a2dd", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 833, + "text": "Increasing alcohol consumption" + }, + { + "answer_start": 1808, + "text": "Low to moderate alcohol consumption in women" + } + ] + } + ] +} \ No newline at end of file diff --git a/7610b775-b112-4442-ba39-10cc11082877.json b/7610b775-b112-4442-ba39-10cc11082877.json new file mode 100644 index 0000000000000000000000000000000000000000..bf3de0997e0a297cd9e8639183996dd0249c58f5 --- /dev/null +++ b/7610b775-b112-4442-ba39-10cc11082877.json @@ -0,0 +1,50 @@ +{ + "id": "7610b775-b112-4442-ba39-10cc11082877", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "16801583", + "text": "OBJECTIVE:\nTo examine ethnic differences in risk of type 2 diabetes, taking dietary and lifestyle risk factors into account.\n\nRESEARCH DESIGN AND METHODS:\nA prospective (1980-2000) cohort (from The Nurses' Health Study) including 78,419 apparently healthy women (75,584 whites, 801 Asians, 613 Hispanics, and 1,421 blacks) was studied. Detailed dietary and lifestyle information for each participant was repeatedly collected every 4 years.\n\nRESULTS:\nDuring 1,294,799 person-years of follow-up, we documented 3,844 incident cases of diabetes. Compared with whites, the age-adjusted relative risks (RRs) were 1.43 (95% CI 1.08-1.90) for Asians, 1.76 (1.32-2.34) for Hispanics, and 2.18 (1.82-2.61) for blacks. After adjustment for BMI, the RRs changed to 2.26 (1.70-2.99) for Asians, 1.86 (1.40-2.47) for Hispanics, and 1.34 (1.12-1.61) for blacks. For each 5-unit increment in BMI, the multivariate RR of diabetes was 2.36 (1.83-3.04) for Asians, 2.21 (1.75-2.79) for Hispanics, 1.96 (1.93-2.00) for whites, and 1.55 (1.36-1.77) for blacks (P for interaction \u003c0.001). For each 5-kg weight gain between age 18 and the year 1980, the risk of diabetes was increased by 84% (95% CI 58-114) for Asians, 44% (26-63) for Hispanics, 38% (28-49) for blacks, and 37% (35-38%) for whites. A healthy diet high in cereal fiber and polyunsaturated fat and low in trans fat and glycemic load was more strongly associated with a lower risk of diabetes among minorities (RR 0.54 [95% CI 0.39-0.73]) than among whites (0.77 [0.72-0.84]).\n\nCONCLUSIONS:\nThe risk of diabetes is significantly higher among Asians, Hispanics, and blacks than among whites before and after taking into account differences in BMI. Weight gain is particularly detrimental for Asians. Our data suggest that the inverse association of a healthy diet with diabetes is stronger for minorities than for whites." + }, + "questions": [ + { + "id": "5232a7af-79e7-492a-8a33-e55454e0510e", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1584, + "text": "Asians" + }, + { + "answer_start": 1592, + "text": "Hispanics" + }, + { + "answer_start": 1607, + "text": "blacks" + }, + { + "answer_start": 1688, + "text": " Weight gain" + }, + { + "answer_start": 1071, + "text": "each 5-kg weight gain between age 18" + } + ] + } + ] +} \ No newline at end of file diff --git a/76e0757a-e0f3-49d3-aa59-26565a077e1a.json b/76e0757a-e0f3-49d3-aa59-26565a077e1a.json new file mode 100644 index 0000000000000000000000000000000000000000..474e6fdf16a2b1c65339ed003ed410861e296d07 --- /dev/null +++ b/76e0757a-e0f3-49d3-aa59-26565a077e1a.json @@ -0,0 +1,34 @@ +{ + "id": "76e0757a-e0f3-49d3-aa59-26565a077e1a", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "17164760", + "text": "In a prospective cohort study, a close to two-fold elevated risk of bladder cancer was found among men reporting a history of gonorrhoea (relative risk=1.92, 95% CI=1.10-3.33). Our finding warrants further examination of the role of gonorrhoea in bladder carcinogenesis." + }, + "questions": [ + { + "id": "5d75f92f-6fad-4157-85cd-4871f81c5b25", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 99, + "text": "men reporting a history of gonorrhoea" + } + ] + } + ] +} \ No newline at end of file diff --git a/77a664d5-046c-4efb-8c77-b2f3b23729b5.json b/77a664d5-046c-4efb-8c77-b2f3b23729b5.json new file mode 100644 index 0000000000000000000000000000000000000000..09c45abffdfcdccbb4067d635495de1727152919 --- /dev/null +++ b/77a664d5-046c-4efb-8c77-b2f3b23729b5.json @@ -0,0 +1,37 @@ +{ + "id": "77a664d5-046c-4efb-8c77-b2f3b23729b5", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "8658039", + "text": "BACKGROUND:\nIt has been suggested that there is an increased risk of colorectal cancer after cholecystectomy due to increased levels of secondary bile acids. Some studies suggest the risk is higher for women and for the development of right-sided tumours.\n\nMETHODS:\nA review of the literature yielded 95 relevant studies, of which 35 were suitable for a meta-analysis involving age- and sex-matched controls.\n\nRESULTS:\nThe pooled odds ratio for a positive association between cholecystectomy and colorectal cancer was 1.11 (95% confidence interval (CI), 1.02 to 1.21). For women the odds ratio was 1.14 (95 % CI, 10.01 to 1.28) and for right-sided cancer 1.86 (95% CI, 1.31 to 2.65).\n\nCONCLUSIONS:\nIt is possible that this small observed association may be due to a publication bias for positive results or bias within the included studies. If it is indeed a real effect, the risk to an individual is very small." + }, + "questions": [ + { + "id": "ec31f738-0c85-427b-ab47-62d806caff14", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 476, + "text": "cholecystectomy" + } + ] + } + ] +} \ No newline at end of file diff --git a/77baeda3-8eed-499c-8f64-888aa4738667.json b/77baeda3-8eed-499c-8f64-888aa4738667.json new file mode 100644 index 0000000000000000000000000000000000000000..f111b79bb4bcd2a24b61e2f571563b6a4cd4f41a --- /dev/null +++ b/77baeda3-8eed-499c-8f64-888aa4738667.json @@ -0,0 +1,38 @@ +{ + "id": "77baeda3-8eed-499c-8f64-888aa4738667", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "23549584", + "text": "IMPORTANCE:\nLoss-of-function mutations in the melatonin receptor are associated with insulin resistance and type 2 diabetes. Additionally, in a cross-sectional analysis of persons without diabetes, lower nocturnal melatonin secretion was associated with increased insulin resistance.\n\nOBJECTIVE:\nTo study the association between melatonin secretion and the risk of developing type 2 diabetes.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nCase-control study nested within the Nurses' Health Study cohort. Among participants without diabetes who provided urine and blood samples at baseline in 2000, we identified 370 women who developed type 2 diabetes from 2000-2012 and matched 370 controls using risk-set sampling.\n\nMAIN OUTCOME MEASURES:\nAssociations between melatonin secretion at baseline and incidence of type 2 diabetes were evaluated with multivariable conditional logistic regression controlling for demographic characteristics, lifestyle habits, measures of sleep quality, and biomarkers of inflammation and endothelial dysfunction.\n\nRESULTS:\nThe median urinary ratios of 6-sulfatoxymelatonin to creatinine were 28.2 ng/mg (5%-95% range, 5.5-84.2 ng/mg) among cases and 36.3 ng/mg (5%-95% range, 6.9-110.8 ng/mg) among controls. Women with lower ratios of 6-sulfatoxymelatonin to creatinine had increased risk of diabetes (multivariable odds ratio, 1.48 [95% CI, 1.11-1.98] per unit decrease in the estimated log ratio of 6-sulfatoxymelatonin to creatinine). Compared with women in the highest ratio category of 6-sulfatoxymelatonin to creatinine, those in the lowest category had a multivariable odds ratio of 2.17 (95% CI, 1.18-3.98) of developing type 2 diabetes. Women in the highest category of melatonin secretion had an estimated diabetes incidence rate of 4.27 cases/1000 person-years compared with 9.27 cases/1000 person-years in the lowest category.\n\nCONCLUSIONS AND RELEVANCE:\nLower melatonin secretion was independently associated with a higher risk of developing type 2 diabetes. Further research is warranted to assess if melatonin secretion is a modifiable risk factor for diabetes within the general population." + }, + "questions": [ + { + "id": "ede6461e-34c9-4137-911f-1cfe29c7ca76", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1230, + "text": "Women with lower ratios of 6-sulfatoxymelatonin to creatinine" + }, + { + "answer_start": 1889, + "text": "Lower melatonin secretion" + } + ] + } + ] +} \ No newline at end of file diff --git a/77f4b374-b550-4f78-b519-9cc79ac15ab1.json b/77f4b374-b550-4f78-b519-9cc79ac15ab1.json new file mode 100644 index 0000000000000000000000000000000000000000..4204bcf9da787732e8a7747d8a17b4ac98e3ad4b --- /dev/null +++ b/77f4b374-b550-4f78-b519-9cc79ac15ab1.json @@ -0,0 +1,35 @@ +{ + "id": "77f4b374-b550-4f78-b519-9cc79ac15ab1", + "disease": { + "id": "H00056", + "names": [ + "Alzheimer disease", + "Dementia due to Alzheimer disease" + ], + "dbLinks": { + "icd10": [ + "G30" + ], + "mesh": [ + "D000544" + ] + }, + "category": "Neurodegenerative disease" + }, + "article": { + "id": "17503514", + "text": "OBJECTIVE:\nExamine the effects of subcortical infarcts with Alzheimer's disease (AD) pathology on dementia, episodic memory, and other cognitive abilities in older persons.\n\nMETHODS:\nParticipants included 148 autopsied subjects of the Rush Memory and Aging Project (mean age, 88.0 years), a longitudinal clinicopathological study. Cognition was assessed yearly with 21 neuropsychological tests. Infarcts were visualized on coronal slabs, and plaques and neurofibrillary tangles were counted and standardized to form a composite measure of AD pathology. Multiple regression analyses were used controlling for age, sex, and education.\n\nRESULTS:\nFifty-three (35.8%) subjects had cerebral infarcts. After accounting for AD pathology, infarcts increased the odds of dementia by 5.1-fold (95% confidence interval, 1.98-12.92) and lowered cognitive function by 0.50 standard unit (p = 0.001). After controlling for cortical infarcts and AD pathology, subcortical infarcts, present in 39 of 53 (73.6%) subjects with infarcts, increased the odds of dementia by almost 4-fold and reduced cognitive function by more than a third of a unit (parameter estimate = -0.37; p = 0.03). In analyses with cognitive abilities, subcortical infarcts were associated with lower episodic, semantic, and working memory (p \u003c or = 0.05), and had an interaction with AD pathology to further worsen working memory (p = 0.02).\n\nINTERPRETATION:\nSubcortical infarcts add to deleterious effects of AD pathology by increasing the odds of dementia and lowering memory function." + }, + "questions": [ + { + "id": "5091875a-e1b7-485b-9b3c-27d77044a820", + "text": "What are the risk factors of Alzheimer disease?", + "answers": [ + { + "answer_start": 1413, + "text": "Subcortical infarcts" + } + ] + } + ] +} \ No newline at end of file diff --git a/78a7a514-4b84-43ec-a528-76587f721e0b.json b/78a7a514-4b84-43ec-a528-76587f721e0b.json new file mode 100644 index 0000000000000000000000000000000000000000..c89b76ae28308340cc995fd190d3dff31c30e76d --- /dev/null +++ b/78a7a514-4b84-43ec-a528-76587f721e0b.json @@ -0,0 +1,39 @@ +{ + "id": "78a7a514-4b84-43ec-a528-76587f721e0b", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "8223814", + "text": "Using cross-sectional data of an epidemiological study, risk factors for asthma and recurrent wheezy bronchitis were investigated in 1812 primary school children. Children with asthma (n = 63) had a similar pattern but a higher frequency of chronic respiratory symptoms than those with recurrent wheezy bronchitis (n = 136). Logistic regression analyses showed similar risk factors for both disorders, however, more pronounced for asthma. Prematurity was a significant risk factor for asthma and for recurrent wheezy bronchitis. Children with asthma more often had a family history of paternal or maternal asthma and their mothers tended to be younger. Effects of paternal asthma and prematurity were also found when the atopic status of the child (defined as skin test positivity to any of seven aero allergens) was taken into account. Next to genetic effects, adverse circumstances in early life seem to be important for the development of asthma. In school children recurrent wheezy bronchitis and asthma seem to be similar disorders which differ in quantitative but not qualitative aspects." + }, + "questions": [ + { + "id": "eb5fc33e-b0a0-4d93-bff3-7b373efdac60", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 439, + "text": "Prematurity" + }, + { + "answer_start": 567, + "text": "family history of paternal or maternal asthma" + } + ] + } + ] +} \ No newline at end of file diff --git a/78c2ce48-1cd3-42da-ac9f-9e4ecd02491d.json b/78c2ce48-1cd3-42da-ac9f-9e4ecd02491d.json new file mode 100644 index 0000000000000000000000000000000000000000..3ae2029606653c19e0e6b126f16157ca228a1008 --- /dev/null +++ b/78c2ce48-1cd3-42da-ac9f-9e4ecd02491d.json @@ -0,0 +1,42 @@ +{ + "id": "78c2ce48-1cd3-42da-ac9f-9e4ecd02491d", + "disease": { + "id": "H00408", + "names": [ + "Type 1 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E10" + ], + "mesh": [ + "D003922" + ] + }, + "category": "Metabolic disease; Immune system disease; Endocrine disease" + }, + "article": { + "id": "3792666", + "text": "The families of 554 type I (insulin-dependent) diabetics were genetically analyzed according to probands' sex and age at onset applying a modification of Strömgren's method of age correction. Lifetime recurrence risk of type I diabetes (risk up to age 80 yr) for first-degree relatives in three consecutive generations was calculated. The overall risk (+/- 1 SE) for siblings was 6.6 +/- 1.1% and for children was 4.9 +/- 1.7%. The similar risks among siblings and children argue against a simple autosomal recessive trait. The results do not permit a conclusion about a distinct mode of inheritance. Regardless of age at onset, offspring of male probands always had a higher risk than offspring of female probands. Among all probands, fathers were significantly more often affected with type I diabetes (about twice) than mothers (4.1 +/- 0.9 vs. 1.7 +/- 0.6%, respectively). The risk for further siblings of the proband was significantly increased in the presence of a type I diabetic parent (25.2 +/- 10.3 vs. 5.8 +/- 1.0% for remaining probands), indicating a nonrandom clustering type I diabetes in families. Younger age at onset (less than 25 yr) was not associated with an increased risk to siblings. Type II diabetes was not more frequent among parents and siblings of type I diabetics than in the general population. The calculated risk estimates are of practical value in genetic counseling and are important for genetic models concerning type I diabetes." + }, + "questions": [ + { + "id": "9b9635b5-7cd5-42cd-a924-07ebd1b61e4f", + "text": "What are the risk factors of Type 1 diabetes mellitus?", + "answers": [ + { + "answer_start": 629, + "text": "offspring of male probands" + }, + { + "answer_start": 736, + "text": "fathers" + }, + { + "answer_start": 898, + "text": "siblings of the proband" + } + ] + } + ] +} \ No newline at end of file diff --git a/79b037a0-19d1-44a0-8757-157f2c8ca18f.json b/79b037a0-19d1-44a0-8757-157f2c8ca18f.json new file mode 100644 index 0000000000000000000000000000000000000000..e55516102e443bbe10986a688586a4265b9da6c5 --- /dev/null +++ b/79b037a0-19d1-44a0-8757-157f2c8ca18f.json @@ -0,0 +1,42 @@ +{ + "id": "79b037a0-19d1-44a0-8757-157f2c8ca18f", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "34274065", + "text": "BACKGROUND:\nThe prevalence of overweight, obesity, and diabetes is rising rapidly in low-income and middle-income countries (LMICs), but there are scant empirical data on the association between body-mass index (BMI) and diabetes in these settings.\n\nMETHODS:\nIn this cross-sectional study, we pooled individual-level data from nationally representative surveys across 57 LMICs. We identified all countries in which a WHO Stepwise Approach to Surveillance (STEPS) survey had been done during a year in which the country fell into an eligible World Bank income group category. For LMICs that did not have a STEPS survey, did not have valid contact information, or declined our request for data, we did a systematic search for survey datasets. Eligible surveys were done during or after 2008; had individual-level data; were done in a low-income, lower-middle-income, or upper-middle-income country; were nationally representative; had a response rate of 50% or higher; contained a diabetes biomarker (either a blood glucose measurement or glycated haemoglobin [HbA]); and contained data on height and weight. Diabetes was defined biologically as a fasting plasma glucose concentration of 7·0 mmol/L (126·0 mg/dL) or higher; a random plasma glucose concentration of 11·1 mmol/L (200·0 mg/dL) or higher; or a HbA of 6·5% (48·0 mmol/mol) or higher, or by self-reported use of diabetes medication. We included individuals aged 25 years or older with complete data on diabetes status, BMI (defined as normal [18·5-22·9 kg/m], upper-normal [23·0-24·9 kg/m], overweight [25·0-29·9 kg/m], or obese [≥30·0 kg/m]), sex, and age. Countries were categorised into six geographical regions: Latin America and the Caribbean, Europe and central Asia, east, south, and southeast Asia, sub-Saharan Africa, Middle East and north Africa, and Oceania. We estimated the association between BMI and diabetes risk by multivariable Poisson regression and receiver operating curve analyses, stratified by sex and geographical region.\n\nFINDINGS:\nOur pooled dataset from 58 nationally representative surveys in 57 LMICs included 685 616 individuals. The overall prevalence of overweight was 27·2% (95% CI 26·6-27·8), of obesity was 21·0% (19·6-22·5), and of diabetes was 9·3% (8·4-10·2). In the pooled analysis, a higher risk of diabetes was observed at a BMI of 23 kg/m or higher, with a 43% greater risk of diabetes for men and a 41% greater risk for women compared with a BMI of 18·5-22·9 kg/m. Diabetes risk also increased steeply in individuals aged 35-44 years and in men aged 25-34 years in sub-Saharan Africa. In the stratified analyses, there was considerable regional variability in this association. Optimal BMI thresholds for diabetes screening ranged from 23·8 kg/m among men in east, south, and southeast Asia to 28·3 kg/m among women in the Middle East and north Africa and in Latin America and the Caribbean.\n\nINTERPRETATION:\nThe association between BMI and diabetes risk in LMICs is subject to substantial regional variability. Diabetes risk is greater at lower BMI thresholds and at younger ages than reflected in currently used BMI cutoffs for assessing diabetes risk. These findings offer an important insight to inform context-specific diabetes screening guidelines.\n\nFUNDING:\nHarvard T H Chan School of Public Health McLennan Fund: Dean's Challenge Grant Program." + }, + "questions": [ + { + "id": "c3bfd2ca-82bb-460a-a3ed-e007b86a2dc8", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 2323, + "text": " a BMI of 23 kg/m or higher" + }, + { + "answer_start": 2508, + "text": "individuals aged 35-44 years" + }, + { + "answer_start": 85, + "text": "low-income and middle-income countries (LMICs)" + } + ] + } + ] +} \ No newline at end of file diff --git a/79bd63e1-1bf4-48a1-ad7e-33c07e4b1c6e.json b/79bd63e1-1bf4-48a1-ad7e-33c07e4b1c6e.json new file mode 100644 index 0000000000000000000000000000000000000000..86de6ea7a4a6983d0b352b671fa77077c5542b99 --- /dev/null +++ b/79bd63e1-1bf4-48a1-ad7e-33c07e4b1c6e.json @@ -0,0 +1,39 @@ +{ + "id": "79bd63e1-1bf4-48a1-ad7e-33c07e4b1c6e", + "disease": { + "id": "H01633", + "names": [ + "High blood pressure", + "Hypertension" + ], + "dbLinks": { + "icd10": [ + "I10" + ], + "mesh": [ + "D006973" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "2508915", + "text": "OBJECTIVE:\nTo assess the relations among prevalence of arterial hypertension, history of weight change, and current body weight in the range from normal weight to severe obesity.\n\nDESIGN:\nRetrospective analysis of medical records of men registered with Danish military authorities from 1943 to 1977 and followed up four to 40 years later.\n\nSETTING:\nDraft board of Copenhagen and surrounding counties and the rest of Sjaelland and surrounding islands.\n\nSUBJECTS:\n964 Men who were severely obese (body mass index greater than or equal to kg/m2 at the first examination) and 1134 random controls.\n\nMAIN OUTCOME MEASURES:\nBlood pressure and weight.\n\nRESULTS:\nHypertension was more prevalent in subjects with an unchanged body mass index as that index increased over the range studied. At any body mass index hypertension was more prevalent in subjects who had increased to this index and less common in those who had decreased to it than in those who had stayed the same weight since the first examination. Hypertension among controls was most common in those subjects who had become obese during adulthood.\n\nCONCLUSIONS:\nChanges in body weight have a great influence on arterial hypertension independent of the effect of attained weight, particularly in obese subjects." + }, + "questions": [ + { + "id": "45498611-b3dc-4d46-9871-16483153b356", + "text": "What are the risk factors for Hypertension?", + "answers": [ + { + "answer_start": 1118, + "text": "Changes in body weight" + }, + { + "answer_start": 839, + "text": "subjects who had increased to this index" + } + ] + } + ] +} \ No newline at end of file diff --git a/7a1ddd5a-2c11-4960-85b6-1d7fcef06d29.json b/7a1ddd5a-2c11-4960-85b6-1d7fcef06d29.json new file mode 100644 index 0000000000000000000000000000000000000000..86fbeaa71e15322cae2aace58fcc50de671be7f3 --- /dev/null +++ b/7a1ddd5a-2c11-4960-85b6-1d7fcef06d29.json @@ -0,0 +1,39 @@ +{ + "id": "7a1ddd5a-2c11-4960-85b6-1d7fcef06d29", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "21979000", + "text": "OBJECTIVES:\nStatins offer significant cardiovascular benefits. Their use, however, influences immune regulation, which may potentially facilitate autoimmunity, eventually resulting in autoimmune diseases such as rheumatoid arthritis (RA).The authors studied whether statin use was associated with an increased risk of developing RA by conducting a case-control study using the Netherlands Information Network of General Practice database.\n\nMETHODS:\nThe authors identified 508 patients aged 40 years or older with a first-time diagnosis of RA in the period 2001-2006. Each RA case was matched to five controls for age, sex and index date, which was selected 1 year before the first diagnosis of RA. Odds ratios for the first-time diagnosis of RA were verified by a referral to a rheumatologist and/or at least one prescription of disease-modifying anti-rheumatic drugs and/or two prescriptions of corticosteroids after the date of first diagnosis.\n\nRESULTS:\nCases were more often users of statins (15.9%) compared to controls (8.6%). After adjustment for cardiovascular risk factors and use of comedication, statin use was associated with an increased risk of incident RA (adjusted OR, 1.71 (95% CI 1.16 to 2.53); p=0.007). A consistent trend of increasing risk with increased cumulative duration, cumulative defined daily doses and number of prescriptions was not observed. However, a small trend between the potency of statin treatment and the risk of RA was found.\n\nCONCLUSIONS:\nStatin use seems to be associated with an increased risk of developing RA. Our findings should be replicated by additional studies." + }, + "questions": [ + { + "id": "642b4b98-b2b1-4520-b3ba-c1c0cd5b700d", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 1107, + "text": "statin use" + }, + { + "answer_start": 1481, + "text": "Statin use" + } + ] + } + ] +} \ No newline at end of file diff --git a/7a32ffae-d4b3-473f-b05f-201e318162ed.json b/7a32ffae-d4b3-473f-b05f-201e318162ed.json new file mode 100644 index 0000000000000000000000000000000000000000..ece9cc7cf8e3279c2a6a32dc91d1f48bc2409ceb --- /dev/null +++ b/7a32ffae-d4b3-473f-b05f-201e318162ed.json @@ -0,0 +1,41 @@ +{ + "id": "7a32ffae-d4b3-473f-b05f-201e318162ed", + "disease": { + "id": "M2023_04_26_16_38_52", + "names": [ + "Migraine" + ], + "dbLinks": { + "icd10": [ + "G43" + ], + "icd11": [ + "8A80" + ], + "mesh": [ + "C10.228.140.546.399.750" + ] + }, + "description": "Migraine is a chronic neurological disorder characterized by recurrent episodes of unilateral, pulsatile headaches associated with autonomic symptoms such as nausea, vomiting, photophobia, and phonophobia. The pathophysiology of migraine is multifactorial and involves complex interactions between genetic, environmental, and neurochemical factors that modulate cerebral vascular tone and nociception. Migraine attacks can be triggered by a variety of factors, including stress, hormonal changes, sleep disturbances, and certain foods or medications. Treatment options for migraine include pharmacotherapy for acute attacks, preventive medications for frequent or severe headaches, and lifestyle modifications to avoid triggers. In refractory cases, interventional therapies such as nerve blocks or neuromodulation techniques may be considered." + }, + "article": { + "id": "15985108", + "text": "OBJECTIVES:\nThis study characterized sleep parameters and complaints in a large clinical sample of migraineurs and examined sleep complaints in relation to headache frequency and severity.\n\nBACKGROUND:\nThe relationship between headache and sleep has been documented at least anecdotally in medical literature for well over a century and clinical texts allude to the importance of sleep as a headache precipitant. A small number of empirical studies have emerged, but the precise nature and magnitude of the headache/sleep association and underlying mechanisms remain poorly understood.\n\nMETHODS:\nIn this investigation, 1283 migraineurs were drawn from 1480 consecutive headache sufferers presenting for evaluation to a tertiary headache clinic. Patients underwent a physical examination and structured interview assessing a variety of sleep, headache, and demographic variables. Migraine was diagnosed according the IHS criteria (1.1 to 1.6 diagnostic codes). Migraineurs were 84% female, with a mean age of 37.4 years. Groups were formed based on patient's average nocturnal sleep patterns, including short, normal, and long sleep groups, and were compared on headache variables.\n\nRESULTS:\nSleep complaints were common and associated with headache in a sizeable proportion of patients. Over half of migraineurs reported difficulty initiating and maintaining sleep at least occasionally. Many in this sample reported chronically shortened sleep patterns similar to that observed in persons with insomnia, with 38% of patients sleeping on average 6 hours per night. Migraines were triggered by sleep disturbance in 50% of patients. \"Awakening headaches\" or headaches awakening them from sleep were reported by 71% of patients. Interestingly, sleep was also a common palliative agent for headache; 85% of migraineurs indicated that they chose to sleep or rest because of headache and 75% were forced to sleep or rest because of headache. Patients with chronic migraine reported shorter nightly sleep times than those with episodic migraine, and were more likely to exhibit trouble falling asleep, staying asleep, sleep triggering headache, and choosing to sleep because of headache. Short sleepers (ie, average sleep period 6 hours) exhibited significantly more frequent and more severe headaches than individuals who slept longer and were more likely to exhibit morning headaches on awakening.\n\nCONCLUSIONS:\nThese data support earlier research and anecdotal observations of a substantial sleep/migraine relationship, and implicate sleep disturbance in specific headache patterns and severity. The short sleep group, who routinely slept 6 hours per night, exhibited the more severe headache patterns and more sleep-related headache. Sleep complaints occurred with greater frequency among chronic than episodic migraineurs. Future research may identify possible mediating factors such as primary sleep and mood disorders. Prospective studies are needed to determine if normalizing sleep times in the short sleeps would impact headache threshold." + }, + "questions": [ + { + "id": "4a03b312-8d8e-415d-b4e9-26da5fbb5f21", + "text": "what are the risk factors of Migraine?", + "answers": [ + { + "answer_start": 2530, + "text": "sleep disturbance" + }, + { + "answer_start": 2596, + "text": "short sleep group, who routinely slept 6 hours per night" + } + ] + } + ] +} \ No newline at end of file diff --git a/7aa7f5ad-9a61-4ebf-8755-416af66c0188.json b/7aa7f5ad-9a61-4ebf-8755-416af66c0188.json new file mode 100644 index 0000000000000000000000000000000000000000..ac92013771881977bbda9e7b957c5b924b1fec7c --- /dev/null +++ b/7aa7f5ad-9a61-4ebf-8755-416af66c0188.json @@ -0,0 +1,34 @@ +{ + "id": "7aa7f5ad-9a61-4ebf-8755-416af66c0188", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "22719024", + "text": "AIMS:\nFamilial risks for coronary heart disease (CHD) in families with multiple affected siblings have not been thoroughly studied. This nationwide cohort study aimed to determine familial risks for hospitalization or death due to CHD in families with multiple affected siblings.\n\nMETHODS AND RESULTS:\nThe study is a nationwide follow-up study. The Swedish Multigeneration Register data on 0-76-year-old subjects were linked to Hospital Discharge Register and Cause of Death Register data for 1964-2008. Standardized incidence ratios (SIRs) were calculated for individuals whose siblings were hospitalized or died (without previous hospitalization, i.e., primary fatal cases) due to CHD compared with those whose siblings were not affected. The procedure was repeated for spouses. Among a total of 185 810 cases of hospitalization or death due to CHD, the SIRs for hospitalization and death in the siblings of affected probands were 1.82 (95% CI: 1.27-2.60) and 1.60 (95% CI: 1.10-2.36), respectively. The SIRs for hospitalization in siblings of two and three affected probands were 6.92 (95% CI: 4.77-10.03) and 7.88 (95% CI: 5.31-11.70), respectively. The SIRs for death in siblings of two and three affected probands were 7.31 (95% CI: 4.76-11.19) and 6.61 (95% CI: 3.91-11.10), respectively. Spouses had low overall familial risks (SIR = 1.05, 95% CI: 1.05-1.06).\n\nCONCLUSION:\nFamily history of multiple affected siblings increases the CHD risk. Family history is not a binary trait. There are degrees of risk associated with family history with more than one affected sibling." + }, + "questions": [ + { + "id": "ab66ecb9-e81e-4ff9-a297-007f5c2912a1", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1381, + "text": "Family history of multiple affected siblings" + } + ] + } + ] +} \ No newline at end of file diff --git a/7ba4f018-f93b-4436-81be-d27b7c767af3.json b/7ba4f018-f93b-4436-81be-d27b7c767af3.json new file mode 100644 index 0000000000000000000000000000000000000000..f1afcf9eb1279ff8e2d5ef49ee1bdd2449e34e9f --- /dev/null +++ b/7ba4f018-f93b-4436-81be-d27b7c767af3.json @@ -0,0 +1,35 @@ +{ + "id": "7ba4f018-f93b-4436-81be-d27b7c767af3", + "disease": { + "id": "H00056", + "names": [ + "Alzheimer disease", + "Dementia due to Alzheimer disease" + ], + "dbLinks": { + "icd10": [ + "G30" + ], + "mesh": [ + "D000544" + ] + }, + "category": "Neurodegenerative disease" + }, + "article": { + "id": "28784822", + "text": "BACKGROUND:\nSeveral observational studies have reported that higher visit-to-visit blood pressure variability is a risk factor for cognitive impairment and dementia. However, no studies have investigated the association of day-to-day blood pressure variability assessed by home blood pressure measurement with the development of dementia.\n\nMETHODS:\nA total of 1674 community-dwelling Japanese elderly without dementia, ≥60 years of age, were followed up for 5 years (2007-2012). Home blood pressure was measured 3 times every morning for a median of 28 days. Day-to-day systolic (SBP) and diastolic blood pressure variabilities, calculated as coefficients of variation (CoV) of home SBP and diastolic blood pressure, were categorized into quartiles. The hazard ratios and their 95% confidence intervals of the CoV levels of home blood pressure on the development of all-cause dementia, vascular dementia (VaD), and Alzheimer disease (AD) were computed with a Cox proportional hazards model.\n\nRESULTS:\nDuring the follow-up, 194 subjects developed all-cause dementia; of these, 47 had VaD and 134 had AD. The age- and sex-adjusted incidences of all-cause dementia, VaD, and AD increased significantly with increasing CoV levels of home SBP (all for trend \u003c0.05). These associations remained unchanged after adjustment for potential confounding factors, including home SBP. Compared with subjects in the first quartile of CoV levels of home SBP, the risks of the development of all-cause dementia, VaD, and AD were significantly higher in those in the fourth quartile (hazard ratio=2.27, 95% confidence interval=1.45-3.55, \u003c0.001 for all-cause dementia; hazard ratio=2.79, 95% confidence interval=1.04-7.51, =0.03 for VaD; hazard ratio=2.22, 95% confidence interval=1.31-3.75, \u003c0.001 for AD). Similar associations were observed for CoV levels of home diastolic blood pressure. Meanwhile, home SBP levels were significantly associated with the risk of VaD but not with the risks of all-cause dementia and AD. There was no interaction between home SBP levels and CoV levels of home SBP on the risk of each subtype of dementia.\n\nCONCLUSIONS:\nOur findings suggest that increased day-to-day blood pressure variability is, independently of average home blood pressure, a significant risk factor for the development of all-cause dementia, VaD, and AD in the general elderly Japanese population." + }, + "questions": [ + { + "id": "66758c07-55f5-4213-824d-5d5eefac0ab5", + "text": "What are the risk factors of Alzheimer disease?", + "answers": [ + { + "answer_start": 2162, + "text": "increased day-to-day blood pressure variability" + } + ] + } + ] +} \ No newline at end of file diff --git a/7be25697-d1f7-43bb-8db9-35cd12758260.json b/7be25697-d1f7-43bb-8db9-35cd12758260.json new file mode 100644 index 0000000000000000000000000000000000000000..19c3085bc758d5b85317b760ae67082ed9bff548 --- /dev/null +++ b/7be25697-d1f7-43bb-8db9-35cd12758260.json @@ -0,0 +1,46 @@ +{ + "id": "7be25697-d1f7-43bb-8db9-35cd12758260", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "26546245", + "text": "Studies on active and passive tobacco smoking and breast cancer have found inconsistent results. A meta-analysis of observational studies on tobacco smoking and breast cancer occurrence was conducted based on systematic searches for studies with retrospective (case-control) and prospective (cohort) designs. Eligible studies were identified, and relative risk measurements were extracted for active and passive tobacco exposures. Random-effects meta-analyses were used to compute summary relative risks (SRR). Heterogeneity of results between studies was evaluated using the (I (2)) statistics. For ever active smoking, in 27 prospective studies, the SRR for breast cancer was 1.10 (95 % CI [1.09-1.12]) with no heterogeneity (I (2) = 0 %). In 44 retrospective studies, the SRR was 1.08 (95 % CI [1.02-1.14]) with high heterogeneity (I (2) = 59 %). SRRs for current active smoking were 1.13 (95 % CI [1.09-1.17]) in 27 prospective studies and 1.08 (95 % CI [0.97-1.20]) in 22 retrospective studies. The results were stable across different subgroup analyses, notably pre/post-menopause, alcohol consumption adjustments, including/excluding passive smokers from the referent group. For ever passive smoking, in 11 prospective studies, the SRR for breast cancer was 1.07 (95 % CI [1.02-1.13]) with no heterogeneity (I (2) = 1 %). In 20 retrospective studies, the SRR was 1.30 (95 % CI [1.10-1.54]) with high heterogeneity (I (2) = 74 %). Too few prospective studies were available for meaningful subgroup analyses. There is consistent evidence for a moderate increase in the risk of breast cancer in women who smoke tobacco. The evidence for a moderate increase in risk with passive smoking is more substantial than a few years ago." + }, + "questions": [ + { + "id": "b40478ab-509a-4dbc-acfb-d1e87f22236b", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1186, + "text": "ever passive smoking" + }, + { + "answer_start": 859, + "text": "current active smoking" + }, + { + "answer_start": 1599, + "text": "women who smoke tobacco" + }, + { + "answer_start": 1674, + "text": "passive smoking" + } + ] + } + ] +} \ No newline at end of file diff --git a/7c189f56-5f04-4f2c-bea1-caa56f952c59.json b/7c189f56-5f04-4f2c-bea1-caa56f952c59.json new file mode 100644 index 0000000000000000000000000000000000000000..91f147f7ce337c266d1f105cefe926becf63e395 --- /dev/null +++ b/7c189f56-5f04-4f2c-bea1-caa56f952c59.json @@ -0,0 +1,41 @@ +{ + "id": "7c189f56-5f04-4f2c-bea1-caa56f952c59", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "10203281", + "text": "BACKGROUND:\nInsulin-like growth factor-I (IGF-I) is a potent mitogen for normal and neoplastic cells, whereas IGF-binding protein-3 (IGFBP-3) inhibits cell growth in many experimental systems. Acromegalics, who have abnormally high levels of growth hormone and IGF-I, have higher rates of colorectal cancer. We therefore examined associations of plasma levels of IGF-I and IGFBP-3 with the risk of colorectal cancer in a prospective case-control study nested in the Physicians' Health Study.\n\nMETHODS:\nPlasma samples were collected at baseline from 14916 men without diagnosed cancer. IGF-I, IGF-II, and IGFBP-3 were assayed among 193 men later diagnosed with colorectal cancer during 14 years of follow-up and among 318 age- and smoking-matched control subjects. All P values are two-sided.\n\nRESULTS:\nIGFBP-3 levels correlated with IGF-I levels (r=.64) and with IGF-II levels (r=.90). After controlling for IGFBP-3, age, smoking, body mass index (weight in kg/[height in m]2), and alcohol intake, men in the highest quintile for IGF-I had an increased risk of colorectal cancer compared with men in the lowest quintile (relative risk [RR]=2.51; 95% confidence interval [CI]=1.15-5.46; P for trend = .02). After controlling for IGF-I and other covariates, men with higher IGFBP-3 had a lower risk (RR=0.28; 95% CI=0.12-0.66; P for trend = .005, comparing extreme quintiles). The associations were consistent during the first and the second 7-year follow-up intervals and among younger and older men. IGF-II was not associated with risk.\n\nCONCLUSIONS:\nOur findings suggest that circulating IGF-I and IGFBP-3 are related to future risk of colorectal cancer." + }, + "questions": [ + { + "id": "3fcdaf4a-b24c-4277-9175-f92509473e36", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1577, + "text": "circulating IGF-I and IGFBP-3" + }, + { + "answer_start": 998, + "text": "men in the highest quintile for IGF-I" + } + ] + } + ] +} \ No newline at end of file diff --git a/7c245594-5d19-43a7-ab11-877054d1e12e.json b/7c245594-5d19-43a7-ab11-877054d1e12e.json new file mode 100644 index 0000000000000000000000000000000000000000..b966e7159cd7e54ce7f9e3846cbfb968f8dfa21a --- /dev/null +++ b/7c245594-5d19-43a7-ab11-877054d1e12e.json @@ -0,0 +1,45 @@ +{ + "id": "7c245594-5d19-43a7-ab11-877054d1e12e", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "19088354", + "text": "CONTEXT:\nColorectal cancer is the third most common form of cancer and the fourth most frequent cause of cancer deaths worldwide. The association between cigarette smoking and colorectal cancer has been inconsistent among studies.\n\nOBJECTIVE:\nTo clarify the association of cigarette smoking and colorectal cancer, we performed a comprehensive literature search and a meta-analysis of observational studies considering both incidence and mortality.\n\nDATA SOURCES:\nWe performed a literature search using PubMed, ISI Web of Science (Science Citation Index Expanded), and EMBASE to May 2008, with no restrictions. We also reviewed references from all retrieved articles.\n\nSTUDY SELECTION:\nAll articles that were independent and contained the minimum information necessary to estimate the colorectal cancer risk associated with cigarette smoking and a corresponding measure of uncertainty.\n\nDATA EXTRACTION:\nArticles were reviewed and data were extracted and cross-checked independently by 3 investigators, and any disagreement was resolved by consensus among all 3.\n\nRESULTS:\nOne hundred six observational studies were included in the analysis of incidence. Twenty-six studies provided adjusted risk estimates for ever smokers vs never smokers, leading to a pooled relative risk of 1.18 (95% confidence interval [CI], 1.11-1.25). Smoking was associated with an absolute risk increase of 10.8 cases per 100,000 person-years (95% CI, 7.9-13.6). We found a statistically significant dose-relationship with an increasing number of pack-years and cigarettes per day. However, the association was statistically significant only after 30 years of smoking. Seventeen cohort studies were included in the analysis of mortality. The pooled risk estimate for ever vs never smokers was 1.25 (95% CI, 1.14-1.37). Smoking was associated with an absolute risk increase of 6.0 deaths per 100,000 person-years (95% CI, 4.2-7.6). For both incidence and mortality, the association was stronger for cancer of the rectum than of the colon.\n\nCONCLUSION:\nCigarette smoking is significantly associated with colorectal cancer incidence and mortality." + }, + "questions": [ + { + "id": "3da86d1a-0bd3-498b-8911-868367749244", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1326, + "text": "Smoking" + }, + { + "answer_start": 1624, + "text": "30 years of smoking" + }, + { + "answer_start": 2027, + "text": "Cigarette smoking" + } + ] + } + ] +} \ No newline at end of file diff --git a/7c31b237-64a6-4dd3-b20e-36bff0faf065.json b/7c31b237-64a6-4dd3-b20e-36bff0faf065.json new file mode 100644 index 0000000000000000000000000000000000000000..6f8035f6ff46eff3086a9d35591b27b024ceba9e --- /dev/null +++ b/7c31b237-64a6-4dd3-b20e-36bff0faf065.json @@ -0,0 +1,46 @@ +{ + "id": "7c31b237-64a6-4dd3-b20e-36bff0faf065", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "11251984", + "text": "A population-based case-control study was conducted in Los Angeles, California, which involved 1,514 incident cases of bladder cancer and an equal number of age-, sex- and ethnicity-matched controls. Information on personal use of hair dyes was obtained from 897 cases and their matched controls. After adjustment for cigarette smoking, a major risk factor for bladder cancer, women who used permanent hair dyes at least once a month experienced a 2.1-fold risk of bladder cancer relative to non-users (p for trend = 0.04). Risk increased to 3.3 (95% CI = 1.3-8.4) among regular (at least monthly) users of 15 or more years. Occupational exposure to hair dyes was associated with an increased risk of bladder cancer in this study. Subjects who worked for 10 or more years as hairdressers or barbers experienced a 5-fold (95% CI = 1.3-19.2) increase in risk compared to individuals not exposed." + }, + "questions": [ + { + "id": "d149084d-e4a2-4cf4-8c5a-74c3d0c9be26", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 377, + "text": "women who used permanent hair dyes at least once a month" + }, + { + "answer_start": 571, + "text": "regular (at least monthly) users of 15 or more years" + }, + { + "answer_start": 625, + "text": "Occupational exposure to hair dyes" + }, + { + "answer_start": 731, + "text": "Subjects who worked for 10 or more years as hairdressers or barbers" + } + ] + } + ] +} \ No newline at end of file diff --git a/7f080050-b944-4b74-80ba-e43bd340827c.json b/7f080050-b944-4b74-80ba-e43bd340827c.json new file mode 100644 index 0000000000000000000000000000000000000000..f265096dc97f230fdf21bade9b173d44bdc0fd2c --- /dev/null +++ b/7f080050-b944-4b74-80ba-e43bd340827c.json @@ -0,0 +1,40 @@ +{ + "id": "7f080050-b944-4b74-80ba-e43bd340827c", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "20139228", + "text": "BACKGROUND:\nAlthough many studies have suggested that biomass smoke is a risk factor for COPD, the relationship between the two has not been firmly established. In particular, the extent of the association between exposure of biomass smoke and COPD in different populations, as well as the relationship between biomass smoke and cigarette smoke, is not clear. To ascertain the relationship between biomass smoke and COPD, we performed a metaanalysis.\n\nMETHODS:\nWe searched MEDLINE, EMBASE, and the Latin American and Caribbean Literature in Health Sciences Database and analyzed 15 epidemiologic (11 cross-sectional and four case-control) studies that met our criteria. Data were extracted and analyzed independently by two investigators using a standardized protocol.\n\nRESULTS:\nOverall, people exposed to biomass smoke have an odds ratio (OR) of 2.44 (95% CI, 1.9-3.33) for developing COPD, relative to those not exposed to biomass smoke. Biomass smoke exposure was clearly identified as a risk factor for developing COPD in both women (OR, 2.73; 95% CI, 2.28-3.28) and men (OR, 4.30; 95% CI, 1.85-10.01), and in both the Asian population (OR, 2.31; 95% CI, 1.41-3.78) and the non-Asian population (OR, 2.56; 95% CI, 1.71-3.83). This risk factor has also been revealed in patients with chronic bronchitis (OR, 2.56; 95% CI, 1.77-3.70) and COPD (OR, 2.65; 95% CI, 1.75-4.03), and in cigarette smokers (OR, 4.39; 95% CI, 1.40-4.66) and non-cigarette smokers (OR, 2.55; 95% CI, 2.06-3.15).\n\nCONCLUSIONS:\nExposure to biomass smoke is a risk factor for COPD." + }, + "questions": [ + { + "id": "84eac3f4-d705-40d2-b9c0-5a42cf0dedef", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 788, + "text": "people exposed to biomass smoke" + }, + { + "answer_start": 940, + "text": "Biomass smoke exposure" + } + ] + } + ] +} \ No newline at end of file diff --git a/7fb5fedc-d1e1-41fd-85c7-0075fc00e45e.json b/7fb5fedc-d1e1-41fd-85c7-0075fc00e45e.json new file mode 100644 index 0000000000000000000000000000000000000000..4da92265be2e9c93d774b8c4af6a3a7193dd3972 --- /dev/null +++ b/7fb5fedc-d1e1-41fd-85c7-0075fc00e45e.json @@ -0,0 +1,38 @@ +{ + "id": "7fb5fedc-d1e1-41fd-85c7-0075fc00e45e", + "disease": { + "id": "H00408", + "names": [ + "Type 1 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E10" + ], + "mesh": [ + "D003922" + ] + }, + "category": "Metabolic disease; Immune system disease; Endocrine disease" + }, + "article": { + "id": "29937434", + "text": "Insulin-dependent diabetes may occur in patients with cancers who are treated with checkpoint inhibitors (CPIs). We reviewed cases occurring over a 6-year period at two academic institutions and identified 27 patients in whom this developed, or an incidence of 0.9%. The patients had a variety of solid-organ cancers, but all had received either anti-PD-1 or anti-PD-L1 antibodies. Diabetes presented with ketoacidosis in 59%, and 42% had evidence of pancreatitis in the peridiagnosis period. Forty percent had at least one positive autoantibody and 21% had two or more. There was a predominance of HLA-DR4, which was present in 76% of patients. Other immune adverse events were seen in 70%, and endocrine adverse events in 44%. We conclude that autoimmune, insulin-dependent diabetes occurs in close to 1% of patients treated with anti-PD-1 or -PD-L1 CPIs. This syndrome has similarities and differences compared with classic type 1 diabetes. The dominance of HLA-DR4 suggests an opportunity to identify those at highest risk of these complications and to discover insights into the mechanisms of this adverse event." + }, + "questions": [ + { + "id": "a0429ec7-316d-4b30-9f6f-d577a5f3d994", + "text": "What are the risk factors of Type 1 diabetes mellitus?", + "answers": [ + { + "answer_start": 330, + "text": "received either anti-PD-1 or anti-PD-L1 antibodies" + }, + { + "answer_start": 961, + "text": "HLA-DR4" + } + ] + } + ] +} \ No newline at end of file diff --git a/7fcf7aec-453a-4b7f-bd7c-9ebb6c74d333.json b/7fcf7aec-453a-4b7f-bd7c-9ebb6c74d333.json new file mode 100644 index 0000000000000000000000000000000000000000..a678c0bad2d710d9e38b8d82a9ae543a05ba99ca --- /dev/null +++ b/7fcf7aec-453a-4b7f-bd7c-9ebb6c74d333.json @@ -0,0 +1,36 @@ +{ + "id": "7fcf7aec-453a-4b7f-bd7c-9ebb6c74d333", + "disease": { + "id": "M2023_04_26_16_49_01", + "names": [ + "Metabolic syndrome" + ], + "dbLinks": { + "mesh": [ + "C18.452.394.968.500.570", + "C18.452.625" + ] + }, + "description": "Metabolic syndrome is a complex constellation of metabolic derangements that increase the risk of atherosclerotic cardiovascular disease, type 2 diabetes, and all-cause mortality. The key features of metabolic syndrome include central obesity, insulin resistance, dyslipidemia, and hypertension. These abnormalities are believed to arise from a combination of genetic predisposition and environmental factors, such as sedentary behavior, poor dietary habits, and chronic stress. Diagnosis of metabolic syndrome requires meeting three or more established criteria, based on standardized guidelines. Management of metabolic syndrome involves a comprehensive approach, including lifestyle modifications such as weight loss, physical activity, and dietary changes, as well as pharmacotherapy to address underlying risk factors such as hypertension, dyslipidemia, and hyperglycemia. Early intervention and aggressive management of metabolic syndrome are critical to preventing or delaying the onset of complications and improving long-term health outcomes." + }, + "article": { + "id": "16816234", + "text": "OBJECTIVE:\nThis study compared the prevalence of the metabolic syndrome among outpatients with schizophrenia and schizoaffective disorder receiving clozapine with a matched comparison group from the National Health and Nutrition Examination Survey.\n\nMETHOD:\nNinety-three outpatients and a matched group of 2,701 comparison subjects were compared according to National Cholesterol Education Program criteria. Outpatient data were obtained through physical assessments, laboratory testing, and reviews of medical records.\n\nRESULTS:\nThe prevalence of the metabolic syndrome was significantly higher among clozapine patients (53.8%) than among the comparison group (20.7%). For clozapine patients, logistic regression analysis revealed significant associations with age, body mass index, and duration of clozapine treatment. Only age and body mass index were associated with the prevalence of metabolic syndrome in both groups.\n\nCONCLUSIONS:\nPatients receiving clozapine are at significantly increased risk for developing the metabolic syndrome. Psychiatrists and other providers should consider performing regular physical health monitoring to prevent long-term adverse health consequences." + }, + "questions": [ + { + "id": "b0407746-2d1b-43fa-98dd-d7440d1b4622", + "text": "What is a risk factor for Metabolic Syndrome?", + "answers": [ + { + "answer_start": 602, + "text": "clozapine" + }, + { + "answer_start": 938, + "text": "Patients receiving clozapine" + } + ] + } + ] +} \ No newline at end of file diff --git a/7ffd6048-9253-4252-9ae9-466996654398.json b/7ffd6048-9253-4252-9ae9-466996654398.json new file mode 100644 index 0000000000000000000000000000000000000000..8c51669eec9f0239ba7dc27e1f3c25ddaff6ab39 --- /dev/null +++ b/7ffd6048-9253-4252-9ae9-466996654398.json @@ -0,0 +1,43 @@ +{ + "id": "7ffd6048-9253-4252-9ae9-466996654398", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "25387276", + "text": "RATIONALE:\nEvidence linking active or passive smoking to the incidence of adult-onset asthma is inconsistent with both positive and inverse associations being reported. Most previous studies of active smoking have not accounted for passive smoke exposure, which may have introduced bias.\n\nOBJECTIVES:\nTo assess the separate associations of active and passive smoking to the incidence of adult-onset asthma in the U.S. Black Women's Health Study, a prospective cohort of African American women followed since 1995 with mailed biennial questionnaires.\n\nMETHODS:\nActive smoking status was reported at baseline and updated on all follow-up questionnaires. Passive smoke exposure during childhood, adolescence, and adulthood was ascertained in 1997. Asthma cases comprised women who reported doctor-diagnosed asthma with concurrent asthma medication use. Cox regression models were used to derive multivariable hazard ratios (HRs) and 95% confidence intervals (CIs) for former and current smoking and for passive smoking among nonsmokers compared with a reference category of never active or passive smokers.\n\nMEASUREMENTS AND MAIN RESULTS:\nAmong 46,182 participants followed from 1995 to 2011, 1,523 reported incident asthma. The multivariable HRs for former active smoking, current active smoking, and passive smoking only were, respectively, 1.36 (95% CI, 1.11-1.67), 1.43 (95% CI, 1.15-1.77), and 1.21 (95% CI, 1.00-1.45), compared with never active/passive smoking.\n\nCONCLUSIONS:\nIn this large population with 16 years of follow-up, active smoking increased the incidence of adult-onset asthma, and passive smoke exposure increased the risk among nonsmokers. Continued efforts to reduce exposure to tobacco smoke may have a beneficial effect on the incidence of adult-onset asthma." + }, + "questions": [ + { + "id": "d574df78-6935-46e5-ac34-8234c8358a10", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1248, + "text": "former active smoking" + }, + { + "answer_start": 1271, + "text": "current active smoking" + }, + { + "answer_start": 1299, + "text": "passive smoking only" + } + ] + } + ] +} \ No newline at end of file diff --git a/800aaa5b-f889-438f-a21b-145503bfc62f.json b/800aaa5b-f889-438f-a21b-145503bfc62f.json new file mode 100644 index 0000000000000000000000000000000000000000..31988b62badbbb248edc31f285ea5283491f7c8e --- /dev/null +++ b/800aaa5b-f889-438f-a21b-145503bfc62f.json @@ -0,0 +1,41 @@ +{ + "id": "800aaa5b-f889-438f-a21b-145503bfc62f", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "31250012", + "text": "BACKGROUND:\nThe role of Helicobacter pylori (H. pylori) infection in the development of colorectal neoplasia has been a matter of scientific debate with controversial findings.\n\nAIMS:\nThis study examined the association between H. pylori infection and colorectal cancer (CRC) in a nationwide population-based Chinese cohort study.\n\nMETHODS:\nA total of approximately 3936 individuals with newly diagnosed H. pylori infection (the H. pylori-infected cohort) and 15 744 age- and sex-matched patients with diagnoses absence of H. pylori infection (the comparison cohort) from 2000 to 2005 were identified from Taiwan's National Health Insurance Research Database. The Kaplan-Meier method was used for measuring the cumulative incidence of CRC in each cohort. Cox proportional hazards models were used to compute hazard ratios (HRs) and accompanying 95% confidence intervals (CIs) for the estimation of the association between H. pylori infection and CRC.\n\nRESULTS:\nThe cumulative incidence of CRC was higher in H. pylori-infected cohort than that in the comparison cohort (log-rank test, P \u003c 0.001). After adjustment for potential confounders, H. pylori infection was associated with a significantly increased risk of CRC (adjusted HR 1.87; 95% CI 1.37-2.57). In addition, the HR of CRC appeared to increase with increasing frequency of clinical visits for H. pylori infection.\n\nCONCLUSIONS:\nOur study demonstrated that H. pylori infection was associated with an increased risk of CRC, which warrants confirmation and exploration of the underlying biologic mechanisms by future studies." + }, + "questions": [ + { + "id": "03c188c7-56c0-4ab6-85cf-c9336d44ea44", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1140, + "text": "H. pylori infection" + }, + { + "answer_start": 1416, + "text": "H. pylori infection" + } + ] + } + ] +} \ No newline at end of file diff --git a/80c16425-2f8b-44a0-ba18-f8d3131e590f.json b/80c16425-2f8b-44a0-ba18-f8d3131e590f.json new file mode 100644 index 0000000000000000000000000000000000000000..f5256e65bca1d51a9f94fa9a5d7b8455138f9787 --- /dev/null +++ b/80c16425-2f8b-44a0-ba18-f8d3131e590f.json @@ -0,0 +1,42 @@ +{ + "id": "80c16425-2f8b-44a0-ba18-f8d3131e590f", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "3652049", + "text": "The hypothesis that the frequency distribution of indices of oxidative drug-metabolizing activity is different between patients with bladder cancer (n = 98) and age, sex-matched control subjects (n = 110) has been investigated. Urinary recovery ratios of debrisoquine and R/S ratios of mephenytoin have been measured in an 8-h urine sample after simultaneous administration of debrisoquine (10 mg) and racemic mephenytoin (100 mg). In addition, alcohol consumption, smoking habit, and acetylation phenotype (using 100 mg dapsone as a substrate) have been measured. Patients with bladder cancer were classified on histological criteria as having aggressive (Stage III) (34%) or nonaggressive (Stages I and II) (66%) disease. The median of the frequency distribution of the debrisoquine urinary recovery ratio in patients with aggressive bladder cancer was greater than in control subjects, and only four patients had recovery ratios lower than the mean of the control group. Using logistic regression analysis, efficient debrisoquine metabolism and a synergistic interaction between smoking and ethanol consumption were significant, independent risk factors, while S-mephenytoin hydroxylation and acetylation phenotype were not significant risk factors. In contrast, patients with non-aggressive bladder cancer had a significant, but weaker, association with rapid hydroxylation of S-mephenytoin, which was independent of a significant synergistic interaction between smoking and alcohol consumption. Acetylation phenotype and debrisoquine urinary recovery ratio were not associated with increased risk of nonaggressive cancer. These results are consistent with the concept that oxidative isozymes might be responsible for conversion of environmental agents to proximate bladder carcinogens in nonindustrial-related bladder cancer. They also suggest that different etiological factors are involved in the pathogenesis of aggressive and nonaggressive bladder cancer." + }, + "questions": [ + { + "id": "a3f45b9e-ebe9-46d3-9e95-d020e959c730", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 1010, + "text": "efficient debrisoquine metabolism" + }, + { + "answer_start": 1050, + "text": "synergistic interaction between smoking and ethanol consumption" + }, + { + "answer_start": 1358, + "text": "rapid hydroxylation of S-mephenytoin," + } + ] + } + ] +} \ No newline at end of file diff --git a/82368c86-cde2-4589-a375-54c14290950e.json b/82368c86-cde2-4589-a375-54c14290950e.json new file mode 100644 index 0000000000000000000000000000000000000000..405a67292f522aec9a62605b5e4df1bfa91dc869 --- /dev/null +++ b/82368c86-cde2-4589-a375-54c14290950e.json @@ -0,0 +1,37 @@ +{ + "id": "82368c86-cde2-4589-a375-54c14290950e", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "9934729", + "text": "OBJECTIVE:\nThe relationship between cholecystectomy and the occurrence of subsequent colon cancer has been controversial. Using data collected as part of an incident case-control study of colon cancer conducted in northern California, Minnesota, and Utah, we evaluated this association.\n\nMETHODS:\nParticipants were between 30 and 79 yr of age and had a first primary colon cancer diagnosed between October 1, 1991 and September 30, 1994. Analyses were adjusted for age, gender, family history of colorectal cancer, body mass index, dietary energy and fiber intake, use of aspirin or nonsteroidal antiinflammatory drugs, and long-term leisure-time vigorous physical activity.\n\nRESULTS:\nA weak positive association between cholecystectomy and proximal colon cancer (odds ratio [OR] and 95% confidence interval [CI] 1.3 [1.0-1.6]) was observed. This was counterbalanced by a weak, nonsignificant negative association (OR 0.8, 95% CI 0.6-1.1) with distal colon cancer leading to no overall association (OR 1.0, 95% CI 0.9-1.2). The association between colon cancer and cholecystectomy did not differ by gender or race, but it did differ by study area, with most of the increased association being attributed to the Minnesota population. The elevated risk of proximal colon cancer increased after cholecystectomy but disappeared after 14 years.\n\nCONCLUSIONS:\nOur results suggest that cholecystectomy or the underlying gallstone disease that prompts it may be related weakly to the risk of subsequent proximal colon cancer. However, the association may differ by geographic area of the country, and may be artifactual at least in part." + }, + "questions": [ + { + "id": "49714cea-9102-4748-9ae1-1a648e78c3ea", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 721, + "text": "cholecystectomy " + } + ] + } + ] +} \ No newline at end of file diff --git a/82b41a91-ee5c-46a3-8f17-f32d2325f873.json b/82b41a91-ee5c-46a3-8f17-f32d2325f873.json new file mode 100644 index 0000000000000000000000000000000000000000..ad9fda889547dbdf3dedbc49dc9fdd367860cfb0 --- /dev/null +++ b/82b41a91-ee5c-46a3-8f17-f32d2325f873.json @@ -0,0 +1,40 @@ +{ + "id": "82b41a91-ee5c-46a3-8f17-f32d2325f873", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "7735588", + "text": "An increased level of airway responsiveness has been proposed as a risk factor associated with the onset and prognosis of chronic airway obstruction. To determine this, longitudinal studies are necessary, with measurement of both the level of airway responsiveness and of additional risk factors, such as cigarette smoking, made before measurement of pulmonary function decline. The association of airways responsiveness with decline in FEV1 has been prospectively studied in a random sample of the Dutch population. Longitudinal data from 921 males, providing 2,376 paired observations, and 698 females, providing 1,682 paired observations, were used for analysis. Differences between responders and nonresponders (PC10 \u003c or = 16 mg/ml of histamine) were estimated from linear regression analyses stratified by gender and smoking status, with adjustment for age, residential area, the presence of respiratory symptoms, indicators for each interval, and residuals of FEV1 at the beginning of the interval. Responders had a greater mean yearly decline in FEV1, and the differences between responders and nonresponders were similar for all gender and smoking subgroups. In an overall regression model, subjects with airway hyperresponsiveness had a significantly steeper decline in FEV1, independent of the other variables (males: beta = -12.5 ml/yr, SEM = 3.22, p \u003c 0.001; females: beta = -11.50 ml/yr, SEM = 2.98, p \u003c 0.001). The current analyses conclusively demonstrated that increased airway responsiveness is an independent risk factor for an accelerated decline in FEV1 and, hence, for the development of chronic obstructive lung disease. The mechanisms by which increased airway responsiveness leads to an accelerated decline in FEV, are imperfectly understood and require further study." + }, + "questions": [ + { + "id": "94eb5e1b-8b7b-4200-bc6d-ff9aacd74893", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 1200, + "text": "subjects with airway hyperresponsiveness" + }, + { + "answer_start": 1478, + "text": "increased airway responsiveness" + } + ] + } + ] +} \ No newline at end of file diff --git a/83860e53-8180-425f-b27a-be830c4bd157.json b/83860e53-8180-425f-b27a-be830c4bd157.json new file mode 100644 index 0000000000000000000000000000000000000000..c835807997f06cd9fb4472f738eb27b3d55d5d46 --- /dev/null +++ b/83860e53-8180-425f-b27a-be830c4bd157.json @@ -0,0 +1,35 @@ +{ + "id": "83860e53-8180-425f-b27a-be830c4bd157", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "22957782", + "text": "BACKGROUND:\nThe association between neonatal jaundice and childhood asthma is a new finding of two reports. The purpose of the study was to verify their results.\n\nMETHODS:\nData from 11,321 children were collected from the National Health Insurance Research Database. Their claims data were evaluated from birth to 10 yr old. Children were analyzed as case (those with neonatal jaundice) and controls (those without neonatal jaundice). The diagnostic criteria for asthma were as follows: at least four asthma diagnoses at outpatient services and emergency department (ED), or one asthma diagnosis during an admission. In children fitting the asthma criteria, those with no asthma diagnosis after 1 yr of age were excluded. Mantel-Haenszel's odds ratios were calculated after adjustment for the following confounders: preterm/low birth weight, neonatal infection, other respiratory conditions, other birth conditions, and gender. Asthma rate, onset time, the use of drugs, upper respiratory infection and lower respiratory infection (LRI) rates, hospital admission/ED visit rates, and the effect of phototherapy were evaluated.\n\nRESULTS:\nAfter adjustment for the confounding factors, the rate of asthma was higher in icteric children (OR: 1.64, 95% CI 1.36-1.98, p \u003c 0.001), and the influence in females was stronger. There still was an association between neonatal jaundice and late onset asthma (asthma onset after 3 yr of age). In asthmatic children, those with neonatal jaundice have increased asthma onset rate before age 6, increased use of inhalant steroids, LRI rates, and ED visits for respiratory disease.\n\nCONCLUSIONS:\nNeonatal jaundice increased the rate and severity of childhood asthma in subjects aged up to 10 yr and may be a risk factor for childhood asthma." + }, + "questions": [ + { + "id": "00a9b25f-85c1-42f0-bd9d-46039a4a03b6", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1628, + "text": "Neonatal jaundice" + } + ] + } + ] +} \ No newline at end of file diff --git a/845aad35-ea60-4da4-8150-6fc371a7f5e2.json b/845aad35-ea60-4da4-8150-6fc371a7f5e2.json new file mode 100644 index 0000000000000000000000000000000000000000..c77d59c66de3b6579e6e14953fc14a64aee2af09 --- /dev/null +++ b/845aad35-ea60-4da4-8150-6fc371a7f5e2.json @@ -0,0 +1,42 @@ +{ + "id": "845aad35-ea60-4da4-8150-6fc371a7f5e2", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "17320658", + "text": "OBJECTIVES:\nTo determine the pathologic features of bladder tumors after nephroureterectomy or segmental ureterectomy for upper urinary tract transitional cell carcinoma (UUT-TCC).\n\nMETHODS:\nFrom 1993 to 2003, 82 patients without a history of bladder cancer underwent nephroureterectomy or segmental distal ureterectomy for UUT-TCC. We reviewed the pathologic features of the subsequent bladder tumors, including stage, grade, and progression to cystectomy in these patients at a median follow-up of 44.1 months.\n\nRESULTS:\nA total of 36 (44%) of 82 patients developed bladder tumors after definitive therapy for UUT-TCC at a mean interval of 13.9 months. The mean number of bladder tumors diagnosed per patient in the follow-up interval was 2.1 (range 1 to 6), for a total of 74 bladder tumors. Of the 74 bladder tumors, 71 (96%) were superficial (Stage Ta, Tis, T1), 49 of these superficial tumors (69%) being low grade (grade 1 and 2) and 22 (31%) high grade (grade 3). Three patients had high-grade, muscle-invasive disease, and all progressed to cystectomy during follow-up. A greater than 75% concordance was found in pathologic grade between the UUT lesion and subsequent bladder tumors. The stage of the UUT malignancy, however, did not correlate with subsequent bladder tumor pathologic findings.\n\nCONCLUSIONS:\nBladder tumors developed in 44% of patients after treatment of UUT-TCC. Of these bladder tumors, over 60% were superficial, low-grade lesions, yielding a similar pathologic distribution to that of bladder cancer de novo. The grade, but not the stage, of the UUT tumors correlated with the pathologic findings of subsequent bladder tumor recurrence. Aggressive surveillance with cystoscopy and urinary cytology after surgical management of UUT-TCC is imperative." + }, + "questions": [ + { + "id": "f3a8e564-cb82-4964-8340-950a94be60dd", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 122, + "text": "upper urinary tract transitional cell carcinoma (UUT-TCC)" + }, + { + "answer_start": 589, + "text": "definitive therapy for UUT-TCC" + }, + { + "answer_start": 1354, + "text": "patients after treatment of UUT-TCC" + } + ] + } + ] +} \ No newline at end of file diff --git a/849aebf0-0a33-4e5f-8c61-4195fb70df26.json b/849aebf0-0a33-4e5f-8c61-4195fb70df26.json new file mode 100644 index 0000000000000000000000000000000000000000..351df9bb0621add57fed0aa6862d591e13278050 --- /dev/null +++ b/849aebf0-0a33-4e5f-8c61-4195fb70df26.json @@ -0,0 +1,37 @@ +{ + "id": "849aebf0-0a33-4e5f-8c61-4195fb70df26", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "29912394", + "text": "BACKGROUND:\nExperimental and epidemiological studies suggest a protective role for vitamin D in colorectal carcinogenesis, but evidence is inconclusive. Circulating 25-hydroxyvitamin D (25(OH)D) concentrations that minimize risk are unknown. Current Institute of Medicine (IOM) vitamin D guidance is based solely on bone health.\n\nMETHODS:\nWe pooled participant-level data from 17 cohorts, comprising 5706 colorectal cancer case participants and 7107 control participants with a wide range of circulating 25(OH)D concentrations. For 30.1% of participants, 25(OH)D was newly measured. Previously measured 25(OH)D was calibrated to the same assay to permit estimating risk by absolute concentrations. Study-specific relative risks (RRs) for prediagnostic season-standardized 25(OH)D concentrations were calculated using conditional logistic regression and pooled using random effects models.\n\nRESULTS:\nCompared with the lower range of sufficiency for bone health (50-\u003c62.5 nmol/L), deficient 25(OH)D (\u003c30 nmol/L) was associated with 31% higher colorectal cancer risk (RR = 1.31, 95% confidence interval [CI] = 1.05 to 1.62); 25(OH)D above sufficiency (75-\u003c87.5 and 87.5-\u003c100 nmol/L) was associated with 19% (RR = 0.81, 95% CI = 0.67 to 0.99) and 27% (RR = 0.73, 95% CI = 0.59 to 0.91) lower risk, respectively. At 25(OH)D of 100 nmol/L or greater, risk did not continue to decline and was not statistically significantly reduced (RR = 0.91, 95% CI = 0.67 to 1.24, 3.5% of control participants). Associations were minimally affected when adjusting for body mass index, physical activity, or other risk factors. For each 25 nmol/L increment in circulating 25(OH)D, colorectal cancer risk was 19% lower in women (RR = 0.81, 95% CI = 0.75 to 0.87) and 7% lower in men (RR = 0.93, 95% CI = 0.86 to 1.00) (two-sided Pheterogeneity by sex = .008). Associations were inverse in all subgroups, including colorectal subsite, geographic region, and season of blood collection.\n\nCONCLUSIONS:\nHigher circulating 25(OH)D was related to a statistically significant, substantially lower colorectal cancer risk in women and non-statistically significant lower risk in men. Optimal 25(OH)D concentrations for colorectal cancer risk reduction, 75-100 nmol/L, appear higher than current IOM recommendations." + }, + "questions": [ + { + "id": "a4152a97-6ed6-46d9-975a-1e2e4609929e", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 979, + "text": "deficient 25(OH)D (\u003c30 nmol/L)" + } + ] + } + ] +} \ No newline at end of file diff --git a/84c27440-3f83-4967-9407-8fdce48bd8b3.json b/84c27440-3f83-4967-9407-8fdce48bd8b3.json new file mode 100644 index 0000000000000000000000000000000000000000..607398a07b772b1afbdcc4f6736e9074a0f37b18 --- /dev/null +++ b/84c27440-3f83-4967-9407-8fdce48bd8b3.json @@ -0,0 +1,35 @@ +{ + "id": "84c27440-3f83-4967-9407-8fdce48bd8b3", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "27589676", + "text": "BACKGROUND:\nApproximately 70% of rural Nigerian households rely on biomass fuels for cooking. The International Study of Asthma and Allergies in Childhood (ISAAC) estimates the prevalence of current wheeze among children in Nigeria to have risen from 10.7% in 1999 to approximately 20% in 2014.\n\nOBJECTIVE:\nTo examine the effects of biomass smoke exposure on asthma symptom prevalence in rural children in Nigeria.\n\nMETHODS:\nWe conducted a cross-sectional survey in rural communities in Nigeria. Asthma symptoms were defined according to ISAAC definitions. Biomass smoke exposure was determined by the types of fuel used for cooking. Logistic regression was used to explore associations between biomass smoke and asthma symptoms.\n\nRESULTS:\nThe study population comprised 1,690 school children, of which 865 lived in households cooking with biomass and 825 lived in households not using biomass. Asthma symptoms were reported in 481 (28.5%) children. Biomass fuel was associated with increased odds of asthma symptoms. Adjusted odds ratios (aORs) were 1.38 (95% CI: 1.05-1.80) for nocturnal cough, 1.26 (95% CI: 1.00-1.61) for current wheeze, and 1.33 (95% CI: 1.05-1.69) for report of any asthma-related symptoms. Sex modified the associations between asthma symptoms with biomass fuel: aORs were stronger and significant for males (nocturnal cough = 1.85, 95% CI: 1.24-2.76; current wheeze = 1.48, 95% CI: 1.03-2.13; report of any asthma-related symptoms = 1.60, 95% CI: 1.12-2.28), but weaker and non-significant for females.\n\nCONCLUSION:\nThe risk of asthma symptoms related to biomass smoke exposure appears to differ by sex." + }, + "questions": [ + { + "id": "5d47c686-6655-447e-9bcc-9abb995cddb7", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 950, + "text": "Biomass fuel" + } + ] + } + ] +} \ No newline at end of file diff --git a/85026313-7da1-43ea-af71-4cd0eb894836.json b/85026313-7da1-43ea-af71-4cd0eb894836.json new file mode 100644 index 0000000000000000000000000000000000000000..e993cec9e87bb7467f0ff325ab3a7df9b0bd934b --- /dev/null +++ b/85026313-7da1-43ea-af71-4cd0eb894836.json @@ -0,0 +1,42 @@ +{ + "id": "85026313-7da1-43ea-af71-4cd0eb894836", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "23297314", + "text": "AIMS:\nFamily history is an established risk factor for myocardial infarction (MI), but it is not clear how this risk changes with number and gender of first-degree relatives with MI. We used the entire Danish population to examine the importance of MI in siblings and parents.\n\nMETHODS AND RESULTS:\nThis study is a retrospective nationwide register-based cohort study including registered relatives to all Danish citizens diagnosed with MI in the period 1978-2010. In the entire Danish population we identified siblings to 7552 patients with a first-time MI. The rate ratios (RR) calculated by Poisson models showed an RR of 4.30 (95% confidence interval 3.53-5.23) for siblings of a patient with MI. Children of parents with MI also showed high risk: for children of a maternal case RR 2.40 (2.20-2.60), and of a paternal case RR 1.98 (1.98-2.09), respectively; P value for gender interaction \u003c0.0001. A paternal case with MI at an age \u003c50 years was associated with an RR of 3.30 (2.92-3.72) while a case \u003e50 years was associated with a risk of 1.83 (1.73-1.93). For maternal cases below and above 50 years of age the risks were 3.23 (2.56-4.10) and 2.31 (2.11-2.52), respectively.\n\nCONCLUSION:\nFirst-degree relatives of a patient with myocardial infarction themselves have a substantial higher risk of myocardial infarction. The risk is particularly elevated when the MI case is the mother or a sibling, and when the MI case has the infarction before the age of 50 years." + }, + "questions": [ + { + "id": "2bb8d179-24d2-43e2-9c1e-4261291610f3", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 670, + "text": "siblings of a patient with MI" + }, + { + "answer_start": 701, + "text": "Children of parents with MI" + }, + { + "answer_start": 1196, + "text": "First-degree relatives of a patient with myocardial infarction" + } + ] + } + ] +} \ No newline at end of file diff --git a/857b24c2-78d7-46c5-86d0-1b74f0aa9423.json b/857b24c2-78d7-46c5-86d0-1b74f0aa9423.json new file mode 100644 index 0000000000000000000000000000000000000000..10cd0e34857bc6b9b51337efc03cf4ef4f3b37fa --- /dev/null +++ b/857b24c2-78d7-46c5-86d0-1b74f0aa9423.json @@ -0,0 +1,41 @@ +{ + "id": "857b24c2-78d7-46c5-86d0-1b74f0aa9423", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "23208272", + "text": "OBJECTIVES:\nIt has been suggested that Helicobacter pylori (H. pylori) constitutes a risk for the development of adenomatous polyps and adenocarcinoma of the colon. Our aim was to study the association between H. pylori-positive gastritis and the occurrence of any colonic neoplasm.\n\nMETHODS:\nFrom a computerized database of surgical pathology reports, we selected 156,000 subjects who underwent colonoscopy and esophago-gastro-duodenoscopy with biopsy results from both procedures.\n\nRESULTS:\nCompared with normal gastric mucosa, H. pylori gastritis occurred more frequently among patients with hyperplastic polyps (OR=1.24, 95% CI: 1.18-1.30), adenomatous polyps (1.52, 1.46-1.57), advanced adenomas (1.80, 1.69-1.92), villous adenomas or adenomas with high-grade dysplasia (1.97, 1.82-2.14), and adenocarcinomas (2.35, 1.98-2.80). Similarly, the strength of the association between H. pylori-positive gastritis and colonic neoplasm increased with size and number of the adenomas. The association between H. pylori gastritis and the occurrence of colonic neoplasm was similar for different locations of the large bowel. Other gastric conditions etiologically associated with H. pylori, such as intestinal metaplasia, adenoma, lymphoma, and adenocarcinoma, were also significantly associated with an increased risk of colonic neoplasm.\n\nCONCLUSIONS:\nVarious forms of gastritis related to H. pylori infection confer an increased risk for colonic neoplasm. In the past, when H. pylori infection was more prevalent, its attributable risk to the occurrence of colorectal neoplasm may have been quite substantial." + }, + "questions": [ + { + "id": "dca3f4c7-d40a-4dbf-96da-243778352020", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 530, + "text": "H. pylori gastritis" + }, + { + "answer_start": 1350, + "text": "Various forms of gastritis related to H. pylori infection" + } + ] + } + ] +} \ No newline at end of file diff --git a/868a462a-01f6-4513-bb04-a6c2ef533487.json b/868a462a-01f6-4513-bb04-a6c2ef533487.json new file mode 100644 index 0000000000000000000000000000000000000000..2d681510238b427ba89435b02a3bf0b65c584978 --- /dev/null +++ b/868a462a-01f6-4513-bb04-a6c2ef533487.json @@ -0,0 +1,38 @@ +{ + "id": "868a462a-01f6-4513-bb04-a6c2ef533487", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "24881994", + "text": "BACKGROUND:\nThe associations of blood pressure with the different manifestations of incident cardiovascular disease in a contemporary population have not been compared. In this study, we aimed to analyse the associations of blood pressure with 12 different presentations of cardiovascular disease.\n\nMETHODS:\nWe used linked electronic health records from 1997 to 2010 in the CALIBER (CArdiovascular research using LInked Bespoke studies and Electronic health Records) programme to assemble a cohort of 1·25 million patients, 30 years of age or older and initially free from cardiovascular disease, a fifth of whom received blood pressure-lowering treatments. We studied the heterogeneity in the age-specific associations of clinically measured blood pressure with 12 acute and chronic cardiovascular diseases, and estimated the lifetime risks (up to 95 years of age) and cardiovascular disease-free life-years lost adjusted for other risk factors at index ages 30, 60, and 80 years. This study is registered at ClinicalTrials.gov, number NCT01164371.\n\nFINDINGS:\nDuring 5·2 years median follow-up, we recorded 83,098 initial cardiovascular disease presentations. In each age group, the lowest risk for cardiovascular disease was in people with systolic blood pressure of 90-114 mm Hg and diastolic blood pressure of 60-74 mm Hg, with no evidence of a J-shaped increased risk at lower blood pressures. The effect of high blood pressure varied by cardiovascular disease endpoint, from strongly positive to no effect. Associations with high systolic blood pressure were strongest for intracerebral haemorrhage (hazard ratio 1·44 [95% CI 1·32-1·58]), subarachnoid haemorrhage (1·43 [1·25-1·63]), and stable angina (1·41 [1·36-1·46]), and weakest for abdominal aortic aneurysm (1·08 [1·00-1·17]). Compared with diastolic blood pressure, raised systolic blood pressure had a greater effect on angina, myocardial infarction, and peripheral arterial disease, whereas raised diastolic blood pressure had a greater effect on abdominal aortic aneurysm than did raised systolic pressure. Pulse pressure associations were inverse for abdominal aortic aneurysm (HR per 10 mm Hg 0·91 [95% CI 0·86-0·98]) and strongest for peripheral arterial disease (1·23 [1·20-1·27]). People with hypertension (blood pressure ≥140/90 mm Hg or those receiving blood pressure-lowering drugs) had a lifetime risk of overall cardiovascular disease at 30 years of age of 63·3% (95% CI 62·9-63·8) compared with 46·1% (45·5-46·8) for those with normal blood pressure, and developed cardiovascular disease 5·0 years earlier (95% CI 4·8-5·2). Stable and unstable angina accounted for most (43%) of the cardiovascular disease-free years of life lost associated with hypertension from index age 30 years, whereas heart failure and stable angina accounted for the largest proportion (19% each) of years of life lost from index age 80 years.\n\nINTERPRETATION:\nThe widely held assumptions that blood pressure has strong associations with the occurrence of all cardiovascular diseases across a wide age range, and that diastolic and systolic associations are concordant, are not supported by the findings of this high-resolution study. Despite modern treatments, the lifetime burden of hypertension is substantial. These findings emphasise the need for new blood pressure-lowering strategies, and will help to inform the design of randomised trials to assess them.\n\nFUNDING:\nMedical Research Council, National Institute for Health Research, and Wellcome Trust." + }, + "questions": [ + { + "id": "bd4d0e92-a7d8-4dfc-8972-fcc6bcc39b82", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1830, + "text": "raised systolic blood pressure" + }, + { + "answer_start": 2253, + "text": "People with hypertension (blood pressure ≥140/90 mm Hg or those receiving blood pressure-lowering drugs)" + } + ] + } + ] +} \ No newline at end of file diff --git a/872e1ad0-ef48-43f8-afc3-f6028d2d7a39.json b/872e1ad0-ef48-43f8-afc3-f6028d2d7a39.json new file mode 100644 index 0000000000000000000000000000000000000000..2303c40cd09a3548324d328d468de4c904eeb860 --- /dev/null +++ b/872e1ad0-ef48-43f8-afc3-f6028d2d7a39.json @@ -0,0 +1,59 @@ +{ + "id": "872e1ad0-ef48-43f8-afc3-f6028d2d7a39", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "16125929", + "text": "A systematic meta-analysis of observational studies of melanoma and family history, actinic damage and phenotypic factors was conducted as part of a comprehensive meta-analysis of all major risk factors for melanoma. Following a systematic literature search, relative risks were extracted from 60 studies published before September 2002. Fixed and random effects models were used to obtain pooled estimates for family history (RR = 1.74, 1.41-2.14), skin type (I vs. IV: RR = 2.09, 1.67-2.58), high density of freckles (RR = 2.10, 1.80-2.45), skin colour (Fair vs. Dark: RR = 2.06, 1.68-2.52), eye colour (Blue vs. Dark: RR = 1.47, 1.28-1.69) and hair colour (Red vs. Dark: RR = 3.64, 2.56-5.37), pre-malignant and skin cancer lesions (RR = 4.28, 2.80-6.55) and actinic damage indicators (RR = 2.02, 1.24-3.29). Sub-group analysis and meta-regression were carried out to explore sources of between-study variation and bias. Sensitivity analyses investigated reliability of results and publication bias. Latitude and adjustment for phenotype were two study characteristics that significantly influenced the estimates." + }, + "questions": [ + { + "id": "210117b1-63b3-4a13-ac82-0587280aa03b", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 411, + "text": "family history" + }, + { + "answer_start": 450, + "text": "skin type" + }, + { + "answer_start": 494, + "text": "high density of freckles" + }, + { + "answer_start": 543, + "text": "skin colour" + }, + { + "answer_start": 594, + "text": "eye colour" + }, + { + "answer_start": 697, + "text": "pre-malignant and skin cancer lesions" + }, + { + "answer_start": 762, + "text": "actinic damage indicators" + } + ] + } + ] +} \ No newline at end of file diff --git a/87867fbe-476d-4228-b1d2-a83751e6d332.json b/87867fbe-476d-4228-b1d2-a83751e6d332.json new file mode 100644 index 0000000000000000000000000000000000000000..a7f4d96c1dc66f435543822b41503aef18d4b2e3 --- /dev/null +++ b/87867fbe-476d-4228-b1d2-a83751e6d332.json @@ -0,0 +1,43 @@ +{ + "id": "87867fbe-476d-4228-b1d2-a83751e6d332", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "30790475", + "text": "OBJECTIVE:\nTo investigate the impact and timing of smoking cessation on developing rheumatoid arthritis (RA) and serologic phenotypes.\n\nMETHODS:\nWe investigated smoking cessation and RA risk in the Nurses' Health Study (NHS) (1976-2014) and the NHS II (1989-2015). Smoking exposures and covariates were obtained by biennial questionnaires. Self-reported RA was confirmed by medical record review for American College of Rheumatology/European League Against Rheumatism criteria. Cox regression was used to estimate hazard ratios (HRs) and 95% confidence intervals (95% CIs) for RA serologic phenotypes (all, seropositive, seronegative) according to smoking status, intensity, pack-years, and years since cessation.\n\nRESULTS:\nAmong 230,732 women, we identified 1,528 incident cases of RA (63.4% of which were seropositive) during 6,037,151 person-years of follow-up. Compared with never smoking, current smoking increased the risk of all RA (multivariable HR 1.47, 95% CI 1.27-1.72) and seropositive RA (HR 1.67, 95% CI 1.38-2.01) but not seronegative RA (HR 1.20, 95% CI 0.93-1.55). An increasing number of smoking pack-years was associated with an increased trend for the risk of all RA (P \u003c 0.0001) and seropositive RA (P \u003c 0.0001). With increasing duration of smoking cessation, a decreased trend for the risk of all RA was observed (P = 0.009) and seropositive RA (P = 0.002). Compared to recent quitters (\u003c5 years), those who quit ≥30 years ago had an HR of 0.63 (95% CI 0.44-0.90) for seropositive RA. However, a modestly increased risk of RA was still detectable 30 years after quitting smoking (for all RA, HR 1.25 [95% CI 1.02-1.53]; for seropositive RA, HR 1.30 [95% CI 1.01-1.68]; reference, never smoking).\n\nCONCLUSION:\nThese results confirm that smoking is a strong risk factor for developing seropositive RA and demonstrate for the first time that a behavior change of sustained smoking cessation could delay or even prevent seropositive RA." + }, + "questions": [ + { + "id": "13895321-c0ac-43b5-8816-b4a813fe3c54", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 894, + "text": "current smoking" + }, + { + "answer_start": 1082, + "text": "An increasing number of smoking pack-years" + }, + { + "answer_start": 1758, + "text": "smoking" + } + ] + } + ] +} \ No newline at end of file diff --git a/878b324a-8370-4d69-866d-03f5c9e88ded.json b/878b324a-8370-4d69-866d-03f5c9e88ded.json new file mode 100644 index 0000000000000000000000000000000000000000..a259b6f7e875121fc2ea39e35a88d03058537af0 --- /dev/null +++ b/878b324a-8370-4d69-866d-03f5c9e88ded.json @@ -0,0 +1,42 @@ +{ + "id": "878b324a-8370-4d69-866d-03f5c9e88ded", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "23052052", + "text": "AIMS/HYPOTHESIS:\nAlthough a family history of type 2 diabetes is a strong risk factor for the disease, the factors mediating this excess risk are poorly understood. In the InterAct case-cohort study, we investigated the association between a family history of diabetes among different family members and the incidence of type 2 diabetes, as well as the extent to which genetic, anthropometric and lifestyle risk factors mediated this association.\n\nMETHODS:\nA total of 13,869 individuals (including 6,168 incident cases of type 2 diabetes) had family history data available, and 6,887 individuals had complete data on all mediators. Country-specific Prentice-weighted Cox models were fitted within country, and HRs were combined using random effects meta-analysis. Lifestyle and anthropometric measurements were performed at baseline, and a genetic risk score comprising 35 polymorphisms associated with type 2 diabetes was created.\n\nRESULTS:\nA family history of type 2 diabetes was associated with a higher incidence of the condition (HR 2.72, 95% CI 2.48, 2.99). Adjustment for established risk factors including BMI and waist circumference only modestly attenuated this association (HR 2.44, 95% CI 2.03, 2.95); the genetic score alone explained only 2% of the family history-associated risk of type 2 diabetes. The greatest risk of type 2 diabetes was observed in those with a biparental history of type 2 diabetes (HR 5.14, 95% CI 3.74, 7.07) and those whose parents had been diagnosed with diabetes at a younger age (\u003c50 years; HR 4.69, 95% CI 3.35, 6.58), an effect largely confined to a maternal family history.\n\nCONCLUSIONS/INTERPRETATION:\nProminent lifestyle, anthropometric and genetic risk factors explained only a marginal proportion of the excess risk associated with family history, highlighting the fact that family history remains a strong, independent and easily assessed risk factor for type 2 diabetes. Discovering factors that will explain the association of family history with type 2 diabetes risk will provide important insight into the aetiology of type 2 diabetes." + }, + "questions": [ + { + "id": "cc5debbb-1042-4735-b203-e9b068b21012", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 942, + "text": "A family history of type 2 diabetes" + }, + { + "answer_start": 1367, + "text": "those with a biparental history of type 2 diabetes" + }, + { + "answer_start": 1451, + "text": "those whose parents had been diagnosed with diabetes at a younger age (\u003c50 years" + } + ] + } + ] +} \ No newline at end of file diff --git a/87c08b7c-7ca5-4364-9e47-44b2740ab358.json b/87c08b7c-7ca5-4364-9e47-44b2740ab358.json new file mode 100644 index 0000000000000000000000000000000000000000..a34fce7cc9159fca3abe887d9a04177e0d66aff1 --- /dev/null +++ b/87c08b7c-7ca5-4364-9e47-44b2740ab358.json @@ -0,0 +1,45 @@ +{ + "id": "87c08b7c-7ca5-4364-9e47-44b2740ab358", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "9634428", + "text": "BACKGROUND:\nThe risk for colorectal cancer among family members of patients with colorectal cancer is well established, but the risk among family members of patients with colorectal adenomas is less well established.\n\nOBJECTIVE:\nTo examine the risk for colorectal cancer among first-degree relatives of patients with adenoma compared with that among first-degree relatives of controls without adenoma.\n\nDESIGN:\nReconstructed cohort study.\n\nSETTING:\nThree university-based colonoscopy practices in New York City.\n\nPATIENTS:\n1554 first-degree relatives of 244 patients with newly diagnosed adenomas and 2173 first-degree relatives of 362 endoscopically normal controls.\n\nMEASUREMENTS:\nStructured interviews were used to obtain family history. Adjusted relative risks (RR) were estimated from Cox proportional hazards regression models.\n\nRESULTS:\nThe risk for colorectal cancer was elevated (RR, 1.74 [95% CI, 1.24 to 2.45]) among first-degree relatives of patients with newly diagnosed adenomas compared with the risk among first-degree relatives of controls. This increased risk was the same for parents (RR, 1.58 [CI, 1.07 to 2.34]) and siblings (RR, 1.58 [CI, 0.81 to 3.08]). First-degree relatives of patients with adenomas did not have elevated risk for other cancers. The risk for colorectal cancer among family members increased with decreasing age at diagnosis of adenoma in probands. Among first-degree relatives of patients who were 50 years of age or younger when the adenoma was diagnosed, the risk was more than four times greater (RR, 4.36 [CI, 2.24 to 8.51]) than that among first-degree relatives of patients who were older than 60 years of age when the adenoma was diagnosed.\n\nCONCLUSIONS:\nFirst-degree relatives of patients with newly diagnosed adenomas, particularly of patients who are 50 years of age or younger at diagnosis, are at increased risk for colorectal cancer and should undergo screening similar to that recommended for relatives of patients with colorectal cancer." + }, + "questions": [ + { + "id": "4925be6c-cfdb-45f5-9167-b90f6315679a", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 928, + "text": "first-degree relatives of patients with newly diagnosed adenomas" + }, + { + "answer_start": 1397, + "text": "first-degree relatives of patients who were 50 years of age or younger when the adenoma was diagnosed" + }, + { + "answer_start": 1705, + "text": "First-degree relatives of patients with newly diagnosed adenomas" + } + ] + } + ] +} \ No newline at end of file diff --git a/87d129a1-021e-4cb0-82c2-91d71bd83ad6.json b/87d129a1-021e-4cb0-82c2-91d71bd83ad6.json new file mode 100644 index 0000000000000000000000000000000000000000..45caa41f272dbb89afd92ea9ea8e5d6bfcf6b8c8 --- /dev/null +++ b/87d129a1-021e-4cb0-82c2-91d71bd83ad6.json @@ -0,0 +1,45 @@ +{ + "id": "87d129a1-021e-4cb0-82c2-91d71bd83ad6", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "16288121", + "text": "BACKGROUND:\nDiabetes has been associated with an increased risk of colorectal cancer in most, but not all, studies. Findings have also been inconclusive with regard to sex and subsite in the colorectum. To resolve these inconsistencies, we conducted a meta-analysis of published data on the association between diabetes and the incidence and mortality of colorectal cancer.\n\nMETHODS:\nWe identified studies by a literature search of Medline from January 1, 1966, through July 31, 2005, and by searching the reference lists of pertinent articles. Summary relative risks (RRs) with 95% confidence intervals (CIs) were calculated with a random-effects model. All statistical tests were two-sided.\n\nRESULTS:\nAnalysis of 15 studies (six case-control and nine cohort studies), including 2 593 935 participants, found that diabetes was associated with an increased risk of colorectal cancer, compared with no diabetes (summary RR of colorectal cancer incidence = 1.30, 95% CI = 1.20 to 1.40), without heterogeneity between studies (P(heterogeneity) = .21). These results were consistent between case-control and cohort studies and between studies conducted in the United States and in Europe. The association between diabetes and colorectal cancer incidence did not differ statistically significantly by sex (summary RR among women = 1.33, 95% CI = 1.23 to 1.44; summary RR among men = 1.29, 95% CI = 1.15 to 1.44; P(heterogeneity) = .26) or by cancer subsite (summary RR for colon = 1.43, 95% CI = 1.28 to 1.60; summary RR for rectum = 1.33, 95% CI = 1.14 to 1.54; P(heterogeneity) = .42). Diabetes was positively associated with colorectal cancer mortality (summary RR = 1.26, 95% CI = 1.05 to 1.50), but there was evidence for heterogeneity between studies (P(heterogeneity) = .04).\n\nCONCLUSIONS:\nOur findings strongly support a relationship between diabetes and increased risk of colon and rectal cancer in both women and men." + }, + "questions": [ + { + "id": "228df03e-142e-41f5-93c1-824228512b25", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 815, + "text": "diabetes" + }, + { + "answer_start": 1583, + "text": "Diabetes" + }, + { + "answer_start": 1845, + "text": "diabetes" + } + ] + } + ] +} \ No newline at end of file diff --git a/882da8fa-eec4-4fd0-a96f-54a596697fd2.json b/882da8fa-eec4-4fd0-a96f-54a596697fd2.json new file mode 100644 index 0000000000000000000000000000000000000000..43cecc044f130d7f643c3c659002daac27a41ddf --- /dev/null +++ b/882da8fa-eec4-4fd0-a96f-54a596697fd2.json @@ -0,0 +1,35 @@ +{ + "id": "882da8fa-eec4-4fd0-a96f-54a596697fd2", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "19035450", + "text": "A \"divergent pathway\" model for the development of cutaneous melanoma has been proposed. The model hypothesizes that melanomas occurring in people with a low tendency to develop nevi will, on average, arise more commonly on habitually sun-exposed body sites such as the head and neck. In contrast, people with an inherent propensity to develop nevi will tend to develop melanomas most often on body sites with large melanocyte populations, such as on the back. We conducted a collaborative analysis to test this hypothesis using the original data from 10 case-control studies of melanoma in women (2,406 cases and 3,119 controls), with assessment of the potential confounding effects of socioeconomic, pigmentary and sun exposure-related factors. Higher nevus count on the arm was associated specifically with an increased risk of melanoma of the trunk (p for trend = 0.0004) and limbs (both upper and lower limb p for trends = 0.01), but not of the head and neck (p for trend = 0.25). The pooled odds ratios for the highest quartile of nonzero nevus count versus none were 4.6 (95% confidence interval (CI) 2.7-7.6) for melanoma of the trunk, 2.0 (95% CI 0.9-4.5) for the head and neck, 4.2 (95% CI 2.3-7.5) for the upper limbs and 3.4 (95% CI 1.5-7.9) for the lower limbs. Aggregate data from these studies suggest that high nevus counts are strongly associated with melanoma of the trunk but less so if at all of the head and neck. This finding supports different etiologic pathways of melanoma development by anatomic site." + }, + "questions": [ + { + "id": "f5d24b98-45e8-4e08-a1e5-800cb761b138", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 1322, + "text": "high nevus counts" + } + ] + } + ] +} \ No newline at end of file diff --git a/88adc678-c233-460e-ac31-d62586a922c6.json b/88adc678-c233-460e-ac31-d62586a922c6.json new file mode 100644 index 0000000000000000000000000000000000000000..1921c554217a4814000349b743e461a5e1b5f7a6 --- /dev/null +++ b/88adc678-c233-460e-ac31-d62586a922c6.json @@ -0,0 +1,34 @@ +{ + "id": "88adc678-c233-460e-ac31-d62586a922c6", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "22623718", + "text": "BACKGROUND:\nFamily history of coronary heart disease (CHD) has been well studied as an independent risk factor for CHD events in the short term (\u003c10 years). However, data are sparse on the association between family history and risk for CHD across long-term follow-up.\n\nMETHODS AND RESULTS:\nWe included 49 255 men from the Cooper Center Longitudinal Study. Premature family history of CHD was defined as the presence of angina, myocardial infarction, angioplasty, or bypass surgery in a relative \u003c50 years of age. Cause-specific mortality was obtained from the National Death Index. The association between premature family history and cardiovascular disease (CVD) or CHD death was compared across 3 unique follow-up periods (0-10, \u003e10-20, and \u003e20 years). Lifetime risk was estimated by use of a modified survival analytic technique adjusted for competing risk with non-CVD death as the competing event. After 811 708 person-years of follow-up, there were 919 CHD deaths and 1456 CVD deaths. After adjustment for traditional risk factors, premature family history was associated with CHD mortality \u003e10 to 20 years (1.59; 95% confidence interval, 1.14-2.22) and \u003e20 years (1.43; 95% confidence interval, 1.05-1.95) with wider confidence intervals at 0 to 10 years (1.32; 95% confidence interval, 0.76-2.31). Similar findings were observed for CVD mortality. Compared with men without a family history of coronary artery disease, premature family history was associated with an ≈50% higher lifetime risk for both CHD and CVD mortality (13.7% versus 8.9% and 21% versus 14.1%, respectively).\n\nCONCLUSION:\nPremature family history was associated with a persistent increase in both CHD and CVD mortality risk across long-term follow-up, resulting in significantly higher lifetime risk estimates." + }, + "questions": [ + { + "id": "42d2362b-7d84-4c4f-9556-c791fc1f2bc2", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1602, + "text": "Premature family history" + } + ] + } + ] +} \ No newline at end of file diff --git a/88cb894b-5128-4cbc-b648-63e5a51c1a50.json b/88cb894b-5128-4cbc-b648-63e5a51c1a50.json new file mode 100644 index 0000000000000000000000000000000000000000..bc591f47b8ddf45b98fb4d2e9e375ce82ffe3d11 --- /dev/null +++ b/88cb894b-5128-4cbc-b648-63e5a51c1a50.json @@ -0,0 +1,42 @@ +{ + "id": "88cb894b-5128-4cbc-b648-63e5a51c1a50", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "18591398", + "text": "OBJECTIVE:\nOur objective was to perform a quantitative review of prospective studies examining the association between the metabolic syndrome and incident diabetes.\n\nRESEARCH DESIGN AND METHODS:\nUsing the title terms \"diabetes\" and \"metabolic syndrome\" in PubMed, we searched for articles published since 1998.\n\nRESULTS:\nBased on the results from 16 cohorts, we performed a meta-analysis of estimates of relative risk (RR) and incident diabetes. The random-effects summary RRs were 5.17 (95% CI 3.99-6.69) for the 1999 World Health Organization definition (ten cohorts); 4.45 (2.41-8.22) for the 1999 European Group for the Study of Insulin Resistance definition (four cohorts); 3.53 (2.84-4.39) for the 2001 National Cholesterol Education Program definition (thirteen cohorts); 5.12 (3.26-8.05) for the 2005 American Heart Association/National Heart, Lung, and Blood Institute definition (five cohorts); and 4.42 (3.30-5.92) for the 2005 International Diabetes Federation definition (nine cohorts). The fixed-effects summary RR for the 2004 National Heart, Lung, and Blood Institute/American Heart Association definition was 5.16 (4.43-6.00) (six cohorts). Higher number of abnormal components was strongly related to incident diabetes. Compared with participants without an abnormality, estimates of RR for those with four or more abnormal components ranged from 10.88 to 24.4. Limited evidence suggests fasting glucose alone may be as good as metabolic syndrome for diabetes prediction.\n\nCONCLUSIONS:\nThe metabolic syndrome, however defined, has a stronger association with incident diabetes than that previously demonstrated for coronary heart disease. Its clinical value for diabetes prediction remains uncertain." + }, + "questions": [ + { + "id": "1e7fbcb4-e1e7-4468-89ef-2dc6448a49b7", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1508, + "text": "metabolic syndrome" + }, + { + "answer_start": 1158, + "text": "Higher number of abnormal components" + }, + { + "answer_start": 1320, + "text": "four or more abnormal components" + } + ] + } + ] +} \ No newline at end of file diff --git a/893aff4c-e952-4695-bc13-26025d95e9f2.json b/893aff4c-e952-4695-bc13-26025d95e9f2.json new file mode 100644 index 0000000000000000000000000000000000000000..11648cb71bac3af5a585f40e9d13f1a8a32e263c --- /dev/null +++ b/893aff4c-e952-4695-bc13-26025d95e9f2.json @@ -0,0 +1,38 @@ +{ + "id": "893aff4c-e952-4695-bc13-26025d95e9f2", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "18505952", + "text": "CONTEXT:\nContinuing advances in genotyping technologies and the inclusion of DNA collection in observational studies have resulted in an increasing number of genetic association studies.\n\nOBJECTIVE:\nTo evaluate the overall progress and contribution of candidate gene association studies to current understanding of the genetic susceptibility to cancer.\n\nDATA SOURCES:\nWe systematically examined the results of meta-analyses and pooled analyses for genetic polymorphisms and cancer risk published through March 2008.\n\nSTUDY SELECTION:\nWe identified 161 meta-analyses and pooled analyses, encompassing 18 cancer sites and 99 genes. Analyses had to meet the following criteria: include at least 500 cases, have cancer risk as outcome, not be focused on HLA antigen genetic markers, and be published in English.\n\nDATA EXTRACTION:\nInformation on cancer site, gene name, variant, point estimate and 95% confidence interval (CI), allelic frequency, number of studies and cases, tests of study heterogeneity, and publication bias were extracted by 1 investigator and reviewed by other investigators.\n\nRESULTS:\nThese 161 analyses evaluated 344 gene-variant cancer associations and included on average 7.3 studies and 3551 cases (range, 508-19 729 cases) per investigated association. The summary odds ratio (OR) for 98 (28%) statistically significant associations (P value \u003c.05) were further evaluated by estimating the false-positive report probability (FPRP) at a given prior probability and statistical power. At a prior probability level of 0.001 and statistical power to detect an OR of 1.5, 13 gene-variant cancer associations remained noteworthy (FPRP \u003c0.2). Assuming a very low prior probability of 0.000001, similar to a probability assumed for a randomly selected single-nucleotide polymorphism in a genome-wide association study, and statistical power to detect an OR of 1.5, 4 associations were considered noteworthy as denoted by an FPRP value \u003c0.2: GSTM1 null and bladder cancer (OR, 1.5; 95% CI, 1.3-1.6; P = 1.9 x 10(-14)), NAT2 slow acetylator and bladder cancer (OR, 1.46; 95% CI, 1.26-1.68; P = 2.5 x 10(-7)), MTHFR C677T and gastric cancer (OR, 1.52; 95% CI, 1.31-1.77; P = 4.9 x 10(-8)), and GSTM1 null and acute leukemia (OR, 1.20; 95% CI, 1.14-1.25; P = 8.6 x 10(-15)). When the OR used to determine statistical power was lowered to 1.2, 2 of the 4 noteworthy associations remained so: GSTM1 null with bladder cancer and acute leukemia.\n\nCONCLUSION:\nIn this review of candidate gene association studies, nearly one-third of gene-variant cancer associations were statistically significant, with variants in genes encoding for metabolizing enzymes among the most consistent and highly significant associations." + }, + "questions": [ + { + "id": "375ed932-6baf-45e2-8220-8a524ced40c4", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 2031, + "text": "NAT2 slow acetylator" + }, + { + "answer_start": 1954, + "text": "GSTM1 null" + } + ] + } + ] +} \ No newline at end of file diff --git a/898c402f-0c10-42f3-848b-998ef8c64d00.json b/898c402f-0c10-42f3-848b-998ef8c64d00.json new file mode 100644 index 0000000000000000000000000000000000000000..65731a1279ee0e5c0e1f3114b5438faac63899bc --- /dev/null +++ b/898c402f-0c10-42f3-848b-998ef8c64d00.json @@ -0,0 +1,46 @@ +{ + "id": "898c402f-0c10-42f3-848b-998ef8c64d00", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "15117811", + "text": "Epidemiological studies have shown an association between low folate intake and an increased cancer risk. Major genes involved in folate metabolism include methylene-tetrahydrofolate reductase (MTHFR) and methionine synthase (MS). We investigated joint effects of polymorphisms of the MTHFR (677 C--\u003eT, 1298A--\u003eC) and MS genes (2756 A--\u003eG), dietary folate intake and cigarette smoking on the risk of bladder cancer in a case-control study. The study population consisted of 457 bladder cancer patients and 457 healthy controls, matched to the cases in terms of age, gender and ethnicity. Genotype data were analyzed in a subset of 410 Caucasian cases and 410 controls. Compared with individuals carrying the MTHFR 677 wild-type (CC) and reporting a high folate intake, those carrying the variant genotype (CT or TT) and reporting a low folate intake were at a significantly 3.51-fold increased risk of bladder cancer (95% CI: 1.59-6.52). In contrast, individuals carrying a variant genotype and reporting a high folate intake were at only a 1.39-fold increased risk (95% CI: 0.71-2.70), and those carrying the wild-type and reporting a low folate intake were at only 1.56-fold increased risk (95% CI: 0.82-2.97). The interaction between genetic polymorphisms and folate intake was significant on the multiplicative scale (P = 0.01). When analyzed in the context of smoking status, compared with never smokers with the MTHFR 677 wild-type, the risk increased to 6.56-fold (95% CI: 3.28-13.12) in current smokers carrying the variant genotype. Analyses of the MTHFR 1298, MS 2756 genes revealed similar results. In addition, age at cancer onset in former smokers increased as the proportion of the heteromorphic haplotype in the individual increased (P = 0.005). Our results strongly suggest that polymorphisms of the MTHFR and MS genes act together with low folate intake and smoking to increase bladder cancer risk. These results have important implications for cancer prevention in susceptible populations." + }, + "questions": [ + { + "id": "0eb61c36-73d1-40df-b89a-281e4eff02fe", + "text": "What are the risk factors of Bladder Cancer?", + "answers": [ + { + "answer_start": 1795, + "text": "polymorphisms of the MTHFR and MS genes" + }, + { + "answer_start": 1853, + "text": "low folate intake and smoking" + }, + { + "answer_start": 775, + "text": "carrying the variant genotype (CT or TT) and reporting a low folate intake" + }, + { + "answer_start": 264, + "text": "polymorphisms of the MTHFR (677 C--\u003eT, 1298A--\u003eC)" + } + ] + } + ] +} \ No newline at end of file diff --git a/8995b030-ad36-4582-990d-7cb1747850a6.json b/8995b030-ad36-4582-990d-7cb1747850a6.json new file mode 100644 index 0000000000000000000000000000000000000000..84c2db2091f753f18994c29acddebe867ea40d69 --- /dev/null +++ b/8995b030-ad36-4582-990d-7cb1747850a6.json @@ -0,0 +1,39 @@ +{ + "id": "8995b030-ad36-4582-990d-7cb1747850a6", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "8664138", + "text": "The atypical mole syndrome (AMS) phenotype, characterised by a large number of common naevi as well as atypical naevi, has been described in families with a genetic susceptibility to melanoma. However, the importance of this phenotype for melanoma in the general population has not been conclusively determined. This study was designed to examine the types and distribution of naevi as well as the prevalence of the AMS phenotype in melanoma patients in England compared with controls. A total of 426 cutaneous melanoma cases (61% of all incident cases) aged 16-75 years were recruited between 1989 and 1993 from the north-east Thames region of the UK and 416 controls from the same age group were recruited over the same period and from the same region. Each subject answered a questionnaire covering demographic details, sun exposure history and other risk factors and underwent a skin examination with total body naevus count performed by a dermatologist. The AMS phenotype was defined using a scoring system. Atypical naevi gave the highest relative risk for cutaneous melanoma, with an odds ratio (OR) of 28.7 (P \u003c 0.0001) for four or more atypical naevi compared with none. Many common naevi were also an important risk factor: the OR for 100 or more naevi 2 mm or above in diameter compared with 0-4 naevi was 7.7 (P \u003c 0.0001). Melanoma was also associated with naevi on sun-exposed sites but also with naevi on non-sun-exposed sites such as the dorsum of the feet, buttocks and anterior scalp. Sixteen per cent of the cases had the AMS phenotype compared with 2% of the controls (OR 10.4, P \u003c 0.0001). The AMS phenotype was more common in males than females (P = 0.008). The odds ratio for the presence of the AMS phenotype was dependent on age, with an odds ratio of 16.1 (95% CI 4.6-57.5) for the presence of the AMS phenotype if aged less than 40 compared with an odds ratio of 6.9 (95% CI 2.9-16.6) if aged 40 or more. The AMS phenotype was strongly predictive of an increased risk of melanoma outside the familial context." + }, + "questions": [ + { + "id": "54702765-33ba-4975-8b0a-559e53b9ebac", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 1935, + "text": "AMS phenotype" + }, + { + "answer_start": 4, + "text": "atypical mole syndrome (AMS) phenotype" + } + ] + } + ] +} \ No newline at end of file diff --git a/8a438d0e-348d-4444-8ab1-a1a4ecc60d8c.json b/8a438d0e-348d-4444-8ab1-a1a4ecc60d8c.json new file mode 100644 index 0000000000000000000000000000000000000000..4bb87b1424abdfc1e3948905d1f37b153af90553 --- /dev/null +++ b/8a438d0e-348d-4444-8ab1-a1a4ecc60d8c.json @@ -0,0 +1,45 @@ +{ + "id": "8a438d0e-348d-4444-8ab1-a1a4ecc60d8c", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "8531963", + "text": "BACKGROUND:\nThe adenoma-adenocarcinoma sequence in colorectal cancer suggests an increased risk of colorectal cancer in the families of patients with adenomatous polyps.\n\nMETHODS:\nA random sample of participants in the National Polyp Study who had newly diagnosed adenomatous polyps were interviewed for information on the history of colorectal cancer in their parents and siblings. The risk of colorectal cancer in family members was analyzed according to the characteristics of the patients with adenomas and in comparison with a sample of patients' spouses, who served as controls.\n\nRESULTS:\nAmong the patients with adenomas, 1199 provided information on whether they had a family history of colorectal cancer. After the exclusion of families for which information was incomplete and of 48 patients who had been referred for colonoscopy solely because they had a family history of colorectal cancer, there were 1031 patients with adenomas, 1865 parents, 2381 siblings, and 1411 spouse controls. The relative risk of colorectal cancer, adjusted for the year of birth and sex, was 1.78 for the parents and siblings of the patients with adenomas as compared with the spouse controls (95 percent confidence interval, 1.18 to 2.67). The relative risk for siblings of patients in whom adenomas were diagnosed before 60 years of age was 2.59 (95 percent confidence interval, 1.46 to 4.58) as compared with the siblings of patients who were 60 or older at the time of diagnosis and after adjustment for the sibling's year of birth and sex and a parental history of colorectal cancer. The risk increased with decreasing age at the time of the diagnosis of adenoma (P for trend \u003c 0.001). The relative risk for the siblings of patients who had a parent with colorectal cancer, as compared with those who had no parent with cancer, was 3.25 (95 percent confidence interval, 1.92 to 5.52), after adjustment for the sibling's year of birth and sex and the patient's age at diagnosis.\n\nCONCLUSIONS:\nSiblings and parents of patients with adenomatous polyps are at increased risk for colorectal cancer, particularly when the adenoma is diagnosed before the age of 60 or--in the case of siblings--when a parent has had colorectal cancer." + }, + "questions": [ + { + "id": "6beef6ed-5b01-4ab7-a92b-505a866341ef", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1253, + "text": "siblings of patients in whom adenomas were diagnosed before 60 years of age" + }, + { + "answer_start": 1707, + "text": "siblings of patients who had a parent with colorectal cancer" + }, + { + "answer_start": 1987, + "text": "Siblings and parents of patients with adenomatous polyps" + } + ] + } + ] +} \ No newline at end of file diff --git a/8ac94ed8-595c-4879-986c-83c4c0cfa2fc.json b/8ac94ed8-595c-4879-986c-83c4c0cfa2fc.json new file mode 100644 index 0000000000000000000000000000000000000000..12caa66ad36a29d325ea07373bcf29180b2be81f --- /dev/null +++ b/8ac94ed8-595c-4879-986c-83c4c0cfa2fc.json @@ -0,0 +1,45 @@ +{ + "id": "8ac94ed8-595c-4879-986c-83c4c0cfa2fc", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "21960713", + "text": "BACKGROUND:\nStreptococcus bovis has long been associated with colorectal cancer (CRC). However, not all genospecies are as closely related to CRC. With this systematic review, we aim to increase the awareness of the association between S. bovis biotype I (Streptococcus gallolyticus) and CRC and urge for uniform molecular microbiological classification.\n\nMETHODS:\nIn January 2011, the PubMed database was searched for all studies that investigated the association between S. bovis, infective endocarditis (IE), and CRC. A total of 191 studies were screened for eligibility and yielded 52 case reports and 31 case series, of which 11 were used for meta-analysis on the association between S. bovis biotype, IE, and adenomas/carcinomas (CRC).\n\nRESULTS:\nAmong the S. bovis-infected patients who underwent colonic evaluation, the median percentage of patients who had concomitant adenomas/carcinomas was 60% (interquartile range, 22%), which largely exceeds the disease rate reported in the general asymptomatic population. Meta-analysis showed that patients with S. bovis biotype I infection had a strongly increased risk of having CRC (pooled odds ratio [OR], 7.26; 95% confidence interval [CI], 3.94-13.36) and IE (pooled OR, 16.61; 95% CI, 8.85-31.16), compared with S. bovis biotype II-infected patients. Notably, CRC occurred more often among patients with S. bovis IE than among patients with S. bovis infection at other sites (pooled OR, 3.72; 95% CI, 2.03-6.81).\n\nCONCLUSIONS:\nOur meta-analysis clearly indicates that S. bovis should no longer be regarded as a single species in clinical practice, because S. gallolyticus (S. bovis biotype I) infection, in particular, has an unambiguous association with CRC." + }, + "questions": [ + { + "id": "b2529b79-aef5-49a4-b3e6-17a84e5dbb65", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1047, + "text": "patients with S. bovis biotype I infection" + }, + { + "answer_start": 1346, + "text": "patients with S. bovis IE" + }, + { + "answer_start": 1612, + "text": "S. gallolyticus (S. bovis biotype I) infection" + } + ] + } + ] +} \ No newline at end of file diff --git a/8affd63d-00c8-46a8-8f33-9759e8f59408.json b/8affd63d-00c8-46a8-8f33-9759e8f59408.json new file mode 100644 index 0000000000000000000000000000000000000000..387dfb3b5f0b60a330ab2d9e1941602048b63643 --- /dev/null +++ b/8affd63d-00c8-46a8-8f33-9759e8f59408.json @@ -0,0 +1,47 @@ +{ + "id": "8affd63d-00c8-46a8-8f33-9759e8f59408", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "9714052", + "text": "Epidemiological data strongly implicate sunlight as the principal environmental cause of melanoma; however, critical molecular targets for ultraviolet (UV)-induced melanoma remain to be identified. The p53 tumor suppressor gene is one possible target, being abnormally expressed in 20-40% of primary melanomas. We undertook a population-based molecular epidemiological study with the aim of determining the environmental and phenotypic factors associated with p53-positive and p53-negative melanomas. One hundred fifty cases of melanoma were randomly ascertained from the Queensland Cancer Registry and matched to 150 electoral roll controls. Data on environmental and phenotypic exposures were collected through interviews and physical examination of all participants. Sections of tumor tissue were obtained from 134 (89%) cases and stained with the anti-p53 DO-7 monoclonal antibody (MAb) following microwave antigen retrieval. Of 121 useable sections, 22 tumors (18%) had more than 1% cells with positive staining consistent with abnormalities in p53 expression. Strongest predictors of p53-positive melanoma were inability to tan [odds ratio (OR) 6.8], history of non-melanoma skin cancer (OR 3.2) and site of melanoma: head/neck (OR 2.2) and lower limbs (OR 2.3). In contrast, factors such as nevus density and freckling propensity were strongly associated only with p53-immunonegative melanoma (OR 8.6 for \u003e25 moles; OR 3.0 for heavy facial freckling). Overall, the determinants of p53-positive and p53-negative melanomas were independent and complementary, the former being associated with features of sun-sensitivity and chronic sun exposure, the latter with phenotypic markers of melanocytic proliferation. Our findings are consistent with at least 2 independent pathways in the pathogenesis of melanoma, characterized by environmental induction and p53 overexpression on the one hand and pigment cell instability on the other." + }, + "questions": [ + { + "id": "5fdb7342-4227-49c8-94c4-41c72d25c353", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 1859, + "text": "p53 overexpression" + }, + { + "answer_start": 1117, + "text": "inability to tan" + }, + { + "answer_start": 1157, + "text": "history of non-melanoma skin cancer" + }, + { + "answer_start": 1298, + "text": "nevus density" + } + ] + } + ] +} \ No newline at end of file diff --git a/8b8a4294-c457-4bc5-abe5-ef8b754ae0a2.json b/8b8a4294-c457-4bc5-abe5-ef8b754ae0a2.json new file mode 100644 index 0000000000000000000000000000000000000000..b055f2f6bc7d3600ef3788d5e9eee3b8b17e83c0 --- /dev/null +++ b/8b8a4294-c457-4bc5-abe5-ef8b754ae0a2.json @@ -0,0 +1,54 @@ +{ + "id": "8b8a4294-c457-4bc5-abe5-ef8b754ae0a2", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "12420953", + "text": "OBJECTIVE:\nBody size is an important modifiable risk factor for breast cancer. Although obesity has generally been found to be associated with increased risk for postmenopausal breast cancer, there remain questions concerning the role of body fat distribution, lifetime weight history, and effects within specific subgroups of women.\n\nMETHODS:\nWe assessed the relationship of several anthropometric measures and risk of postmenopausal breast cancer in 85,917 women aged 50-79 at entry in the Women's Health Initiative Observational Study. Women were enrolled during 1993-1998 at 40 clinics in the US and 1030 developed invasive breast cancer by April 2000. Upon entry, trained clinical center staff measured each woman's height, weight, and waist and hip circumference.\n\nRESULTS:\nAnthropometric factors were not associated with breast cancer among women who had ever used hormone replacement therapy (HRT). Among HRT non-users, heavier women (baseline body mass index (BMI) \u003e31.1) had an elevated risk of postmenopausal breast cancer (relative risk (RR) = 2.52; 95% confidence interval (CI) = 1.62-3.93), compared to slimmer women (baseline BMI \u003c 22.6). The elevation in risk associated with increasing BMI appeared to be most pronounced among younger postmenopausal women. Change in BMI since age 18, maximum BMI, and weight were also associated with breast cancer in HRT non-users. While both waist and hip circumference were associated with breast cancer risk, their ratio, a measure of fat distribution, was not (RR = 1.33; 95% CI = 0.88-2.01).\n\nCONCLUSIONS:\nOur study confirms previously reported findings that generalized obesity is an important risk factor for postmenopausal breast cancer, but only among women who have never taken HRT. Lifetime weight gain is also a strong predictor of breast cancer. Waist to hip ratio, a measure of weight distribution, does not appear to be related to postmenopausal breast cancer risk." + }, + "questions": [ + { + "id": "38a21688-30a4-42c1-b058-d93e6ec5fddd", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 906, + "text": " Among HRT non-users, heavier women (baseline body mass index (BMI) \u003e31.1)" + }, + { + "answer_start": 1192, + "text": "increasing BMI" + }, + { + "answer_start": 1274, + "text": "Change in BMI since age 18" + }, + { + "answer_start": 1302, + "text": "maximum BMI" + }, + { + "answer_start": 1318, + "text": " weight" + }, + { + "answer_start": 1395, + "text": "waist and hip circumference" + } + ] + } + ] +} \ No newline at end of file diff --git a/8c0582a0-6b53-4733-93aa-bdc5536a5150.json b/8c0582a0-6b53-4733-93aa-bdc5536a5150.json new file mode 100644 index 0000000000000000000000000000000000000000..ed01a325256dccc406c1ad3cc359ecbe8eec72c8 --- /dev/null +++ b/8c0582a0-6b53-4733-93aa-bdc5536a5150.json @@ -0,0 +1,38 @@ +{ + "id": "8c0582a0-6b53-4733-93aa-bdc5536a5150", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "19240061", + "text": "OBJECTIVE:\nOur previous coeliac disease genome-wide association study (GWAS) implicated risk variants in the human leucocyte antigen (HLA) region and eight novel risk regions. To identify more coeliac disease loci, we selected 458 single nucleotide polymorphisms (SNPs) that showed more modest association in the GWAS for genotyping and analysis in four independent cohorts.\n\nDESIGN:\n458 SNPs were assayed in 1682 cases and 3258 controls from three populations (UK, Irish and Dutch). We combined the results with the original GWAS cohort (767 UK cases and 1422 controls); six SNPs showed association with p\u003c1 x 10(-04) and were then genotyped in an independent Italian coeliac cohort (538 cases and 593 controls).\n\nRESULTS:\nWe identified two novel coeliac disease risk regions: 6q23.3 (OLIG3-TNFAIP3) and 2p16.1 (REL), both of which reached genome-wide significance in the combined analysis of all 2987 cases and 5273 controls (rs2327832 p = 1.3 x 10(-08), and rs842647 p = 5.2 x 10(-07)). We investigated the expression of these genes in the RNA isolated from biopsies and from whole blood RNA. We did not observe any changes in gene expression, nor in the correlation of genotype with gene expression.\n\nCONCLUSIONS:\nBoth TNFAIP3 (A20, at the protein level) and REL are key mediators in the nuclear factor kappa B (NF-kappaB) inflammatory signalling pathway. For the first time, a role for primary heritable variation in this important biological pathway predisposing to coeliac disease has been identified. Currently, the HLA risk factors and the 10 established non-HLA risk factors explain approximately 40% of the heritability of coeliac disease." + }, + "questions": [ + { + "id": "01451e77-ddc2-4c87-a6fe-7447f20d5703", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 778, + "text": "6q23.3 (OLIG3-TNFAIP3)" + }, + { + "answer_start": 805, + "text": "2p16.1 (REL)" + } + ] + } + ] +} \ No newline at end of file diff --git a/8c238c42-2d1a-4cc3-9370-1de3bd3ce537.json b/8c238c42-2d1a-4cc3-9370-1de3bd3ce537.json new file mode 100644 index 0000000000000000000000000000000000000000..576c5b634638c384427e2a92d90fd7c253aa90ac --- /dev/null +++ b/8c238c42-2d1a-4cc3-9370-1de3bd3ce537.json @@ -0,0 +1,35 @@ +{ + "id": "8c238c42-2d1a-4cc3-9370-1de3bd3ce537", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "7804999", + "text": "BACKGROUND:\nThis study was designed to determine the risk of developing malignant melanoma (MM) in patients with a history of basal cell and/or squamous cell skin cancer (BCC/SCC) and to determine whether surveillance efforts can be directed toward these patients for the detection of early MMs.\n\nMETHODS:\nThe study cohort was followed by annual total cutaneous examination (TCE). Controls consisted of individuals from the United States population matched for age, sex, and length of follow-up. The anatomic locations of the study cohorts' newly diagnosed MMs were plotted on an anatomic chart. The setting was a private dermatology practice. Two hundred, ninety consecutive white patients with a history of BCC/SCC but with no personal or family history of MM were followed by annual TCEs. The main outcome measures were the relative risk of developing MM and their prognosis.\n\nRESULTS:\nTen of the 290 patients developed an MM within an average of 109 months of follow-up (range, 3-17 years). All MMs were less than 0.70 mm in Breslow thickness and 80% occurred on usually clothed cutaneous sites. The expected number of MMs in the control population was 0.59 (P = 0.006), resulting in a relative risk of 17.\n\nCONCLUSION:\nPatients with BCC/SCC skin cancer are at substantial increased risk for developing MM. Regular and life-long surveillance TCE is an inexpensive and effective method for detecting curable MMs in such patients." + }, + "questions": [ + { + "id": "cf342339-2a56-4068-aaeb-7e57d8c14d10", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 1224, + "text": "Patients with BCC/SCC skin cancer" + } + ] + } + ] +} \ No newline at end of file diff --git a/8c4cda6b-9b5a-437d-a68a-c76b1d3cd3bf.json b/8c4cda6b-9b5a-437d-a68a-c76b1d3cd3bf.json new file mode 100644 index 0000000000000000000000000000000000000000..6ff536addf19feb078959af67dcd83dc85cd4776 --- /dev/null +++ b/8c4cda6b-9b5a-437d-a68a-c76b1d3cd3bf.json @@ -0,0 +1,35 @@ +{ + "id": "8c4cda6b-9b5a-437d-a68a-c76b1d3cd3bf", + "disease": { + "id": "H00056", + "names": [ + "Alzheimer disease", + "Dementia due to Alzheimer disease" + ], + "dbLinks": { + "icd10": [ + "G30" + ], + "mesh": [ + "D000544" + ] + }, + "category": "Neurodegenerative disease" + }, + "article": { + "id": "9343467", + "text": "OBJECTIVE:\nTo examine more closely the association between apolipoprotein E (APOE) genotype and Alzheimer disease (AD) by age and sex in populations of various ethnic and racial denominations.\n\nDATA SOURCES:\nForty research teams contributed data on APOE genotype, sex, age at disease onset, and ethnic background for 5930 patients who met criteria for probable or definite AD and 8607 controls without dementia who were recruited from clinical, community, and brain bank sources.\n\nMAIN OUTCOME MEASURES:\nOdds ratios (ORs) and 95% confidence intervals (CIs) for AD, adjusted for age and study and stratified by major ethnic group (Caucasian, African American, Hispanic, and Japanese) and source, were computed for APOE genotypes epsilon2/epsilon2, epsilon2/epsilon3, epsilon2/epsilon4, epsilon3/epsilon4, and epsilon4/epsilon4 relative to the epsilon3/epsilon3 group. The influence of age and sex on the OR for each genotype was assessed using logistic regression procedures.\n\nRESULTS:\nAmong Caucasian subjects from clinic- or autopsy-based studies, the risk of AD was significantly increased for people with genotypes epsilon2/epsilon4 (OR=2.6, 95% CI=1.6-4.0), epsilon3/epsilon4 (OR=3.2, 95% CI=2.8-3.8), and epsilon4/epsilon4 (OR=14.9, 95% CI= 10.8-20.6); whereas, the ORs were decreased for people with genotypes epsilon2/epsilon2 (OR=0.6, 95% CI=0.2-2.0) and epsilon2/epsilon3 (OR=0.6, 95% CI=0.5-0.8). The APOE epsilon4-AD association was weaker among African Americans and Hispanics, but there was significant heterogeneity in ORs among studies of African Americans (P\u003c.03). The APOE epsilon4-AD association in Japanese subjects was stronger than in Caucasian subjects (epsilon3/epsilon4: OR=5.6, 95% CI=3.9-8.0; epsilon4/epsilon4: OR=33.1, 95% CI=13.6-80.5). The epsilon2/epsilon3 genotype appears equally protective across ethnic groups. We also found that among Caucasians, APOE genotype distributions are similar in groups of patients with AD whose diagnoses were determined clinically or by autopsy. In addition, we found that the APOE epsilon4 effect is evident at all ages between 40 and 90 years but diminishes after age 70 years and that the risk of AD associated with a given genotype varies with sex.\n\nCONCLUSIONS:\nThe APOE epsilon4 allele represents a major risk factor for AD in all ethnic groups studied, across all ages between 40 and 90 years, and in both men and women. The association between APOE epsilon4 and AD in African Americans requires clarification, and the attenuated effect of APOE epsilon4 in Hispanics should be investigated further." + }, + "questions": [ + { + "id": "6b0f0cc9-1a2f-4915-8cd7-6e1253dcf5c8", + "text": "What are the risk factors of Alzheimer disease?", + "answers": [ + { + "answer_start": 2236, + "text": "APOE epsilon4 allele" + } + ] + } + ] +} \ No newline at end of file diff --git a/8ca5ec6c-f3b4-4ab3-a3a1-df7df65bd6f8.json b/8ca5ec6c-f3b4-4ab3-a3a1-df7df65bd6f8.json new file mode 100644 index 0000000000000000000000000000000000000000..656e2eeee3b5f10bfac9cabcf724589d41e035ea --- /dev/null +++ b/8ca5ec6c-f3b4-4ab3-a3a1-df7df65bd6f8.json @@ -0,0 +1,39 @@ +{ + "id": "8ca5ec6c-f3b4-4ab3-a3a1-df7df65bd6f8", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "20231496", + "text": "OBJECTIVE:\nTo quantify the risk of subsequent primary cancers among patients with primary cutaneous malignant melanoma.\n\nDESIGN:\nPopulation-based registry study.\n\nSETTING:\nWe evaluated data from 9 cancer registries of the Surveillance, Epidemiology, and End Results program from 1973-2006.\n\nPARTICIPANTS:\nWe included 89 515 patients who survived at least 2 months after their initial melanoma diagnosis.\n\nRESULTS:\nOf the patients with melanoma, 10 857 (12.1%) developed 1 or more subsequent primary cancers. The overall risk of a subsequent primary cancer increased by 28% (observed to expected [O:E] ratio = 1.28). One quarter of the cancers were subsequent primary melanomas (O:E = 8.61). Women with head and neck melanoma and patients younger than 30 had markedly increased risks (O:E = 13.22 and 13.40, respectively) of developing a subsequent melanoma. Second melanomas were more likely to be thin than were the first of multiple primary melanomas (thickness at diagnosis \u003c1.00 mm, 77.9% vs 70.3%, respectively; P \u003c .001). Melanoma survivors had increased risk of developing several cancers; the most common cancers with elevated risks were breast, prostate, and non-Hodgkin lymphoma (O:E = 1.10, 1.15, and 1.25, respectively).\n\nCONCLUSIONS:\nMelanoma survivors have an approximately 9-fold increased risk of developing subsequent melanoma compared with the general population. The risk remains elevated more than 20 years after the initial melanoma diagnosis. This increased risk may be owing to behavioral factors, genetic susceptibility, or medical surveillance. Although the percentage of subsequent primary melanomas thicker than 1 mm is lower than for the first of multiple primary melanomas, it is still substantial. Melanoma survivors should remain under surveillance not only for recurrence but also for future primary melanomas and other cancers." + }, + "questions": [ + { + "id": "f64fc302-6334-48d1-b77f-39cb1f47b5d6", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 691, + "text": "Women with head and neck melanoma" + }, + { + "answer_start": 729, + "text": "patients younger than 30" + } + ] + } + ] +} \ No newline at end of file diff --git a/8d5dc422-9601-45a6-9625-d1c418c3accc.json b/8d5dc422-9601-45a6-9625-d1c418c3accc.json new file mode 100644 index 0000000000000000000000000000000000000000..3780a0b660c3644cc772f71f9de323b7a812d1c0 --- /dev/null +++ b/8d5dc422-9601-45a6-9625-d1c418c3accc.json @@ -0,0 +1,34 @@ +{ + "id": "8d5dc422-9601-45a6-9625-d1c418c3accc", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "1591825", + "text": "BACKGROUND:\nA family history of heart disease has been reported to increase the risk of coronary heart disease. We examined the relation between family history of myocardial infarction (MI) and risk of acute MI to establish the independency of this association, the degree of risk in relation to the number and age of relatives affected, and the possible interaction between family history and other major risk factors for MI.\n\nMETHODS AND RESULTS:\nIn a case-control study conducted in Italy within the framework of the GISSI-2 Trial, 916 cases of newly diagnosed MI and 1,106 hospital controls were identified. Using a structured questionnaire, data were collected on the history of MI in first-degree relatives and the age at which the event occurred. Compared with subjects without family history of MI in first-degree relatives, the relative risk (RR) of MI was 2.0 (95% confidence interval, CI, 1.6-2.5) in those with one and 3.0 (95% CI, 2.0-4.4) in those with two or more relatives affected (chi 2(1) test for trend, 54.1; p less than 0.001). Such an increase was not substantially affected by allowance for recognized risk factors. The risk related to family history involving at least two relatives was higher for early MI (less than 55 years) (RR, 20.0; 95% CI, 3.3-121.2) compared with later MI (less than or equal to 65 years) (RR, 3.5; 95% CI, 1.8-6.6). When known risk factors were considered for their interaction with family history, the effect on RR was approximately multiplicative for several variables, including smoking, serum cholesterol, hypertension, and hyperlipidemia but not for diabetes and body mass index. Thus, the presence of both family history and smoking and cholesterol levels greater than or equal to 226 mg/dl led to an RR of 14 (95% CI, 3.7-50.0) and 8.3 (95% CI, 1.8-38.7), respectively.\n\nCONCLUSIONS:\nThis study indicates that a family history of MI is an independent risk factor for MI, and that the number of relatives and the age at which they were affected is related to the strength of the association. There is a multiplicative effect on RR between family history and several major risk factors for MI." + }, + "questions": [ + { + "id": "c96d9053-77e2-4be8-b6ea-e11fed2bae36", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1870, + "text": "family history of MI" + } + ] + } + ] +} \ No newline at end of file diff --git a/8d67a507-1f42-4d30-a0b0-8356d5534262.json b/8d67a507-1f42-4d30-a0b0-8356d5534262.json new file mode 100644 index 0000000000000000000000000000000000000000..bbb0a483e8315747673c06cf95b52d7e9be3e589 --- /dev/null +++ b/8d67a507-1f42-4d30-a0b0-8356d5534262.json @@ -0,0 +1,68 @@ +{ + "id": "8d67a507-1f42-4d30-a0b0-8356d5534262", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "31626315", + "text": "IMPORTANCE:\nExposure to disinfectants in health care workers has been associated with respiratory health outcomes, including asthma. Despite the biological plausibility of an association between disinfectants (irritant chemicals) and risk of chronic obstructive pulmonary disease (COPD), available data are sparse.\n\nOBJECTIVE:\nTo investigate the association between exposure to disinfectants and COPD incidence in a large cohort of US female nurses.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nThe Nurses' Health Study II is a US prospective cohort study of 116 429 female registered nurses from 14 US states who were enrolled in 1989 and followed up through questionnaires every 2 years since. The present study included women who were still in a nursing job and had no history of COPD in 2009, and used data from the 2009 through 2015 questionnaires. Clean and complete data used for this analysis were available in July 2018, and analyses were conducted from September 2018 through August 2019.\n\nEXPOSURES:\nOccupational exposure to disinfectants, evaluated by questionnaire and a job-task-exposure matrix (JTEM).\n\nMAIN OUTCOMES AND MEASURES:\nIncident physician-diagnosed COPD evaluated by questionnaire.\n\nRESULTS:\nAmong the 73 262 women included in the analyses, mean (SD) age at baseline was 54.7 (4.6) years and 70 311 (96.0%) were white, 1235 (1.7%) black, and 1716 (2.3%) other; and 1345 (1.8%) Hispanic, and 71 917 (98.2%) non-Hispanic. Based on 368 145 person-years of follow-up, 582 nurses reported incident physician-diagnosed COPD. Weekly use of disinfectants to clean surfaces only (16 786 [22.9%] of participants exposed) and to clean medical instruments (13 899 [19.0%] exposed) was associated with COPD incidence, with adjusted hazard ratios of 1.38 (95% CI, 1.13-1.68) for cleaning surfaces only and 1.31 (95% CI, 1.07-1.61) for cleaning medical instruments after adjustment for age, smoking (pack-years), race, ethnicity, and body mass index. High-level exposure, evaluated by the JTEM, to several specific disinfectants (ie, glutaraldehyde, bleach, hydrogen peroxide, alcohol, and quaternary ammonium compounds) was significantly associated with COPD incidence, with adjusted hazard ratios ranging from 1.25 (95% CI, 1.04-1.51) to 1.36 (95% CI, 1.13-1.64). Associations were not modified by smoking or asthma status (P for interaction \u003e .15).\n\nCONCLUSIONS AND RELEVANCE:\nThese longitudinal results suggest that regular use of chemical disinfectants among nurses may be a risk factor for developing COPD. If future studies confirm these results, exposure-reduction strategies that are compatible with infection control in health care settings should be developed." + }, + "questions": [ + { + "id": "29828f32-2b96-4efa-a1b7-9f377bfa16c5", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 1536, + "text": "Weekly use of disinfectants to clean surfaces only" + }, + { + "answer_start": 1632, + "text": "to clean medical instruments" + }, + { + "answer_start": 1953, + "text": "High-level exposure, evaluated by the JTEM, to several specific disinfectants" + }, + { + "answer_start": 2036, + "text": "glutaraldehyde" + }, + { + "answer_start": 2052, + "text": "bleach" + }, + { + "answer_start": 2060, + "text": "hydrogen peroxide" + }, + { + "answer_start": 2079, + "text": "alcohol" + }, + { + "answer_start": 2092, + "text": "quaternary ammonium compounds" + }, + { + "answer_start": 2437, + "text": "chemical disinfectants among nurses" + } + ] + } + ] +} \ No newline at end of file diff --git a/8e251d21-8990-4feb-9a1b-5b4a2ec2ad5b.json b/8e251d21-8990-4feb-9a1b-5b4a2ec2ad5b.json new file mode 100644 index 0000000000000000000000000000000000000000..353120dc5b3d9fedaf45e8ae25f729a226318901 --- /dev/null +++ b/8e251d21-8990-4feb-9a1b-5b4a2ec2ad5b.json @@ -0,0 +1,39 @@ +{ + "id": "8e251d21-8990-4feb-9a1b-5b4a2ec2ad5b", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "27626972", + "text": "RATIONALE:\nPreeclampsia reflects an unusual increase in systemic inflammation during pregnancy.\n\nOBJECTIVES:\nWe studied associations between preeclampsia and asthma, allergy, and eczema in Copenhagen Prospective Studies on Asthma in Childhood (COPSAC) and in national registries.\n\nMETHODS:\nCOPSAC is a high-risk birth cohort of 411 Danish children. Asthma, allergy, and eczema were diagnosed prospectively, and lung function measured at age 1 month and 7 years. Sensitization was evaluated at age 6 months, 18 months, 4 years, and 6 years by skin prick tests and IgE measurements. The register-based cohort included 1.7 million children from Danish national registries in the 35-year period 1977-2012. Children born to mothers with preeclampsia were analyzed regarding risk of asthma, allergy, and eczema.\n\nMEASUREMENTS AND MAIN RESULTS:\nIn the COPSAC cohort, 5.6% (n = 23) were diagnosed with preeclampsia. Preeclampsia was associated with increased risk of treatment with inhaled corticosteroids at age 7 years (adjusted odds ratio, 4.01 [95% confidence interval (CI), 1.11-14.43]; P = 0.0337), increased bronchial responsiveness to methacholine (adjusted β-coefficient log-μmol, -0.80 [95% CI, -1.55 to -0.06]; P = 0.0348), and allergic rhinitis (adjusted odds ratio, 4.83 [95% CI, 1.58-14.78]; P = 0.0057) in the 7-year-old children. Furthermore, the children had an increased risk of sensitization to both aeroallergens and food allergens, and increased amount of total IgE during childhood. In the registry-based cohort, 3.7% (n = 62,728) were born to mothers with preeclampsia. Preeclampsia was associated with increased risk of asthma, eczema, and aeroallergen and food allergy, especially pronounced after a duration of preeclampsia of 14 days or more. Maternal asthma increased the risk of preeclampsia.\n\nCONCLUSIONS:\nPreeclampsia is a shared prenatal risk factor for asthma, eczema, and allergy in childhood pointing toward in utero immune programming of the child." + }, + "questions": [ + { + "id": "7babfee1-4a56-4aed-90f4-c702546c61d6", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1828, + "text": "Preeclampsia" + }, + { + "answer_start": 1585, + "text": "Preeclampsia" + } + ] + } + ] +} \ No newline at end of file diff --git a/8f63522a-23fe-49d2-af36-fa26ca22002a.json b/8f63522a-23fe-49d2-af36-fa26ca22002a.json new file mode 100644 index 0000000000000000000000000000000000000000..7633015b52b24ee9bc07af8324a9a29916b593dd --- /dev/null +++ b/8f63522a-23fe-49d2-af36-fa26ca22002a.json @@ -0,0 +1,43 @@ +{ + "id": "8f63522a-23fe-49d2-af36-fa26ca22002a", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "24210922", + "text": "OBJECTIVE:\nTo evaluate the association between gestational age at birth and the risk of subsequent development of asthma.\n\nSTUDY DESIGN:\nWe conducted a retrospective observational hospital-based birth case-control study in a university-based obstetrics and gynecology department in Finland. A total of 44,173 women delivering between 1989 and 2008 were linked with the social insurance register to identify asthma reimbursements for their offspring (n = 2661). Pregnancy factors were recorded during pregnancy. Infants were categorized as moderately preterm (≤ 32 weeks), late preterm (33-36 weeks), early term (37-38 weeks), term (39-40 weeks), or late term and postterm (≥ 41 weeks). The main outcome measure was asthma among the infants.\n\nRESULTS:\nChildren born moderately preterm (≤ 32 weeks gestation) had a significantly increased risk of asthma (aOR, 3.9; 95% CI, 3.2-4.8). The risk of asthma was also increased in those born late preterm (aOR, 1.7; 95% CI, 1.4-2.0) and early term (aOR, 1.2; 95% CI, 1.1-1.4). In contrast, delivery at 41 weeks or later seemed to decrease the risk of asthma (aOR, 0.9; 95% CI, 0.8-1.0). The burden of asthma associated with preterm birth was associated mainly with early term infants, in whom 108 extra cases of asthma were observed.\n\nCONCLUSION:\nEven though the individual risk of asthma was inversely correlated with gestational age at birth, the overall burden brought about by delivery before term was associated with late preterm and early term deliveries. Furthermore, delivery after term was protective against asthma." + }, + "questions": [ + { + "id": "bba4da4e-8e57-4f1a-9eb7-87d5446bbbef", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 751, + "text": "Children born moderately preterm (≤ 32 weeks gestation)" + }, + { + "answer_start": 922, + "text": "those born late preterm" + }, + { + "answer_start": 978, + "text": "early term" + } + ] + } + ] +} \ No newline at end of file diff --git a/8f77b26d-e85c-40e0-93d6-30808c970f0b.json b/8f77b26d-e85c-40e0-93d6-30808c970f0b.json new file mode 100644 index 0000000000000000000000000000000000000000..1780643b78d6b5a32d2aa3c4cc8ca8e7c5ff33ad --- /dev/null +++ b/8f77b26d-e85c-40e0-93d6-30808c970f0b.json @@ -0,0 +1,38 @@ +{ + "id": "8f77b26d-e85c-40e0-93d6-30808c970f0b", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "16043644", + "text": "BACKGROUND:\nInterleukin (IL)-18 plays a key role in atherosclerosis and its complications. The present study investigated the genetic variability of 4 genes of the IL-18 system-IL18, IL18R1, IL18RAP, and IL18BP-in relation to circulating IL-18 levels and cardiovascular mortality.\n\nMETHODS AND RESULTS:\nTwenty-two polymorphisms were genotyped in 1288 patients with coronary artery disease prospectively followed up during a median period of 5.9 years. The end point was death from cardiovascular causes (n=142). Baseline IL-18 levels were predictive of cardiovascular deaths occurring during \u003c or =4 years of follow-up (HR=2.96, 95% CI 1.54 to 5.70, P=0.001 for the top compared with the bottom quartile) but not of later deaths. Haplotypes of the IL18 gene were associated with IL-18 levels (P=0.002) and cardiovascular mortality (P=0.006) after adjustment for cardiovascular risk factors. The same haplotype was associated with both a 9% lowering effect on IL-18 levels and a protective effect on risk (HR=0.57, 95% CI 0.36 to 0.92). IL18 haplotypes explained only 2% of IL-18 variability. Adjustment for baseline IL-18 levels abolished the association of haplotypes with cardiovascular risk. The haplotype associated with phenotypes was the only one carrying the minor allele of the IL18/A+183G polymorphism located in the 3'untranslated region and potentially affecting mRNA stability. The other genes of the system were not related to IL-18 levels or cardiovascular outcome.\n\nCONCLUSIONS:\nVariations of the IL18 gene consistently influence circulating levels of IL-18 and clinical outcome in patients with coronary artery disease, which supports the hypothesis of a causal role of IL-18 in atherosclerosis and its complications." + }, + "questions": [ + { + "id": "e4e637f0-cb69-4265-a597-cf39f5a35093", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1225, + "text": "phenotypes was the only one carrying the minor allele of the IL18/A+183G polymorphism located in the 3'untranslated region" + }, + { + "answer_start": 1686, + "text": "IL-18" + } + ] + } + ] +} \ No newline at end of file diff --git a/8f7bf48a-88ef-409c-9489-49d905a53ab0.json b/8f7bf48a-88ef-409c-9489-49d905a53ab0.json new file mode 100644 index 0000000000000000000000000000000000000000..e8d420318762b2235e4c8e3cbc6801a5f93a6029 --- /dev/null +++ b/8f7bf48a-88ef-409c-9489-49d905a53ab0.json @@ -0,0 +1,62 @@ +{ + "id": "8f7bf48a-88ef-409c-9489-49d905a53ab0", + "disease": { + "id": "H00408", + "names": [ + "Type 1 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E10" + ], + "mesh": [ + "D003922" + ] + }, + "category": "Metabolic disease; Immune system disease; Endocrine disease" + }, + "article": { + "id": "28770319", + "text": "AIMS/HYPOTHESIS:\nRespiratory infections and onset of islet autoimmunity are reported to correlate positively in two small prospective studies. The Environmental Determinants of Diabetes in the Young (TEDDY) study is the largest prospective international cohort study on the environmental determinants of type 1 diabetes that regularly monitors both clinical infections and islet autoantibodies. The aim was to confirm the influence of reported respiratory infections and to further characterise the temporal relationship with autoantibody seroconversion.\n\nMETHODS:\nDuring the years 2004-2009, 8676 newborn babies with HLA genotypes conferring an increased risk of type 1 diabetes were enrolled at 3 months of age to participate in a 15 year follow-up. In the present study, the association between parent-reported respiratory infections and islet autoantibodies at 3 month intervals up to 4 years of age was evaluated in 7869 children. Time-dependent proportional hazard models were used to assess how the timing of respiratory infections related to persistent confirmed islet autoimmunity, defined as autoantibody positivity against insulin, GAD and/or insulinoma antigen-2, concordant at two reference laboratories on two or more consecutive visits.\n\nRESULTS:\nIn total, 87,327 parent-reported respiratory infectious episodes were recorded while the children were under study surveillance for islet autoimmunity, and 454 children seroconverted. The number of respiratory infections occurring in a 9 month period was associated with the subsequent risk of autoimmunity (p \u003c 0.001). For each 1/year rate increase in infections, the hazard of islet autoimmunity increased by 5.6% (95% CI 2.5%, 8.8%). The risk association was linked primarily to infections occurring in the winter (HR 1.42 [95% CI 1.16, 1.74]; p \u003c 0.001). The types of respiratory infection independently associated with autoimmunity were common cold, influenza-like illness, sinusitis, and laryngitis/tracheitis, with HRs (95% CI) of 1.38 (1.11, 1.71), 2.37 (1.35, 4.15), 2.63 (1.22, 5.67) and 1.76 (1.04, 2.98), respectively.\n\nCONCLUSIONS/INTERPRETATION:\nRecent respiratory infections in young children correlate with an increased risk of islet autoimmunity in the TEDDY study. Further studies to identify the potential causative viruses with pathogen-specific assays should focus especially on the 9 month time window leading to autoantibody seroconversion." + }, + "questions": [ + { + "id": "5d120513-4c60-4630-ba26-f270016f07f7", + "text": "What are the risk factors of Type 1 diabetes mellitus?", + "answers": [ + { + "answer_start": 1450, + "text": "number of respiratory infections occurring in a 9 month period" + }, + { + "answer_start": 1586, + "text": "each 1/year rate increase in infections" + }, + { + "answer_start": 1744, + "text": "infections occurring in the winter" + }, + { + "answer_start": 1904, + "text": "common cold" + }, + { + "answer_start": 1917, + "text": "influenza-like illness" + }, + { + "answer_start": 1941, + "text": "sinusitis" + }, + { + "answer_start": 1956, + "text": "laryngitis/tracheitis" + }, + { + "answer_start": 2122, + "text": "Recent respiratory infections in young children" + } + ] + } + ] +} \ No newline at end of file diff --git a/8fd45884-5f06-4c24-939f-713c95a9c4de.json b/8fd45884-5f06-4c24-939f-713c95a9c4de.json new file mode 100644 index 0000000000000000000000000000000000000000..0e2ddaba3e5d40ce09bade33a875656b444ae536 --- /dev/null +++ b/8fd45884-5f06-4c24-939f-713c95a9c4de.json @@ -0,0 +1,40 @@ +{ + "id": "8fd45884-5f06-4c24-939f-713c95a9c4de", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "19820078", + "text": "BACKGROUND:\nPrior pulmonary TB has been shown to be associated with a higher risk of airflow obstruction, which is the hallmark of COPD, but whether smoking modifies this relationship is unclear. We investigated the relationships between prior TB, smoking, and airflow obstruction in a Chinese population sample.\n\nMETHODS:\nParticipants in the Guangzhou Biobank Cohort Study underwent spirometry, chest radiography, and a structured interview on lifestyle and exposures. Prior TB was defined as the presence of radiologic evidence suggestive of inactive TB. Airflow obstruction was based on spirometric criteria.\n\nRESULTS:\nThe prevalence of prior TB in this sample (N = 8,066, mean age: 61.9 years) was 24.2%. After controlling for sex, age, and smoking exposure, prior TB remained independently associated with an increased risk of airflow obstruction (odds ratio = 1.37; 95% CI, 1.13-1.67). Further adjustment for exposure to passive smoking, biomass fuel, and dust did not alter the relationship. Smoking did not modify the relationship between prior TB and airflow obstruction.\n\nCONCLUSIONS:\nPrior TB is an independent risk factor for airflow obstruction, which may partly explain the higher prevalence of COPD in China. Clinicians should be aware of this long-term risk in individuals with prior TB, irrespective of smoking status, particularly in patients from countries with a high TB burden." + }, + "questions": [ + { + "id": "76074341-13c2-4680-98ac-7084add5f3f5", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 763, + "text": "prior TB" + }, + { + "answer_start": 1095, + "text": "Prior TB" + } + ] + } + ] +} \ No newline at end of file diff --git a/90236ffe-fad1-4906-bb4d-d59254f6d2ee.json b/90236ffe-fad1-4906-bb4d-d59254f6d2ee.json new file mode 100644 index 0000000000000000000000000000000000000000..c3e812ba7468f1619b30e01c681b15a6128363ec --- /dev/null +++ b/90236ffe-fad1-4906-bb4d-d59254f6d2ee.json @@ -0,0 +1,41 @@ +{ + "id": "90236ffe-fad1-4906-bb4d-d59254f6d2ee", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "22350783", + "text": "AIM:\nThe purpose of this study was to determine whether diabetes mellitus is associated with an increased risk of colorectal cancer.\n\nMETHODS:\nRelevant studies were identified in MEDLINE and EMBASE (up until November 1st, 2011). Inclusion criteria were original, peer-reviewed publications, with case-control and cohort studies (for studies on diabetes mellitus and colorectal cancer). Summary relative risks with 95% confidence intervals were calculated with a random-effects model.\n\nRESULTS:\nTwenty-four studies including eight case-control and 16 cohort studies, with a total of 3,659,341 participants, were included in this updated systematic review and meta-analysis, and all involved diabetes mellitus and colorectal cancer risk. Meta-analysis of the 24 included studies indicated that diabetes was associated with an increased risk of colorectal cancer, compared with no diabetes (summary RR of colorectal cancer incidence = 1.26, 95% CI = 1.20-1.31), without heterogeneity between studies (P(heterogeneity) = 0.296). Sub-group analyses found that these results were consistent between case-control and cohort studies and among studies conducted in different areas. The association between diabetes and colorectal cancer incidence did not differ significantly by sex and sub-sites. Insulin therapy was also positively associated with risk of colorectal cancer (summary RR = 1.61, 95% CI 1.18-1.35), with evidence of heterogeneity between studies (P(heterogeneity) = 0.014).\n\nCONCLUSIONS:\nOur findings further support a relationship between diabetes and increased risk of colon and rectal cancer in both women and men, and insulin therapy for diabetes may increase this risk." + }, + "questions": [ + { + "id": "b8e207e8-6795-4e50-b786-dcfec32e3e02", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1547, + "text": "diabetes" + }, + { + "answer_start": 792, + "text": "diabetes" + } + ] + } + ] +} \ No newline at end of file diff --git a/91116b22-a9b8-43d4-a4b4-f691f78fb262.json b/91116b22-a9b8-43d4-a4b4-f691f78fb262.json new file mode 100644 index 0000000000000000000000000000000000000000..7964072af5d7e636d324f0be93d2d8653d0ea4d4 --- /dev/null +++ b/91116b22-a9b8-43d4-a4b4-f691f78fb262.json @@ -0,0 +1,47 @@ +{ + "id": "91116b22-a9b8-43d4-a4b4-f691f78fb262", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "22436169", + "text": "BACKGROUND:\nRelationships between indoor air quality (IAQ) found in schools and the allergic and respiratory health of schoolchildren have been insufficiently explored. A survey was conducted in a large sample of classrooms of primary schools in France to provide objective assessments of IAQ to which young schoolchildren are exposed in classrooms, and to relate exposure to major air pollutants found in classrooms to asthma and allergies of schoolchildren.\n\nMETHODS:\nConcentrations of fine particles with aerodynamic diameter ≤2.5 μm (PM(2.5)), nitrogen dioxide (NO(2)) and three aldehydes were objectively assessed in 401 randomly chosen classrooms in 108 primary schools attended by 6590 children (mean age 10.4 years, SD ±0.7) in the French 6 Cities Study. The survey incorporated a medical visit including skin prick testing (SPT) for common allergens, a test for screening exercise-induced asthma (EIA) and a standardised health questionnaire completed by parents.\n\nRESULTS:\nChildren were differently exposed to poor air quality in classrooms, with almost 30% being highly exposed according to available standards. After adjusting for confounders, past year rhinoconjunctivitis was significantly associated with high levels of formaldehyde in classrooms (OR 1.19; 95% CI 1.04 to 1.36). Additionally, an increased prevalence of past year asthma was found in the classrooms with high levels of PM(2.5) (OR 1.21; 95% CI 1.05 to 1.39), acrolein (OR 1.22; 95% CI 1.09 to 1.38) and NO(2) (OR 1.16; 95% CI 0.95 to 1.41) compared with others. The relationship was observed mostly for allergic asthma as defined using SPT. A significant positive correlation was found between EIA and the levels of PM(2.5) and acrolein in the same week.\n\nCONCLUSIONS:\nIn this random sample, air quality in classrooms was poor, varied significantly among schools and cities, and was related to an increased prevalence of clinical manifestations of asthma and rhinitis in schoolchildren. Children with a background of allergies seemed at increased risk." + }, + "questions": [ + { + "id": "f316d864-fdce-4185-8355-6655ea10e84c", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1385, + "text": "high levels of PM(2.5)" + }, + { + "answer_start": 1440, + "text": "acrolein" + }, + { + "answer_start": 1484, + "text": "NO(2)" + }, + { + "answer_start": 1773, + "text": "air quality in classrooms" + } + ] + } + ] +} \ No newline at end of file diff --git a/91652ef6-2052-447f-a117-e3b099df2946.json b/91652ef6-2052-447f-a117-e3b099df2946.json new file mode 100644 index 0000000000000000000000000000000000000000..a14dc207c805408872748f03059e8cadf828f51c --- /dev/null +++ b/91652ef6-2052-447f-a117-e3b099df2946.json @@ -0,0 +1,38 @@ +{ + "id": "91652ef6-2052-447f-a117-e3b099df2946", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "28345789", + "text": "OBJECTIVE:\nThis study investigated how a wide spectrum of body mass index (BMI) values at ages 7 to 13 years are associated with type 2 diabetes throughout adulthood, including potential modifying effects of sex and birth weight.\n\nMETHODS:\nFrom the Copenhagen School Health Records Register, 292,827 individuals, born between 1930 and 1989, were followed in national registers for type 2 diabetes (women, n = 7,472; men, n = 11,548). Heights and weights were measured at ages 7 to 13 years.\n\nRESULTS:\nBelow-average BMIs, with few exceptions, were not associated with type 2 diabetes. Above-average BMIs had positive associations that were stronger in women than men, stronger in younger birth cohorts, and weaker with older age at diagnosis. Women born 1930-1947, 1948-1965, and 1966-1983 with above-average BMIs at 13 years (≥18.2 kg/m ) had hazard ratios (95% confidence intervals) ranging from 2.12 (1.91-2.36) to 2.84 (2.31-3.49) per z score when diagnosed at 30 to 47 years. Birth weight did not modify these associations.\n\nCONCLUSIONS:\nChildhood BMIs below average are not associated with type 2 diabetes, whereas childhood BMIs above average are strongly associated with type 2 diabetes in adulthood, corresponding to excess risks even at levels below international definitions of overweight. The associations are stronger in women than men but are not affected by birth weight." + }, + "questions": [ + { + "id": "adb87607-37d9-4138-9b71-bf6c31ea1318", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1120, + "text": "childhood BMIs above average" + }, + { + "answer_start": 794, + "text": "above-average BMIs at 13 years (≥18.2 kg/m )" + } + ] + } + ] +} \ No newline at end of file diff --git a/91a993e9-4d33-4ed2-a738-79ec24643cf0.json b/91a993e9-4d33-4ed2-a738-79ec24643cf0.json new file mode 100644 index 0000000000000000000000000000000000000000..f62831f649ed47be16c79c6fc274a892f9f8a36b --- /dev/null +++ b/91a993e9-4d33-4ed2-a738-79ec24643cf0.json @@ -0,0 +1,34 @@ +{ + "id": "91a993e9-4d33-4ed2-a738-79ec24643cf0", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "25623697", + "text": "OBJECTIVE:\nTo investigate the association of cannabis use and tobacco smoking on the incidence of bladder cancer within the California Men's Health Study cohort.\n\nMETHODS:\nWe evaluated the records of 84,170 participants in a multiethnic cohort of men aged 45-69 years. Information on demographic and lifestyle factors including smoking history and cannabis use was collected using mailed questionnaires between 2002 and 2003. We linked the study data with clinical records including cancer data from electronic health records.\n\nRESULTS:\nOverall 34,000 (41%) cohort members reported cannabis use, 47,092 (57%) reported tobacco use, 22,500 (27%) reported using both, and 23,467 (29%) used neither. Men were followed over an 11-year period and 279 (0.3%) developed incident bladder tumors. Among cannabis users, 89 (0.3%) developed bladder cancer in comparison to 190 (0.4%) men who did not report cannabis use (P \u003c .001). After adjusting for age, race or ethnicity, and body mass index, using tobacco only was associated with an increased risk of bladder cancer (hazard regression [HR], 1.52; 95% confidence interval [CI], 1.12-2.07), whereas cannabis use only was associated with a 45% reduction in bladder cancer incidence (HR, 0.55; 95% CI, 0.31-1.00). Using both cannabis and tobacco was associated with an HR of 1.28 (95% CI, 0.91-1.80).\n\nCONCLUSION:\nAlthough a cause and effect relationship has not been established, cannabis use may be inversely associated with bladder cancer risk in this population." + }, + "questions": [ + { + "id": "fea20fd3-37af-491c-88f1-c46524c520d6", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 985, + "text": "using tobacco only" + } + ] + } + ] +} \ No newline at end of file diff --git a/91e5e851-4cb1-43d5-be53-13e628f7af34.json b/91e5e851-4cb1-43d5-be53-13e628f7af34.json new file mode 100644 index 0000000000000000000000000000000000000000..060ff7934e2e4115411243c71cac7dce8e54951a --- /dev/null +++ b/91e5e851-4cb1-43d5-be53-13e628f7af34.json @@ -0,0 +1,35 @@ +{ + "id": "91e5e851-4cb1-43d5-be53-13e628f7af34", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "16537858", + "text": "OBJECTIVES:\nTo determine the association between antibiotic exposure in the first year of life and the development of childhood asthma.\n\nDESIGN:\nMetaanalysis of observational studies retrieved through systematic search of all available electronic data sources. Studies included in the metaanalyses were those with populations exposed to one or more courses of antibiotics during the first year of life, and asthma diagnosis was defined as diagnosis by a physician between the age of 1 to 18 years.\n\nSETTING:\nRetrospective and prospective studies published in the English-language literature from 1966 to present.\n\nRESULTS:\nEight studies (four prospective and four retrospective) examined the association between exposure to at least one course of antibiotics and development of childhood asthma. The total number of subjects for the analysis comparing exposure to at least one antibiotic to no exposure in the first year of life was 12,082 children and 1,817 asthma cases. In the dose-response analysis, we included data from a total of 27,167 children and 3,392 asthma cases. The pooled odds ratio (OR) for the eight studies was 2.05 (95% confidence interval [CI], 1.41 to 2.99). The association was significantly stronger in the retrospective studies (OR, 2.82; 95% CI, 2.07 to 3.85) than the prospective studies (OR, 1.12; 95% CI, 0.88 to 1.42). Five of the eight studies examined whether the association was related to the number of courses of antibiotics taken in the first year of life. The overall OR for the dose-response analysis was 1.16 (95% CI, 1.05 to 1.28) for each additional course of antibiotics; however, this association was not significantly stronger in the retrospective studies (OR, 1.37; 95% CI, 1.18 to 1.60) relative to the prospective studies (OR, 1.07; 95% CI, 0.95 to 1.20).\n\nCONCLUSIONS:\nExposure to at least one course of antibiotics in the first year of life appears to be a risk factor for the development of childhood asthma. Because of the limitations of the studies conducted to date, additional large-scale, prospective studies are needed to confirm this potential association." + }, + "questions": [ + { + "id": "66317e17-4b08-48a1-98f2-bb2874859f3d", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1817, + "text": "Exposure to at least one course of antibiotics in the first year of life" + } + ] + } + ] +} \ No newline at end of file diff --git a/92c21baf-6d23-4795-b42d-b9bafabae109.json b/92c21baf-6d23-4795-b42d-b9bafabae109.json new file mode 100644 index 0000000000000000000000000000000000000000..5b2f4bee9fee11742d0ec8b92cd2d3053ae7a8c7 --- /dev/null +++ b/92c21baf-6d23-4795-b42d-b9bafabae109.json @@ -0,0 +1,35 @@ +{ + "id": "92c21baf-6d23-4795-b42d-b9bafabae109", + "disease": { + "id": "H00056", + "names": [ + "Alzheimer disease", + "Dementia due to Alzheimer disease" + ], + "dbLinks": { + "icd10": [ + "G30" + ], + "mesh": [ + "D000544" + ] + }, + "category": "Neurodegenerative disease" + }, + "article": { + "id": "18401020", + "text": "OBJECTIVE:\nSubjects with diabetes are reported to have an increased risk of dementia and cognitive impairment. However, the underlying causes remain unknown. We investigated the longitudinal associations between midlife insulin secretion, glucose metabolism, and the subsequent development of Alzheimer disease (AD) and dementia.\n\nMETHODS:\nThe population-based Uppsala Longitudinal Study of Adult Men started 1970 when the 2,322 participants were 50 years old. Investigation at baseline included determinations of acute insulin response and glucose tolerance using the IV glucose tolerance test and Homeostasis Model Assessment insulin resistance index. During a median follow up of 32 years, 102 participants were diagnosed with AD, 57 with vascular dementia, and 394 with any dementia or cognitive impairment. Associations were analyzed using Cox proportional hazard models.\n\nRESULTS:\nA low insulin response at baseline was associated with a higher cumulative risk of AD (hazard ratio for 1 SD decrease, 1.31; 95% CI, 1.10-1.56) also after adjustment for age, systolic blood pressure, body mass index, serum cholesterol, smoking, education level, and insulin resistance. This association was stronger in subjects without the APOE epsilon4 allele. Impaired glucose tolerance increased the risk of vascular dementia (hazard ratio for 1 SD decrease, 1.45; 95% CI, 1.05-2.00) but not AD. Impaired insulin secretion, glucose intolerance, and estimates of insulin resistance were all associated with higher risk of any dementia and cognitive impairment.\n\nCONCLUSIONS:\nIn this longitudinal study, impaired acute insulin response at midlife was associated with an increased risk of Alzheimer disease (AD) up to 35 years later suggesting a causal link between insulin metabolism and the pathogenesis of AD." + }, + "questions": [ + { + "id": "1c0d3c31-a100-4061-a1e1-7ef637df11c3", + "text": "What are the risk factors of Alzheimer disease?", + "answers": [ + { + "answer_start": 1592, + "text": "impaired acute insulin response at midlife" + } + ] + } + ] +} \ No newline at end of file diff --git a/92d109de-37f7-48cc-a95f-6e3e9061af98.json b/92d109de-37f7-48cc-a95f-6e3e9061af98.json new file mode 100644 index 0000000000000000000000000000000000000000..5ec85974387d218f6e215a60047fb1892dbd0129 --- /dev/null +++ b/92d109de-37f7-48cc-a95f-6e3e9061af98.json @@ -0,0 +1,44 @@ +{ + "id": "92d109de-37f7-48cc-a95f-6e3e9061af98", + "disease": { + "id": "M2023_04_26_16_49_01", + "names": [ + "Metabolic syndrome" + ], + "dbLinks": { + "mesh": [ + "C18.452.394.968.500.570", + "C18.452.625" + ] + }, + "description": "Metabolic syndrome is a complex constellation of metabolic derangements that increase the risk of atherosclerotic cardiovascular disease, type 2 diabetes, and all-cause mortality. The key features of metabolic syndrome include central obesity, insulin resistance, dyslipidemia, and hypertension. These abnormalities are believed to arise from a combination of genetic predisposition and environmental factors, such as sedentary behavior, poor dietary habits, and chronic stress. Diagnosis of metabolic syndrome requires meeting three or more established criteria, based on standardized guidelines. Management of metabolic syndrome involves a comprehensive approach, including lifestyle modifications such as weight loss, physical activity, and dietary changes, as well as pharmacotherapy to address underlying risk factors such as hypertension, dyslipidemia, and hyperglycemia. Early intervention and aggressive management of metabolic syndrome are critical to preventing or delaying the onset of complications and improving long-term health outcomes." + }, + "article": { + "id": "14988303", + "text": "OBJECTIVE:\nTo prospectively investigate predictors of the incident metabolic syndrome in nondiabetic adults.\n\nRESEARCH DESIGN AND METHODS:\nThis analysis included 714 white, black, and Hispanic participants in the Insulin Resistance Atherosclerosis Study (IRAS) who were free of the metabolic syndrome at baseline; 139 of these developed the metabolic syndrome in the subsequent 5 years. We examined measures of glucose (fasting and 2 h), insulin (fasting and 2 h, acute insulin response, insulin sensitivity [Si], and proinsulin), lipids (HDL and triglycerides), blood pressure (systolic and diastolic), waist circumference, and baseline physical activity (total energy expenditure) as predictors of the metabolic syndrome. Logistic regression models were adjusted for age, sex, study site, ethnicity, and impaired glucose tolerance. Signal detection analysis was used to identify the characteristics of the highest risk group.\n\nRESULTS:\nThe best predictors of incident metabolic syndrome were waist circumference (odds ratio [OR] 1.7 [1.3-2.0] per 11 cm), HDL cholesterol (0.6 [0.4-0.7] per 15 mg/dl), and proinsulin (1.7 [1.4-2.0] per 3.3 pmol/l). Signal detection analysis identified waist circumference (\u003e89 cm in women, \u003e102 cm in men) as the optimal predictor.\n\nCONCLUSIONS:\nThese findings suggest that obesity may precede the development of other metabolic syndrome components. Interventions that address obesity and reduce waist circumference may reduce the incidence of the metabolic syndrome in nondiabetic adults." + }, + "questions": [ + { + "id": "3f201ed6-eecf-499a-b3e5-cc5017b182c1", + "text": "What is a risk factor for Metabolic Syndrome?", + "answers": [ + { + "answer_start": 994, + "text": "waist circumference" + }, + { + "answer_start": 1057, + "text": "HDL cholesterol" + }, + { + "answer_start": 1107, + "text": "proinsulin" + }, + { + "answer_start": 1309, + "text": "obesity" + } + ] + } + ] +} \ No newline at end of file diff --git a/9392c314-001f-4c8e-8220-c40ff7450a7e.json b/9392c314-001f-4c8e-8220-c40ff7450a7e.json new file mode 100644 index 0000000000000000000000000000000000000000..11536248931fa48419a910ccf8b6c94954a79874 --- /dev/null +++ b/9392c314-001f-4c8e-8220-c40ff7450a7e.json @@ -0,0 +1,47 @@ +{ + "id": "9392c314-001f-4c8e-8220-c40ff7450a7e", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "17662882", + "text": "BACKGROUND:\nThe role of exposure to substances in the workplace in new-onset asthma is not well characterised in population-based studies. We therefore aimed to estimate the relative and attributable risks of new-onset asthma in relation to occupations, work-related exposures, and inhalation accidents.\n\nMETHODS:\nWe studied prospectively 6837 participants from 13 countries who previously took part in the European Community Respiratory Health Survey (1990-95) and did not report respiratory symptoms or a history of asthma at the time of the first study. Asthma was assessed by methacholine challenge test and by questionnaire data on asthma symptoms. Exposures were defined by high-risk occupations, an asthma-specific job exposure matrix with additional expert judgment, and through self-report of acute inhalation events. Relative risks for new onset asthma were calculated with log-binomial models adjusted for age, sex, smoking, and study centre.\n\nFINDINGS:\nA significant excess asthma risk was seen after exposure to substances known to cause occupational asthma (Relative risk=1.6, 95% CI 1.1-2.3, p=0.017). Risks were highest for asthma defined by bronchial hyper-reactivity in addition to symptoms (2.4, 1.3-4.6, p=0.008). Of common occupations, a significant excess risk of asthma was seen for nursing (2.2, 1.3-4.0, p=0.007). Asthma risk was also increased in participants who reported an acute symptomatic inhalation event such as fire, mixing cleaning products, or chemical spills (RR=3.3, 95% CI 1.0-11.1, p=0.051). The population-attributable risk for adult asthma due to occupational exposures ranged from 10% to 25%, equivalent to an incidence of new-onset occupational asthma of 250-300 cases per million people per year.\n\nINTERPRETATION:\nOccupational exposures account for a substantial proportion of adult asthma incidence. The increased risk of asthma after inhalation accidents suggests that workers who have such accidents should be monitored closely." + }, + "questions": [ + { + "id": "35c20df6-db92-46ff-a45f-fbb60e117ee8", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1013, + "text": "exposure to substances known to cause occupational asthma" + }, + { + "answer_start": 1306, + "text": "nursing" + }, + { + "answer_start": 1373, + "text": "participants who reported an acute symptomatic inhalation event such as fire, mixing cleaning products, or chemical spills" + }, + { + "answer_start": 1759, + "text": "Occupational exposures" + } + ] + } + ] +} \ No newline at end of file diff --git a/939abdc2-e40e-4fbb-93ee-e15ee3979f7a.json b/939abdc2-e40e-4fbb-93ee-e15ee3979f7a.json new file mode 100644 index 0000000000000000000000000000000000000000..a05216b43ffb0b892f95341ec322e7fe8ac4a74d --- /dev/null +++ b/939abdc2-e40e-4fbb-93ee-e15ee3979f7a.json @@ -0,0 +1,47 @@ +{ + "id": "939abdc2-e40e-4fbb-93ee-e15ee3979f7a", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "28085997", + "text": "OBJECTIVE:\nTo investigate whether menopausal factors are associated with the development of serologic rheumatoid arthritis (RA) phenotypes.\n\nMETHODS:\nData were analyzed from the Nurses' Health Studies (NHS; 1976-2010 and NHSII 1989-2011). A total of 120,700 female nurses ages 30-55 years in the NHS, and a total of 116,430 female nurses ages 25-42 years in the NHSII, were followed via biennial questionnaires on lifestyle and disease outcomes. In total, 1,096 incident RA cases were confirmed by questionnaire and chart review. Seropositive RA was defined as rheumatoid factor positive (RF) or antibodies to citrullinated protein antigen (ACPA) positive, and seronegative RA was defined as RF negative and ACPA negative. We used Cox proportional hazards models to obtain multivariable-adjusted hazard ratios (HRs) with 95% confidence intervals (95% CIs) of seropositive/seronegative RA associated with menopausal status, age at menopause, type of menopause, ovulatory years, and postmenopausal hormone therapy (PMH) use.\n\nRESULTS:\nPostmenopausal women had a 2-fold increased risk of seronegative RA, compared with premenopausal women (NHS: HR 1.8 [95% CI 1.1-3.0], NHSII: HR 2.4 [95% CI 1.4-3.9], and pooled HR 2.1 [95% CI 1.4-3.0]). Natural menopause at early age (≤44 years) was associated with an increased risk of seronegative RA (pooled HR 2.4 [95% CI 1.5-4.0]). None of the menopausal factors was significantly associated with seropositive RA. We observed no association between PMH use and the risk of seronegative or seropositive RA, except that PMH use of ≥8 years was associated with increased risk of seropositive RA (pooled HR 1.4 [95% CI 1.1-1.9]).\n\nCONCLUSION:\nPostmenopause and natural menopause at an early age were strongly associated with seronegative RA, but only marginally with seropositive RA, suggesting potential differences in the etiology of RA subtypes." + }, + "questions": [ + { + "id": "9132d06f-1af3-4d5e-8a0b-3df516eedb8b", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 1033, + "text": "Postmenopausal women" + }, + { + "answer_start": 1236, + "text": "Natural menopause at early age (≤44 years)" + }, + { + "answer_start": 1677, + "text": "Postmenopause" + }, + { + "answer_start": 1695, + "text": "natural menopause at an early age" + } + ] + } + ] +} \ No newline at end of file diff --git a/93aa8d3c-01e0-4996-93cb-1fdd7f979386.json b/93aa8d3c-01e0-4996-93cb-1fdd7f979386.json new file mode 100644 index 0000000000000000000000000000000000000000..48296108f69f3f1bdbb39e8291d1aeb3d4df7363 --- /dev/null +++ b/93aa8d3c-01e0-4996-93cb-1fdd7f979386.json @@ -0,0 +1,38 @@ +{ + "id": "93aa8d3c-01e0-4996-93cb-1fdd7f979386", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "26215765", + "text": "BACKGROUND:\nVariability of blood pressure (BP) across outpatient visits is frequently dismissed as random fluctuation around a patient's underlying BP.\n\nOBJECTIVE:\nTo examine the association of visit-to-visit variability (VVV) of systolic BP (SBP) and diastolic BP with cardiovascular disease (CVD) and mortality outcomes.\n\nDESIGN:\nProspective cohort study.\n\nSETTING:\nPost hoc analysis of ALLHAT (Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial).\n\nPARTICIPANTS:\n25 814 ALLHAT participants.\n\nMEASUREMENTS:\nThe VVV of SBP was defined as the SD across SBP measurements obtained at 7 visits conducted from 6 to 28 months after ALLHAT enrollment. Participants without CVD events during the first 28 months of follow-up were followed from the 28-month visit through the end of active ALLHAT follow-up. Outcomes included fatal coronary heart disease (CHD) or nonfatal myocardial infarction, all-cause mortality, stroke, and heart failure.\n\nRESULTS:\nDuring follow-up, 1194 fatal CHD or nonfatal MI events, 1948 deaths, 606 strokes, and 921 heart failure events occurred. After multivariable adjustment, including for mean SBP, the hazard ratio comparing participants in the highest versus lowest quintile of SD of SBP (≥14.4 mm Hg vs. \u003c6.5 mm Hg) was 1.30 (95% CI, 1.06 to 1.59) for fatal CHD or nonfatal MI, 1.58 (CI, 1.32 to 1.90) for all-cause mortality, 1.46 (CI, 1.06 to 2.01) for stroke, and 1.25 (CI, 0.97 to 1.61) for heart failure. Higher VVV of diastolic BP was also associated with CVD events and mortality.\n\nLIMITATION:\nLong-term outcomes were not available.\n\nCONCLUSION:\nHigher VVV of SBP is associated with an increased risk for CVD and mortality. Future studies should examine whether reducing VVV of BP lowers this risk.\n\nPRIMARY FUNDING SOURCE:\nNational Institutes of Health." + }, + "questions": [ + { + "id": "bdc8d032-c629-4ff5-a08c-78a19ae594cc", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1604, + "text": "Higher VVV of SBP" + }, + { + "answer_start": 1461, + "text": "Higher VVV of diastolic BP" + } + ] + } + ] +} \ No newline at end of file diff --git a/93d565da-3d6b-4094-ae4d-1e2a2fcf4593.json b/93d565da-3d6b-4094-ae4d-1e2a2fcf4593.json new file mode 100644 index 0000000000000000000000000000000000000000..cd4a13d24b7e7e9a47b732326a14daab0a5cf68f --- /dev/null +++ b/93d565da-3d6b-4094-ae4d-1e2a2fcf4593.json @@ -0,0 +1,40 @@ +{ + "id": "93d565da-3d6b-4094-ae4d-1e2a2fcf4593", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "19364790", + "text": "BACKGROUND:\nOur aim was to determine the combined and independent effects of tobacco and marijuana smoking on respiratory symptoms and chronic obstructive pulmonary disease (COPD) in the general population.\n\nMETHOD:\nWe surveyed a random sample of 878 people aged 40 years or older living in Vancouver, Canada, about their respiratory history and their history of tobacco and marijuana smoking. We performed spirometric testing before and after administration of 200 microg of salbutamol. We examined the association between tobacco and marijuana smoking and COPD.\n\nRESULTS:\nThe prevalence of a history of smoking in this sample was 45.5% (95% confidence interval [CI] 42.2%-48.8%) for marijuana use and 53.1% (95% CI 49.8%-56.4%) for tobacco use. The prevalence of current smoking (in the past 12 months) was 14% for marijuana use and 14% for tobacco use. Compared with nonsmokers, participants who reported smoking only tobacco, but not those who reported smoking only marijuana, experienced more frequent respiratory symptoms (odds ratio [OR] 1.50, 95% CI 1.05-2.14) and were more likely to have COPD (OR 2.74, 95% CI 1.66-4.52). Concurrent use of marijuana and tobacco was associated with increased risk (adjusted for age, asthma and comorbidities) of respiratory symptoms (OR 2.39, 95% CI 1.58-3.62) and COPD (OR 2.90, 95% CI 1.53-5.51) if the lifetime dose of marijuana exceeded 50 marijuana cigarettes. The risks of respiratory symptoms and of COPD were related to a synergistic interaction between marijuana and tobacco.\n\nINTERPRETATION:\nSmoking both tobacco and marijuana synergistically increased the risk of respiratory symptoms and COPD. Smoking only marijuana was not associated with an increased risk of respiratory symptoms or COPD." + }, + "questions": [ + { + "id": "7abd6977-a9ff-4f77-b693-44270d84f913", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 1132, + "text": "Concurrent use of marijuana and tobacco" + }, + { + "answer_start": 1545, + "text": "Smoking both tobacco and marijuana synergistically" + } + ] + } + ] +} \ No newline at end of file diff --git a/945ae384-f784-41f7-bd4a-8b7562e5c7b3.json b/945ae384-f784-41f7-bd4a-8b7562e5c7b3.json new file mode 100644 index 0000000000000000000000000000000000000000..c80c7a6c5c8c8b4e3e1e2d015ca5235e4debf79d --- /dev/null +++ b/945ae384-f784-41f7-bd4a-8b7562e5c7b3.json @@ -0,0 +1,38 @@ +{ + "id": "945ae384-f784-41f7-bd4a-8b7562e5c7b3", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "32353313", + "text": "BACKGROUND:\nEvidence is emerging for a role of opiates in various cancers. In this study, we aimed to investigate the association between regular opium use and cancer incidence.\n\nMETHODS:\nThis study was done in a population-based cohort of 50 045 individuals aged 40-75 years from northeast Iran. Data on participant demographics, diet, lifestyle, opium use, and different exposures were collected upon enrolment using validated questionnaires. We used proportional hazards regression models to estimate hazard ratios (HRs) and corresponding 95% CIs for the association between opium use and different cancer types.\n\nFINDINGS:\nDuring a median 10 years of follow-up, 1833 participants were diagnosed with cancer. Use of opium was associated with an increased risk of developing all cancers combined (HR 1·40, 95% CI 1·24-1·58), gastrointestinal cancers (1·31, 1·11-1·55), and respiratory cancers (2·28, 1·58-3·30) in a dose-dependent manner (p\u003c0·001). For site-specific cancers, use of opium was associated with an increased risk of developing oesophageal (1·38, 1·06-1·80), gastric (1·36, 1·03-1·79), lung (2·21, 1·44-3·39), bladder (2·86, 1·47-5·55), and laryngeal (2·53, 1·21-5·29) cancers in a dose-dependent manner (p\u003c0·05). Only high-dose opium use was associated with pancreatic cancer (2·66, 1·23-5·74). Ingestion of opium (but not smoking opium) was associated with brain (2·15, 1·00-4·63) and liver (2·46, 1·23-4·95) cancers in a dose-dependent manner (p\u003c0·01). We observed consistent associations among ever and never tobacco users, men and women, and individuals with lower and higher socioeconomic status.\n\nINTERPRETATION:\nOpium users have a significantly higher risk of developing cancers in different organs of the respiratory, digestive, and urinary systems and the CNS. The results of this analysis show that regular use of opiates might increase the risk of a range of cancer types.\n\nFUNDING:\nWorld Cancer Research Fund International, Cancer Research UK, Tehran University of Medical Sciences, US National Cancer Institute, International Agency for Research on Cancer." + }, + "questions": [ + { + "id": "c43e916e-8bc9-4553-a154-d7930758eb07", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 712, + "text": "Use of opium" + }, + { + "answer_start": 1635, + "text": "Opium users" + } + ] + } + ] +} \ No newline at end of file diff --git a/9482eaf5-34f4-44f4-a5ad-74d417d8bd83.json b/9482eaf5-34f4-44f4-a5ad-74d417d8bd83.json new file mode 100644 index 0000000000000000000000000000000000000000..88cc65af49df7a1e75a23edc1138c8cb48e797f5 --- /dev/null +++ b/9482eaf5-34f4-44f4-a5ad-74d417d8bd83.json @@ -0,0 +1,50 @@ +{ + "id": "9482eaf5-34f4-44f4-a5ad-74d417d8bd83", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "15601642", + "text": "BACKGROUND:\nLevels of endogenous hormones have been associated with the risk of breast cancer among postmenopausal women. Little research, however, has investigated the association between hormone levels and tumor receptor status or invasive versus in situ tumor status. Nor has the relation between breast cancer risk and postmenopausal progesterone levels been investigated. We prospectively investigated these relations in a case-control study nested within the Nurses' Health Study.\n\nMETHODS:\nBlood samples were prospectively collected during 1989 and 1990. Among eligible postmenopausal women, 322 cases of breast cancer (264 invasive, 41 in situ, 153 estrogen receptor [ER]-positive and progesterone receptor [PR]-positive [ER+/PR+], and 39 ER-negative and PR-negative [ER-/PR-] disease) were reported through June 30, 1998. For each case subject, two control subjects (n = 643) were matched on age and blood collection (by month and time of day). Endogenous hormone levels were measured in blood plasma. We used conditional and unconditional logistic regression analyses to assess associations and to control for established breast cancer risk factors.\n\nRESULTS:\nWe observed a statistically significant direct association between breast cancer risk and the level of both estrogens and androgens, but we did not find any (by year) statistically significant associations between this risk and the level of progesterone or sex hormone binding globulin. When we restricted the analysis to case subjects with ER+/PR+ tumors and compared the highest with the lowest fourths of plasma hormone concentration, we observed an increased risk of breast cancer associated with estradiol (relative risk [RR] = 3.3, 95% confidence interval [CI] = 2.0 to 5.4), testosterone (RR = 2.0, 95% CI = 1.2 to 3.4), androstenedione (RR = 2.5, 95% CI = 1.4 to 4.3), and dehydroepiandrosterone sulfate (RR = 2.3, 95% CI = 1.3 to 4.1). In addition, all hormones tended to be associated most strongly with in situ disease.\n\nCONCLUSION:\nCirculating levels of sex steroid hormones may be most strongly associated with risk of ER+/PR+ breast tumors." + }, + "questions": [ + { + "id": "e1f906fb-537f-4eb9-ab04-b2c4bda77598", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1671, + "text": "estradiol" + }, + { + "answer_start": 1752, + "text": "testosterone" + }, + { + "answer_start": 1798, + "text": "androstenedione" + }, + { + "answer_start": 1851, + "text": "dehydroepiandrosterone sulfate" + }, + { + "answer_start": 2014, + "text": "Circulating levels of sex steroid hormones" + } + ] + } + ] +} \ No newline at end of file diff --git a/94e2e099-7a0a-4b2e-ab23-531ac54452bc.json b/94e2e099-7a0a-4b2e-ab23-531ac54452bc.json new file mode 100644 index 0000000000000000000000000000000000000000..6134869ab86c52084d0f2c0974ff55b140ea20af --- /dev/null +++ b/94e2e099-7a0a-4b2e-ab23-531ac54452bc.json @@ -0,0 +1,34 @@ +{ + "id": "94e2e099-7a0a-4b2e-ab23-531ac54452bc", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "29941778", + "text": "Celiac disease is a small intestinal inflammatory disease with autoimmune features that is triggered and maintained by the ingestion of the storage proteins (gluten) of wheat, barley, and rye. Prevalence of celiac disease is increased in patients with mono- and/or polyglandular autoimmunity and their relatives. We have reviewed the current and pertinent literature that addresses the close association between celiac disease and endocrine autoimmunity. The close relationship between celiac disease and glandular autoimmunity can be largely explained by sharing of a common genetic background. Further, between 10 and 30% of patients with celiac disease are thyroid and/or type 1 diabetes antibody positive, while around 5⁻7% of patients with autoimmune thyroid disease, type 1 diabetes, and/or polyglandular autoimmunity are IgA anti-tissue transglutaminase antibody positive. While a gluten free diet does not reverse glandular autoimmunity, its early institution may delay or even prevent its first manifestation. In conclusion, this brief review highlighting the close association between celiac disease and both monoglandular and polyglandular autoimmunity, aims to underline the need for prospective studies to establish whether an early diagnosis of celiac disease and a prompt gluten-free diet may positively impact the evolution and manifestation of glandular autoimmunity." + }, + "questions": [ + { + "id": "8fd2694a-a6b5-47b7-81e3-c42f95f36c36", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 1119, + "text": "monoglandular and polyglandular autoimmunity" + } + ] + } + ] +} \ No newline at end of file diff --git a/95cc46ee-0b57-4e09-ba58-a52c125e9944.json b/95cc46ee-0b57-4e09-ba58-a52c125e9944.json new file mode 100644 index 0000000000000000000000000000000000000000..ddccd9a5d75f7f0c22e02dac97310230eb1384b0 --- /dev/null +++ b/95cc46ee-0b57-4e09-ba58-a52c125e9944.json @@ -0,0 +1,46 @@ +{ + "id": "95cc46ee-0b57-4e09-ba58-a52c125e9944", + "disease": { + "id": "H00408", + "names": [ + "Type 1 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E10" + ], + "mesh": [ + "D003922" + ] + }, + "category": "Metabolic disease; Immune system disease; Endocrine disease" + }, + "article": { + "id": "15677782", + "text": "OBJECTIVE:\nFamilies of children diagnosed with type 1 diabetes require counseling concerning type 1 diabetes risk in nondiabetic siblings and parents. No U.S. population-specific life-table risk estimates are currently available for parents, and those for siblings (2-6% by age 20 years) are based on family studies completed before 1987.\n\nRESEARCH DESIGN AND METHODS:\nWe analyzed family histories of 1,586 patients in Colorado with type 1 diabetes (83% non-Hispanic white, 10% Hispanic, and 7% other) diagnosed before 16 years of age and interviewed during 1999-2002. Families of probands with type 2, undetermined, or secondary diabetes (n = 53) or those with incomplete data (n = 137) were excluded. The median age at onset of the proband was 7.1 years and the median diabetes duration 3.5 years. Cumulative risk estimates were calculated using survival analysis for 2,081 full siblings and 3,016 biological parents.\n\nRESULTS:\nIn siblings, the overall risk of type 1 diabetes by age 20 years was 4.4%, but it was significantly (P \u003c 0.0001) higher in siblings of probands diagnosed under age 7 years than in those diagnosed later. In parents, the overall risk by age 40 years was 2.6% and higher in fathers (3.6%) than in mothers (1.7%) of probands (P \u003c 0.001). Similar to siblings, the risk was also higher (P = 0.006) in parents of probands diagnosed \u003c7 years of age than in those diagnosed later.\n\nCONCLUSIONS:\nCurrent risks of type 1 diabetes in Colorado siblings and parents of type 1 diabetic probands are higher than in the 1982 Pittsburgh study but similar to contemporary European rates. Recurrence risk of type 1 diabetes is significantly higher in first-degree relatives of probands diagnosed at a young age." + }, + "questions": [ + { + "id": "aa6e7160-4e94-48da-a18e-6a2bf00628a4", + "text": "What are the risk factors of Type 1 diabetes mellitus?", + "answers": [ + { + "answer_start": 933, + "text": "siblings" + }, + { + "answer_start": 1053, + "text": "siblings of probands diagnosed under age 7 years" + }, + { + "answer_start": 1325, + "text": "parents of probands diagnosed \u003c7 years of age" + }, + { + "answer_start": 1661, + "text": "first-degree relatives of probands diagnosed at a young age" + } + ] + } + ] +} \ No newline at end of file diff --git a/95d70c05-bbdd-41d1-9ed7-1f2a68f336f3.json b/95d70c05-bbdd-41d1-9ed7-1f2a68f336f3.json new file mode 100644 index 0000000000000000000000000000000000000000..119d14c9a0f2ba89ce48ec3589787e2aeea1580f --- /dev/null +++ b/95d70c05-bbdd-41d1-9ed7-1f2a68f336f3.json @@ -0,0 +1,38 @@ +{ + "id": "95d70c05-bbdd-41d1-9ed7-1f2a68f336f3", + "disease": { + "id": "H00408", + "names": [ + "Type 1 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E10" + ], + "mesh": [ + "D003922" + ] + }, + "category": "Metabolic disease; Immune system disease; Endocrine disease" + }, + "article": { + "id": "34427600", + "text": "IMPORTANCE:\nChanges in the prevalence of youth-onset diabetes have previously been observed.\n\nOBJECTIVE:\nTo estimate changes in prevalence of type 1 and type 2 diabetes in youths in the US from 2001 to 2017.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nIn this cross-sectional observational study, individuals younger than 20 years with physician-diagnosed diabetes were enumerated from 6 areas in the US (4 geographic areas, 1 health plan, and select American Indian reservations) for 2001, 2009, and 2017.\n\nEXPOSURES:\nCalendar year.\n\nMAIN OUTCOMES AND MEASURES:\nEstimated prevalence of physician-diagnosed type 1 and type 2 diabetes overall and by race and ethnicity, age, and sex.\n\nRESULTS:\nAmong youths 19 years or younger, 4958 of 3.35 million had type 1 diabetes in 2001, 6672 of 3.46 million had type 1 diabetes in 2009, and 7759 of 3.61 million had type 1 diabetes in 2017; among those aged 10 to 19 years, 588 of 1.73 million had type 2 diabetes in 2001, 814 of 1.85 million had type 2 diabetes in 2009, and 1230 of 1.85 million had type 2 diabetes in 2017. The estimated type 1 diabetes prevalence per 1000 youths for those 19 years or younger increased significantly from 1.48 (95% CI, 1.44-1.52) in 2001 to 1.93 (95% CI, 1.88-1.98) in 2009 to 2.15 (95% CI, 2.10-2.20) in 2017, an absolute increase of 0.67 per 1000 youths (95%, CI, 0.64-0.70) and a 45.1% (95% CI, 40.0%-50.4%) relative increase over 16 years. The greatest absolute increases were observed among non-Hispanic White (0.93 per 1000 youths [95% CI, 0.88-0.98]) and non-Hispanic Black (0.89 per 1000 youths [95% CI, 0.88-0.98]) youths. The estimated type 2 diabetes prevalence per 1000 youths aged 10 to 19 years increased significantly from 0.34 (95% CI, 0.31-0.37) in 2001 to 0.46 (95% CI, 0.43-0.49) in 2009 to 0.67 (95% CI, 0.63-0.70) in 2017, an absolute increase of 0.32 per 1000 youths (95% CI, 0.30-0.35) and a 95.3% (95% CI, 77.0%-115.4%) relative increase over 16 years. The greatest absolute increases were observed among non-Hispanic Black (0.85 per 1000 youths [95% CI, 0.74-0.97]) and Hispanic (0.57 per 1000 youths [95% CI, 0.51-0.64]) youths.\n\nCONCLUSIONS AND RELEVANCE:\nIn 6 areas of the US from 2001 to 2017, the estimated prevalence of diabetes among children and adolescents increased for both type 1 and type 2 diabetes." + }, + "questions": [ + { + "id": "a8861a4e-4602-4133-ad60-c9d89f011d55", + "text": "What are the risk factors of Type 1 diabetes mellitus?", + "answers": [ + { + "answer_start": 1465, + "text": "non-Hispanic White" + }, + { + "answer_start": 1531, + "text": "non-Hispanic Black" + } + ] + } + ] +} \ No newline at end of file diff --git a/960c4326-53f2-4eac-a81b-a8d3bd469f3a.json b/960c4326-53f2-4eac-a81b-a8d3bd469f3a.json new file mode 100644 index 0000000000000000000000000000000000000000..41140670788f1d451a5f9689ff2b3477f15e999c --- /dev/null +++ b/960c4326-53f2-4eac-a81b-a8d3bd469f3a.json @@ -0,0 +1,49 @@ +{ + "id": "960c4326-53f2-4eac-a81b-a8d3bd469f3a", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "21068432", + "text": "BACKGROUND:\nAndrogen deprivation with gonadotropin-releasing hormone (GnRH) agonists or orchiectomy is a common but controversial treatment for prostate cancer. Uncertainties remain about its use, particularly with increasing recognition of serious side effects. In animal studies, androgens protect against colonic carcinogenesis, suggesting that androgen deprivation may increase the risk of colorectal cancer.\n\nMETHODS:\nWe identified 107 859 men in the linked Surveillance, Epidemiology, and End Results (SEER)-Medicare database who were diagnosed with prostate cancer in 1993 through 2002, with follow-up available through 2004. The primary outcome was development of colorectal cancer, determined from SEER files on second primary cancers. Cox proportional hazards regression was used to assess the influence of androgen deprivation on the outcome, adjusted for patient and prostate cancer characteristics. All statistical tests were two-sided.\n\nRESULTS:\nMen who had orchiectomies had the highest unadjusted incidence rate of colorectal cancer (6.3 per 1000 person-years; 95% confidence interval [CI] = 5.3 to 7.5), followed by men who had GnRH agonist therapy (4.4 per 1000 person-years; 95% CI = 4.0 to 4.9), and men who had no androgen deprivation (3.7 per 1000 person-years; 95% CI = 3.5 to 3.9). After adjustment for patient and prostate cancer characteristics, there was a statistically significant dose-response effect (P(trend) = .010) with an increasing risk of colorectal cancer associated with increasing duration of androgen deprivation. Compared with the absence of these treatments, there was an increased risk of colorectal cancer associated with use of GnRH agonist therapy for 25 months or longer (hazard ratio [HR] = 1.31, 95% CI = 1.12 to 1.53) or with orchiectomy (HR = 1.37, 95% CI = 1.14 to 1.66).\n\nCONCLUSION:\nLong-term androgen deprivation therapy for prostate cancer is associated with an increased risk of colorectal cancer." + }, + "questions": [ + { + "id": "27a77c67-8141-4ba2-89e6-2d157468eb9f", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1510, + "text": "increasing duration of androgen deprivation" + }, + { + "answer_start": 1667, + "text": "use of GnRH agonist therapy for 25 months or longer" + }, + { + "answer_start": 1777, + "text": "orchiectomy" + }, + { + "answer_start": 1838, + "text": "Long-term androgen deprivation therapy for prostate cancer" + } + ] + } + ] +} \ No newline at end of file diff --git a/96869432-0d86-459b-b983-95a3d57d62c6.json b/96869432-0d86-459b-b983-95a3d57d62c6.json new file mode 100644 index 0000000000000000000000000000000000000000..ceef04af23cd5dbb1a2a86996d4c3e5bbabfb925 --- /dev/null +++ b/96869432-0d86-459b-b983-95a3d57d62c6.json @@ -0,0 +1,39 @@ +{ + "id": "96869432-0d86-459b-b983-95a3d57d62c6", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "21620689", + "text": "A number of studies have focused on possible relationships between characteristics of female endocrine status and melanoma (CM) risk; however, the link between melanoma, oral contraceptive (OC) and hormonal replacement therapy (HRT) use, and reproductive factors remains controversial. A comprehensive, systematic bibliographic search of the medical literature was conducted to identify relevant studies. Random effects models were used to summarise results. Subgroup, meta-regression and sensitivity analyses have been carried out to explore sources of between-study variation and bias. We included thirty-six observational studies published in the last 30 years. Summarising a total of 5626 melanoma cases, we did not find any significant melanoma risk associated with OC and HRT use. Several reproductive factors were also investigated, summarising data on 16787 melanoma cases. We found a significantly increased melanoma risk for late age at first birth, and women with more than one child may be at a lower risk for melanoma; however, socio-economic confounders were found to play a significant role in explaining this association. This study confirmed no increased risk of CM with the use of oral contraceptives and hormone replacement therapy: exogenous female hormones do not contribute to an increased risk of CM. In contrast, significant associations of CM with parity and age at first pregnancy were observed in this meta-analysis finds and warrant further research." + }, + "questions": [ + { + "id": "143047bc-19e2-467c-a0fc-5586b26ec9fe", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 935, + "text": "late age at first birth" + }, + { + "answer_start": 1373, + "text": "parity and age at first pregnancy" + } + ] + } + ] +} \ No newline at end of file diff --git a/96b96570-4972-491d-ac4e-9df75a931e43.json b/96b96570-4972-491d-ac4e-9df75a931e43.json new file mode 100644 index 0000000000000000000000000000000000000000..2ef451f9bc5be3a83f3d3ae65e1f37a4a977cdfe --- /dev/null +++ b/96b96570-4972-491d-ac4e-9df75a931e43.json @@ -0,0 +1,39 @@ +{ + "id": "96b96570-4972-491d-ac4e-9df75a931e43", + "disease": { + "id": "H00056", + "names": [ + "Alzheimer disease", + "Dementia due to Alzheimer disease" + ], + "dbLinks": { + "icd10": [ + "G30" + ], + "mesh": [ + "D000544" + ] + }, + "category": "Neurodegenerative disease" + }, + "article": { + "id": "24473795", + "text": "IMPORTANCE:\nThe causes of late-onset Alzheimer disease (AD) are not yet understood but likely include a combination of genetic, environmental, and lifestyle factors. Limited epidemiological studies suggest that occupational pesticide exposures are associated with AD. Previously, we reported that serum levels of dichlorodiphenyldichloroethylene (DDE), the metabolite of the pesticide dichlorodiphenyltrichloroethane (DDT), were elevated in a small number of patients with AD (n=20).\n\nOBJECTIVE:\nTo evaluate the association between serum levels of DDE and AD and whether the apolipoprotein E (APOE) genotype modifies the association.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nA case-control study consisting of existing samples from patients with AD and control participants from the Emory University Alzheimer's Disease Research Center and the University of Texas Southwestern Medical School's Alzheimer's Disease Center. Serum levels of DDE were measured in 79 control and 86 AD cases.\n\nMAIN OUTCOMES AND MEASURES:\nSerum DDE levels, AD diagnosis, severity of AD measured by the Mini-Mental State Examination score, and interaction with APOE4 status.\n\nRESULTS:\nLevels of DDE were 3.8-fold higher in the serum of those with AD (mean [SEM], 2.64 [0.35] ng/mg cholesterol) when compared with control participants (mean [SEM], 0.69 [0.1] ng/mg cholesterol; P \u003c .001). The highest tertile of DDE levels was associated with an odds ratio of 4.18 for increased risk for AD (95% CI, 2.54-5.82; P \u003c .001) and lower Mini-Mental State Examination scores (-1.605; range, -3.095 to -0.114; P \u003c .0001). The Mini-Mental State Examination scores in the highest tertile of DDE were -1.753 points lower in the subpopulation carrying an APOE ε4 allele compared with those carrying an APOE ε3 allele (P interaction = .04). Serum levels of DDE were highly correlated with brain levels of DDE (ρ = 0.95). Exposure of human neuroblastoma cells to DDT or DDE increased levels of amyloid precursor protein.\n\nCONCLUSIONS AND RELEVANCE:\nElevated serum DDE levels are associated with an increased risk for AD and carriers of an APOE4 ε4 allele may be more susceptible to the effects of DDE. Both DDT and DDE increase amyloid precursor protein levels, providing mechanistic plausibility for the association of DDE exposure with AD. Identifying people who have elevated levels of DDE and carry an APOE ε4 allele may lead to early identification of some cases of AD." + }, + "questions": [ + { + "id": "afed5cd1-40d0-4243-80b0-5c912db2337b", + "text": "What are the risk factors of Alzheimer disease?", + "answers": [ + { + "answer_start": 2326, + "text": "elevated levels of DDE" + }, + { + "answer_start": 1798, + "text": "Serum levels of DDE" + } + ] + } + ] +} \ No newline at end of file diff --git a/9780d047-b10e-4cd0-b1ab-f09e4e001890.json b/9780d047-b10e-4cd0-b1ab-f09e4e001890.json new file mode 100644 index 0000000000000000000000000000000000000000..1162ca5acda57396d313f16815ff95635145fbb8 --- /dev/null +++ b/9780d047-b10e-4cd0-b1ab-f09e4e001890.json @@ -0,0 +1,36 @@ +{ + "id": "9780d047-b10e-4cd0-b1ab-f09e4e001890", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "19608716", + "text": "RATIONALE:\nChronic obstructive pulmonary disease (COPD) is a complex disorder with high mortality worldwide. Studies on the role of candidate genes and their polymorphisms in COPD development have so far produced ambiguous results.\n\nOBJECTIVES:\nThe aim of this study was to reveal the role of COPD candidate genes using data collected in previous research.\n\nMETHODS:\nWe performed meta-analyses on 20 polymorphisms in 12 genes, after searching the PubMed and Embase databases for publications on COPD. These genes involve three main pathways associated with COPD development: the inflammatory, protease-antiprotease balance, and antioxidant pathways.\n\nMEASUREMENTS AND MAIN RESULTS:\nWe obtained significant results for three TGFB1 polymorphisms, although these were based only on a few studies. The IL1RN VNTR polymorphism increases the risk for COPD (odds ratio [OR], 1.7; 95% confidence interval [CI], 1.09-2.65), whereas the TNFA -308 G/A polymorphism does so only in Asian populations (OR, 2.01; 95% CI, 1.21-3.31). The GSTP1 I105V polymorphism was protective for COPD in Asian populations only (OR, 0.69; 95% CI, 0.56-0.85).\n\nCONCLUSIONS:\nThese results demonstrate the importance of ethnicity in identifying specific COPD genes." + }, + "questions": [ + { + "id": "fbc27786-f536-44f0-94d9-f14c7256ab6b", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 798, + "text": "IL1RN VNTR polymorphism" + } + ] + } + ] +} \ No newline at end of file diff --git a/981a5c89-9c32-4c6d-802c-6f8fac3717dc.json b/981a5c89-9c32-4c6d-802c-6f8fac3717dc.json new file mode 100644 index 0000000000000000000000000000000000000000..acecdf6431ce9417404a34c7375e3c1796490153 --- /dev/null +++ b/981a5c89-9c32-4c6d-802c-6f8fac3717dc.json @@ -0,0 +1,47 @@ +{ + "id": "981a5c89-9c32-4c6d-802c-6f8fac3717dc", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "24629998", + "text": "BACKGROUND:\nTanning beds are associated with increased risk of melanoma.\n\nOBJECTIVE:\nWe sought to update the evidence of the association of melanoma and indoor tanning focusing on frequency of use and exposure to newer tanning beds.\n\nMETHODS:\nWe searched Scopus, MEDLINE, and Cumulative Index to Nursing and Allied Health Literature on August 14, 2013. We included all observational studies that included patients with melanoma who had indoor tanned. Odds ratios (OR) with 95% confidence intervals (CI) were extracted and combined using generic inverse variance methods assuming a random effects model.\n\nRESULTS:\nIn all, 31 studies were included with data available on 14,956 melanoma cases and 233,106 controls. Compared with never using, the OR for melanoma associated with ever using indoor tanning beds was 1.16 (95% CI 1.05-1.28). Similar findings were identified in recent studies with enrollment occurring in the year 2000 onward (OR 1.22, 95% CI 1.03-1.45) and in subjects attending more than 10 tanning sessions (OR 1.34, 95% CI 1.05-1.71).\n\nLIMITATIONS:\nThe quality of evidence contributing to review results ranges from poor to mediocre.\n\nCONCLUSION:\nUsing tanning beds is associated with a subsequent melanoma diagnosis. Exposure from more than 10 tanning sessions is most strongly associated and there was no statistically significant difference in this association before and after 2000, suggesting that newer tanning technology is not safer than older models." + }, + "questions": [ + { + "id": "a11ecf8b-ba66-49cb-9a87-30cb707133db", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 775, + "text": " ever using indoor tanning beds" + }, + { + "answer_start": 981, + "text": "attending more than 10 tanning sessions" + }, + { + "answer_start": 1162, + "text": "Using tanning beds" + }, + { + "answer_start": 1233, + "text": "Exposure from more than 10 tanning sessions" + } + ] + } + ] +} \ No newline at end of file diff --git a/985228b2-fdff-4608-b274-7b6589c0709d.json b/985228b2-fdff-4608-b274-7b6589c0709d.json new file mode 100644 index 0000000000000000000000000000000000000000..b29a1e9e8342309c0b0254ac98a437064494d77c --- /dev/null +++ b/985228b2-fdff-4608-b274-7b6589c0709d.json @@ -0,0 +1,35 @@ +{ + "id": "985228b2-fdff-4608-b274-7b6589c0709d", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "21338428", + "text": "BACKGROUND:\nThere is evidence to suggest that the risk of asthma might be increased with exposure to paracetamol in the intrauterine environment, infancy, later childhood and adult life.\n\nOBJECTIVE:\nTo review the evidence from studies investigating the association between paracetamol use in pregnancy and childhood asthma.\n\nMETHODS:\nA systematic review and meta-analysis was undertaken of studies reporting the association between paracetamol use in pregnancy and subsequent asthma in childhood. The primary outcome variable was wheeze in the last 12 months. For tabulated raw data, not adjusted for confounders, random effects odds ratios (OR) were pooled by the inverse variance weighted method.\n\nRESULTS:\nThere were six studies identified that were included in the meta-analysis. The age of children studied ranged from 30 to 84 months. The pooled random effects OR for the risk of current wheeze in the children of women who were exposed to any paracetamol during any stage of pregnancy was 1.21 (95% confidence interval 1.02-1.44). Features of the studies variably included an association with paracetamol use during all trimesters of pregnancy and an association with persistent asthma, severe asthma, and with atopy.\n\nCONCLUSION AND CLINICAL RELEVANCE:\nThe use of paracetamol during pregnancy is associated with an increased risk of childhood asthma. More research is urgently required to determine the impact of paracetamol during pregnancy on the risk of wheezing in offspring so that appropriate public health recommendations can be made." + }, + "questions": [ + { + "id": "5bdcd3f0-345f-47ad-bab0-6b5b981e2765", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1265, + "text": "use of paracetamol during pregnancy" + } + ] + } + ] +} \ No newline at end of file diff --git a/990c620b-a203-422a-8ca5-a1a82d1a0054.json b/990c620b-a203-422a-8ca5-a1a82d1a0054.json new file mode 100644 index 0000000000000000000000000000000000000000..0f16010f7ad6c9fa9c132d81bf479a147caf2abc --- /dev/null +++ b/990c620b-a203-422a-8ca5-a1a82d1a0054.json @@ -0,0 +1,39 @@ +{ + "id": "990c620b-a203-422a-8ca5-a1a82d1a0054", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "25432937", + "text": "OBJECTIVE:\nTo investigate the association between exposure to antibiotics in fetal and early life and asthma in childhood, with adjustment for confounding factors.\n\nDESIGN:\nNationwide prospective population based cohort study, including sibling control design.\n\nSETTING:\nSwedish population identified from national demographic and health registers.\n\nPARTICIPANTS:\n493,785 children born 2006-10; 180,894 of these were eligible for sibling analyses.\n\nMAIN OUTCOME MEASURE:\nAsthma defined as having both an asthma diagnosis and dispensed asthma drugs. The association between antibiotic exposure and asthma was investigated in the whole cohort with Cox proportional hazard regression. A stratified proportional hazards model conditional on sibling group was used to adjust for shared factors within families. Confounding by respiratory infections was assessed by investigating whether specific groups of antibiotics were associated with asthma.\n\nRESULTS:\nAntibiotic exposure in fetal life was associated with an increased risk of asthma in cohort analyses (hazard ratio 1.28, 95% confidence interval 1.25 to 1.32), but not in sibling analyses (0.99, 0.92 to 1.07). In cohort analyses, antibiotics used to treat respiratory infections in childhood were associated with a more pronounced increased risk of asthma (4.12, 3.78 to 4.50) than antibiotics used for urinary tract and skin infections (1.54, 1.24 to 1.92). In sibling analyses, the excess risks after exposure to antibiotics for respiratory infections decreased (2.36, 1.78 to 3.13) and disappeared for antibiotics for urinary tract and skin (0.85, 0.47 to 1.55).\n\nCONCLUSIONS:\nPrevious positive associations between exposure to antibiotics in fetal and early life and subsequent childhood asthma could have been caused by confounding by shared familial factors, in addition to confounding by respiratory infections." + }, + "questions": [ + { + "id": "85658fff-0e9e-4f46-9072-03d206c3fc0f", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1182, + "text": "antibiotics used to treat respiratory infections in childhood" + }, + { + "answer_start": 952, + "text": "Antibiotic exposure in fetal life" + } + ] + } + ] +} \ No newline at end of file diff --git a/9951f864-23fb-4c97-aed8-ee2c27c2b12c.json b/9951f864-23fb-4c97-aed8-ee2c27c2b12c.json new file mode 100644 index 0000000000000000000000000000000000000000..9d81921097d10a24fb7c63bf0e2993f032474568 --- /dev/null +++ b/9951f864-23fb-4c97-aed8-ee2c27c2b12c.json @@ -0,0 +1,34 @@ +{ + "id": "9951f864-23fb-4c97-aed8-ee2c27c2b12c", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "30995175", + "text": "PURPOSE:\nPhthalate exposure is ubiquitous and especially high among users of drug products formulated with phthalates. Some phthalates mimic estradiol and may promote breast cancer. Existing epidemiologic studies on this topic are small, mostly not prospective, and have given inconsistent results. We estimated associations between longitudinal phthalate exposures and breast cancer risk in a Danish nationwide cohort, using redeemed prescriptions for phthalate-containing drug products to measure exposure.\n\nMETHODS:\nWe ascertained the phthalate content of drugs marketed in Denmark using an internal Danish Medicines Agency ingredient database. We enrolled a Danish nationwide cohort of 1.12 million women at risk for a first cancer diagnosis on January 1, 2005. By combining drug ingredient data with the Danish National Prescription registry, we characterized annual, cumulative phthalate exposure through redeemed prescriptions. We then fit multivariable Cox regression models to estimate associations between phthalate exposures and incident invasive breast carcinoma according to tumor estrogen receptor status.\n\nRESULTS:\nOver 9.99 million woman-years of follow-up, most phthalate exposures were not associated with breast cancer incidence. High-level dibutyl phthalate exposure (≥ 10,000 cumulative mg) was associated with an approximately two-fold increase in the rate of estrogen receptor-positive breast cancer (hazard ratio, 1.9; 95% CI, 1.1 to 3.5), consistent with in vitro evidence for an estrogenic effect of this compound. Lower levels of dibutyl phthalate exposure were not associated with breast cancer incidence.\n\nCONCLUSION:\nOur results suggest that women should avoid high-level exposure to dibutyl phthalate, such as through long-term treatment with pharmaceuticals formulated with dibutyl phthalate." + }, + "questions": [ + { + "id": "04dc16c1-e09b-4372-8aef-d4c91dde1e2a", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1249, + "text": "High-level dibutyl phthalate exposure (≥ 10,000 cumulative mg)" + } + ] + } + ] +} \ No newline at end of file diff --git a/995c904e-fdb0-4022-ad62-91391b0baf1f.json b/995c904e-fdb0-4022-ad62-91391b0baf1f.json new file mode 100644 index 0000000000000000000000000000000000000000..b526b5d009f686e0c0c3cae9b92d602fb9ce6523 --- /dev/null +++ b/995c904e-fdb0-4022-ad62-91391b0baf1f.json @@ -0,0 +1,41 @@ +{ + "id": "995c904e-fdb0-4022-ad62-91391b0baf1f", + "disease": { + "id": "M2023_04_26_16_38_52", + "names": [ + "Migraine" + ], + "dbLinks": { + "icd10": [ + "G43" + ], + "icd11": [ + "8A80" + ], + "mesh": [ + "C10.228.140.546.399.750" + ] + }, + "description": "Migraine is a chronic neurological disorder characterized by recurrent episodes of unilateral, pulsatile headaches associated with autonomic symptoms such as nausea, vomiting, photophobia, and phonophobia. The pathophysiology of migraine is multifactorial and involves complex interactions between genetic, environmental, and neurochemical factors that modulate cerebral vascular tone and nociception. Migraine attacks can be triggered by a variety of factors, including stress, hormonal changes, sleep disturbances, and certain foods or medications. Treatment options for migraine include pharmacotherapy for acute attacks, preventive medications for frequent or severe headaches, and lifestyle modifications to avoid triggers. In refractory cases, interventional therapies such as nerve blocks or neuromodulation techniques may be considered." + }, + "article": { + "id": "16864817", + "text": "OBJECTIVE:\nTo assess the influence of the body mass index (BMI) on the prevalence and severity of chronic daily headache (CDH) and its most frequent subtypes, transformed migraine (TM) and chronic tension-type headache (CTTH).\n\nMETHODS:\nThe authors gathered information on headache, medical features, height, and weight using a computer-assisted telephone interview. Participants were divided into five categories, based on BMI: underweight (\u003c18.5), normal weight (18.5 to 24.9), overweight (25 to 29.9), obese (30 to 34.9), and morbidly obese (\u003e35). The prevalence and severity of CDH, TM, and CTTH were assessed. Multivariate analyses modeling these diagnoses as a function of BMI were conducted.\n\nRESULTS:\nAmong 30,215 participants, the prevalence of CDH was 4.1%; 1.3% had TM and 2.8% CTTH. In contrast with the normal weight group (3.9%), the prevalence of CDH was higher in obese (5.0% [odds ratio (OR) = 1.3, 95% CI = 1.1-1.6]) and morbidly obese (6.8% [OR = 1.8, 95% CI = 1.4 to 2.2]). BMI had a strong influence on the prevalence of TM, which ranged from 0.9% of the normal weighted to 1.2% of the overweight (OR = 1.4 [1.1 to 1.8]), 1.6% of the obese (OR = 1.7 [1.2 to 2.43]), and 2.5% of the morbidly obese (OR = 2.2 [1.5 to 3.2]). The effects of the BMI on the prevalence of CTTH were just significant in the morbidly obese group. Adjusted analyses showed that obesity was associated with CDH and TM but not CTTH.\n\nCONCLUSIONS:\nChronic daily headache and obesity are associated. Obesity is a stronger risk factor for transformed migraine than for chronic tension-type headache." + }, + "questions": [ + { + "id": "b396ca4d-2c04-4934-b1f0-82729b4f6f85", + "text": "what are the risk factors of Migraine?", + "answers": [ + { + "answer_start": 1467, + "text": "obesity" + }, + { + "answer_start": 1491, + "text": "Obesity" + } + ] + } + ] +} \ No newline at end of file diff --git a/9a08c583-faa4-4e45-bf9e-99591cb7aecd.json b/9a08c583-faa4-4e45-bf9e-99591cb7aecd.json new file mode 100644 index 0000000000000000000000000000000000000000..9791e56b820b182ad3975fc130f785cf6ba79ddf --- /dev/null +++ b/9a08c583-faa4-4e45-bf9e-99591cb7aecd.json @@ -0,0 +1,39 @@ +{ + "id": "9a08c583-faa4-4e45-bf9e-99591cb7aecd", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "17234901", + "text": "RATIONALE:\nAlthough obesity has been implicated as an asthma risk factor, there is heterogeneity in the published literature regarding its role in asthma incidence, particularly in men.\n\nOBJECTIVES:\nTo quantify the relationship between categories of body mass index (BMI) and incident asthma in adults and to evaluate the impact of sex on this relationship.\n\nMETHODS:\nOnline bibliographic databases were searched for prospective studies evaluating BMI and incident asthma in adults. Independent observers extracted data regarding annualized asthma incidence from studies meeting predetermined criteria, within defined categories of normal weight (BMI \u003c 25), overweight (BMI, 25-29.9), and obesity (BMI \u003eor= 30). Data were analyzed by inverse-variance-weighted, random-effects meta-analysis. Stratified analysis between BMI categories and within sex was performed.\n\nRESULTS:\nSeven studies (n=333,102 subjects) met inclusion criteria. Compared with normal weight, overweight and obesity (BMI \u003eor= 25) conferred increased odds of incident asthma, with an odds ratio (OR) of 1.51 (95% confidence interval [CI], 1.27-1.80). A dose-response effect of elevated BMI on asthma incidence was observed; the OR for incident asthma for normal-weight versus overweight subjects was 1.38 (95% CI, 1.17-1.62) and was further elevated for normal weight versus obesity (OR, 1.92; 95% CI, 1.43-2.59; p\u003c0.0001 for the trend). A similar increase in the OR of incident asthma due to overweight and obesity was observed in men (OR, 1.46; 95% CI, 1.05-2.02) and women (OR, 1.68; 95% CI, 1.45-1.94; p=0.232 for the comparison).\n\nCONCLUSIONS:\nOverweight and obesity are associated with a dose-dependent increase in the odds of incident asthma in men and women, suggesting asthma incidence could be reduced by interventions targeting overweight and obesity." + }, + "questions": [ + { + "id": "b3303d95-4861-4557-8ea7-efa1e7193cb2", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1617, + "text": "Overweight" + }, + { + "answer_start": 1632, + "text": "obesity" + } + ] + } + ] +} \ No newline at end of file diff --git a/9a322350-d108-488f-996e-c7da790f136c.json b/9a322350-d108-488f-996e-c7da790f136c.json new file mode 100644 index 0000000000000000000000000000000000000000..ce536dae248e04fb9fe333b9414ff40929f38427 --- /dev/null +++ b/9a322350-d108-488f-996e-c7da790f136c.json @@ -0,0 +1,34 @@ +{ + "id": "9a322350-d108-488f-996e-c7da790f136c", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "10837285", + "text": "BACKGROUND:\nLittle is known about the effects of the amount and type of carbohydrates on risk of coronary heart disease (CHD).\n\nOBJECTIVE:\nThe objective of this study was to prospectively evaluate the relations of the amount and type of carbohydrates with risk of CHD.\n\nDESIGN:\nA cohort of 75521 women aged 38-63 y with no previous diagnosis of diabetes mellitus, myocardial infarction, angina, stroke, or other cardiovascular diseases in 1984 was followed for 10 y. Each participant's dietary glycemic load was calculated as a function of glycemic index, carbohydrate content, and frequency of intake of individual foods reported on a validated food-frequency questionnaire at baseline. All dietary variables were updated in 1986 and 1990.\n\nRESULTS:\nDuring 10 y of follow-up (729472 person-years), 761 cases of CHD (208 fatal and 553 nonfatal) were documented. Dietary glycemic load was directly associated with risk of CHD after adjustment for age, smoking status, total energy intake, and other coronary disease risk factors. The relative risks from the lowest to highest quintiles of glycemic load were 1.00, 1.01, 1. 25, 1.51, and 1.98 (95% CI: 1.41, 2.77 for the highest quintile; P for trend \u003c 0.0001). Carbohydrate classified by glycemic index, as opposed to its traditional classification as either simple or complex, was a better predictor of CHD risk. The association between dietary glycemic load and CHD risk was most evident among women with body weights above average ¿ie, body mass index (in kg/m(2)) \u003e/= 23.\n\nCONCLUSION:\nThese epidemiologic data suggest that a high dietary glycemic load from refined carbohydrates increases the risk of CHD, independent of known coronary disease risk factors." + }, + "questions": [ + { + "id": "2bfddebf-40ec-48af-9d18-06b8ecdd89f8", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1578, + "text": "high dietary glycemic load from refined carbohydrates" + } + ] + } + ] +} \ No newline at end of file diff --git a/9a4eae5c-7a13-4574-8d04-894e37f06ef9.json b/9a4eae5c-7a13-4574-8d04-894e37f06ef9.json new file mode 100644 index 0000000000000000000000000000000000000000..26375d12d944aeadb89c8bce092b949254402133 --- /dev/null +++ b/9a4eae5c-7a13-4574-8d04-894e37f06ef9.json @@ -0,0 +1,37 @@ +{ + "id": "9a4eae5c-7a13-4574-8d04-894e37f06ef9", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "22294430", + "text": "Evidence concerning the role of Helicobacter pylori infection in the development of colorectal cancer remains controversial. The authors assessed the association of H. pylori seroprevalence with risk of colorectal cancer in a large population-based case-control study from Germany in 2003-2007. Serum antibodies to H. pylori in general and the cytotoxin-associated gene A protein (CagA) were measured in 1,712 incident colorectal cancer cases and 1,669 controls. The association between H. pylori seroprevalence and colorectal cancer risk was estimated by logistic regression, with adjustment for potential confounders and stratification by age group, sex, anatomic subsites, and cancer stage. Overall, H. pylori seroprevalence was higher in cases (46.1%) than in controls (40.1%), resulting in an age- and sex-adjusted odds ratio of 1.30 (95% confidence interval (CI): 1.14, 1.50). Adjustment for established colorectal cancer risk factors decreased the odds ratio to 1.26 (95% CI: 1.09, 1.47), with a further reduction to 1.18 (95% CI: 1.01, 1.38) after additional adjustment for previous colorectal endoscopy. Stratified analyses showed risk elevation to be essentially confined to left-sided colorectal cancer, with an odds ratio of 1.22 (95% CI: 1.02, 1.45), suggesting that H. pylori infection may be associated with a small yet relevant risk increase in the left colorectum." + }, + "questions": [ + { + "id": "d217febf-a763-448d-a492-9ec07463d5b3", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1280, + "text": "H. pylori infection" + } + ] + } + ] +} \ No newline at end of file diff --git a/9a699d45-c6e1-42bd-8b62-03a5aa3d66c4.json b/9a699d45-c6e1-42bd-8b62-03a5aa3d66c4.json new file mode 100644 index 0000000000000000000000000000000000000000..04f838e5cdd16e024932a00a93da85f1b48399d9 --- /dev/null +++ b/9a699d45-c6e1-42bd-8b62-03a5aa3d66c4.json @@ -0,0 +1,43 @@ +{ + "id": "9a699d45-c6e1-42bd-8b62-03a5aa3d66c4", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "25671687", + "text": "IMPORTANCE:\nThe risk of next melanoma in patients with 2 or more previous melanomas stratified by familial and sporadic cases separately has not yet been reported, although a few population-based studies have assessed the risk of second melanoma.\n\nOBJECTIVE:\nTo assess the risk of next melanoma in patients with multiple primary melanomas by number of previous melanomas, stratified by demographic and melanoma characteristics.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nProspective population-based cohort study with follow-up from 1958 to 2010 using the Swedish Family-Cancer Database with information on cancer cases retrieved from the Swedish Cancer Registry. A total of 65,429 patients with invasive or in situ melanoma who received a diagnosis during 1958 through 2010 were observed for next melanoma incidence.\n\nMAIN OUTCOMES AND MEASURES:\nStandardized incidence ratios (SIRs) expressing risk of next melanoma by calculating the incidence of next (second, third, fourth, and fifth) melanoma in melanoma patients who had received a diagnosis of 1, 2, 3, and 4, respectively, previous melanomas, compared with the risk of first melanoma in the Swedish population.\n\nRESULTS:\nFor patients with either familial or sporadic melanoma, we observed a stable 2- to 3-times elevated risk by increasing number of previous melanomas; for example, for 2 previous melanomas, the SIR was 2.8 (95% CI, 2.3-3.4) for patients with familial melanoma and 2.5 (95% CI, 2.3-2.7) for patients with sporadic melanoma. Overall risk of second melanoma was higher in patients with familial melanoma who received a diagnosis at younger than 40 years (SIR, 4.7 [95% CI, 3.9-5.6]), and we found a notable risk in young patients with familial melanoma during the first 5-year follow-up after first melanoma: SIR of 6.1 (95% CI, 4.0-9.0) for interval up to 1 year, 6.2 (95% CI, 3.2-11) for 2 to 3 years, and 19 (95% CI, 10-31) for 4 to 5 years. Risk was notable in young (\u003c40 years) patients with sporadic melanoma within the first year of follow-up (SIR, 5.3 [95% CI, 4.3-6.4]) and afterward remained steadily elevated by 2 to 3 times.\n\nCONCLUSIONS AND RELEVANCE:\nWe found a stable 2- to 3-times elevated risk by number of previous melanomas for patients with either familial or sporadic melanoma. Notable risk in young patients with familial melanoma during first 5-year follow-up after first melanoma may suggest that it is important to refer these patients for clinical genetic testing." + }, + "questions": [ + { + "id": "7c6ec112-42f6-440a-8067-7d3461b15c9a", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 1539, + "text": "patients with familial melanoma who received a diagnosis at younger than 40 years" + }, + { + "answer_start": 1682, + "text": "young patients with familial melanoma during the first 5-year follow-up after first melanoma" + }, + { + "answer_start": 1932, + "text": "young (\u003c40 years) patients with sporadic melanoma within the first year of follow-up" + } + ] + } + ] +} \ No newline at end of file diff --git a/9a811bad-0365-4eed-ad3f-286ab8777465.json b/9a811bad-0365-4eed-ad3f-286ab8777465.json new file mode 100644 index 0000000000000000000000000000000000000000..f8a238c319bca9d96efa6fcdef330ffe6c8b6255 --- /dev/null +++ b/9a811bad-0365-4eed-ad3f-286ab8777465.json @@ -0,0 +1,42 @@ +{ + "id": "9a811bad-0365-4eed-ad3f-286ab8777465", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "9326912", + "text": "BACKGROUND:\nWe have quantified the site-specific risk of second malignant neoplasms among nearly 29,000 survivors (\u003e or = 1 year) of testicular cancer, taking into account the histologic type of initial cancer and the primary therapy used to treat it.\n\nMETHODS:\nThe study cohort consisted of 28,843 men identified within 16 population-based tumor registries in North America and Europe; over 3300 men had survived more than 20 years. New invasive cancers were identified through a search of registry files.\n\nRESULTS:\nSecond cancers were reported in 1406 men (observed-to-expected ratio [O/E] = 1.43; 95% confidence interval = 1.36-1.51), with statistically significant excesses noted for acute lymphoblastic leukemia (O/E = 5.20), acute nonlymphocytic leukemia (O/E = 3.07), melanoma (O/E = 1.69), non-Hodgkin's lymphoma (O/E = 1.88), and cancers of the stomach (O/E = 1.95), colon (O/E = 1.27), rectum (O/E = 1.41), pancreas (O/E = 2.21), prostate (O/E = 1.26), kidney (O/E = 1.50), bladder (O/E = 2.02), thyroid (O/E = 2.92), and connective tissue (O/E = 3.16). Overall risk was similar after seminomas (O/E = 1.42) or nonseminomatous tumors (O/E = 1.50). Risk of solid tumors increased with time since the diagnosis of testicular cancer, yielding an O/E = 1.54 (O = 369) among 20-year survivors (two-sided P for trend = .00002). Secondary leukemia was associated with both radiotherapy and chemotherapy, whereas excess cancers of the stomach, bladder, and, possibly, pancreas were associated mainly with radiotherapy.\n\nCONCLUSIONS:\nMen with testicular cancer continue to be at significantly elevated risk of second malignant neoplasms for more than two decades following initial diagnosis. Patterns of excess second cancers suggest that many factors may be involved, although the precise roles of treatment, natural history, diagnostic surveillance, and other influences are yet to be clarified." + }, + "questions": [ + { + "id": "6385b43e-b0a6-411e-a6f0-a3f245fb337c", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 1535, + "text": "Men with testicular cancer" + }, + { + "answer_start": 1507, + "text": "radiotherapy" + }, + { + "answer_start": 104, + "text": "survivors (\u003e or = 1 year) of testicular cancer" + } + ] + } + ] +} \ No newline at end of file diff --git a/9b2e8a1d-fd3b-42a5-9c23-97c60670f2e9.json b/9b2e8a1d-fd3b-42a5-9c23-97c60670f2e9.json new file mode 100644 index 0000000000000000000000000000000000000000..0a733a809fa83d42c0857d8ffcc1d609ff52f78d --- /dev/null +++ b/9b2e8a1d-fd3b-42a5-9c23-97c60670f2e9.json @@ -0,0 +1,35 @@ +{ + "id": "9b2e8a1d-fd3b-42a5-9c23-97c60670f2e9", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "8348254", + "text": "Screening of total IgE in 1189 cord blood samples was conducted by Phadebas IgE PRIST in a one-year birth cohort 1983-1984 in Viborg, Denmark. 113 children with cord blood IgE levels \u003e or = 0.5 kU/l and 138 children chosen at random among those with cord blood IgE levels \u003c 0.5 kU/l were seen at a follow-up at 5 years of age. Based upon history and physical examination a diagnosis of definite atopy or no atopy was established. Allergy (IgE mediated) was defined as atopic disease combined with increased total IgE levels at 5 years of age. The cumulative prevalence of atopic disease was not influenced by cord blood IgE levels or atopic predisposition. Cord blood IgE levels had a low sensitivity as a predictor of atopic disease. A statistically significant correlation between serum levels of IgE at birth and at 5 years was however found (p \u003c 0.001), and a significantly greater number of children with elevated cord blood IgE levels developed allergic disease before 5 years of age (p \u003c 0.01). A cut-off limit of 0.3 kU/l was superior to the originally suggested limit of 0.5 kU/l. A total IgE level \u003e 63 kU/l (geometric mean + 1 SD) at the age of 5 years can be regarded as being an elevated level. A cord blood IgE level \u003e or = 0.3 kU/l in combination with atopic predisposition was predictive of allergic disease, especially allergic bronchial asthma. With regard to allergic disease, the positive predictive value was 26%, the sensitivity 33% and the rate ratio for development of allergic disease 4.(ABSTRACT TRUNCATED AT 250 WORDS)" + }, + "questions": [ + { + "id": "24e3c120-53dd-448f-bf79-2957bc063625", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1208, + "text": "A cord blood IgE level \u003e or = 0.3 kU/l in combination with atopic predisposition" + } + ] + } + ] +} \ No newline at end of file diff --git a/9b7f79fc-9652-425f-afaf-58c2c64a9a2d.json b/9b7f79fc-9652-425f-afaf-58c2c64a9a2d.json new file mode 100644 index 0000000000000000000000000000000000000000..15bcf519fa13ed2287f62f3f2f0f43143d0f2a6e --- /dev/null +++ b/9b7f79fc-9652-425f-afaf-58c2c64a9a2d.json @@ -0,0 +1,43 @@ +{ + "id": "9b7f79fc-9652-425f-afaf-58c2c64a9a2d", + "disease": { + "id": "H00056", + "names": [ + "Alzheimer disease", + "Dementia due to Alzheimer disease" + ], + "dbLinks": { + "icd10": [ + "G30" + ], + "mesh": [ + "D000544" + ] + }, + "category": "Neurodegenerative disease" + }, + "article": { + "id": "20452461", + "text": "Alzheimer's disease (AD), the most common neurodegenerative disorder, which affects more than 35 million people worldwide, is characterized by a massive accumulation of tangles and amyloid plaques. Several risk factors linked to lipid homeostasis have been identified. Apolipoprotein E (ApoE), which also has a strong impact in coronary artery disease, is besides aging the most prominent risk factor in sporadic AD. High levels of lipoproteins and cholesterol increase the risk of AD and some cholesterol lowering drugs like statins seem to correlate with a reduced risk for dementia. Moreover, cholesterol increases amyloid beta (Abeta) production, which is derived from amyloid precursor protein (APP) by proteolytic processing. Beside cholesterol, other lipids that strongly modulate APP processing could be identified and interestingly the APP cleavage products itself regulate lipid homeostasis resulting in complex regulatory feedback cycles. Here, we review the mechanistic link of cholesterol and sphingolipid homeostasis and APP processing and the consequence of this bidirectional link for and in AD. Although cholesterol is the best studied brain lipid in AD, many other lipids are involved in the Abeta-lipid regulatory system and some of these lipids exceed the cholesterol effect on Abeta production [1-5]. This involvement is bidirectional. On the one hand, lipids control APP processing and, on the other hand, APP processing controls the levels of several key lipids [6, 7]. Beside the physiological function of APP processing in lipid homeostasis, under pathological conditions like AD, these regulating (feedback-) cycles are dysfunctional. Additionally, mutual influence of lipids and APP processing raises the question if altered lipid homeostasis is the cause or consequence of AD." + }, + "questions": [ + { + "id": "3105cb2d-1984-4f2f-92d0-29560cf75dae", + "text": "What are the risk factors of Alzheimer disease?", + "answers": [ + { + "answer_start": 269, + "text": "Apolipoprotein E (ApoE)" + }, + { + "answer_start": 417, + "text": "High levels of lipoproteins and cholesterol" + }, + { + "answer_start": 364, + "text": "aging" + } + ] + } + ] +} \ No newline at end of file diff --git a/9bc8e79d-4f11-4dbb-8a3c-8377ffbc16e0.json b/9bc8e79d-4f11-4dbb-8a3c-8377ffbc16e0.json new file mode 100644 index 0000000000000000000000000000000000000000..9bdb63b09dc6de630b32cf85fb5538a5eb67522b --- /dev/null +++ b/9bc8e79d-4f11-4dbb-8a3c-8377ffbc16e0.json @@ -0,0 +1,34 @@ +{ + "id": "9bc8e79d-4f11-4dbb-8a3c-8377ffbc16e0", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "19500688", + "text": "BACKGROUND \u0026 AIMS:\nSusceptibility to celiac disease (CD) is related to HLA-DQ2 and DQ8 alleles and the heterodimers they encode. The objective of this study was to stratify risk for CD on the basis of HLA-DQ genotype.\n\nMETHODS:\nDNA from 10,191 subjects who are at risk for CD was analyzed for HLA-DQ haplotypes. Individuals with CD were identified as those who tested positive for anti-endomysial immunoglobulin A (EMA+) in an immunofluorescence assay.\n\nRESULTS:\nSamples homozygous for DQ2.5 (HLA-DQA1 05-DQB1 02) or DQ2.2/DQ2.5 (HLA-DQA1 05-DQB1 02 and HLA-DQA1 0201-DQB1 02) comprised 5.38% of the total; 28.28% of these were EMA+ (95% confidence interval [CI], 24.55-32.26). Of the samples that were DQ2.5 heterozygous (HLA-DQA1 05-DQB1 02); 9.09% were EMA+ (95% CI, 7.82-10.51). Among samples in which HLA-DQ8 (HLA-DQA1 03-DQB1 0302) was detected, 8.42% of homozygotes (95% CI, 3.71-15.92) and 2.11% of heterozygotes (95% CI, 1.43-3.00) were EMA+. Samples with DQ2.2/DQ8 or DQ2.5/DQ8 comprised 5.08% of the total, and 11.78% of these were EMA+ (95% CI, 9.13-14.87). HLA-DQ2 and HLA-DQ8 were absent in 4283 samples (42.03% of the total); 0.16% of these samples were EMA+ (95% CI, 0.07-0.34).\n\nCONCLUSIONS:\nHigh-resolution, sequence-specific oligonucleotide probe typing with 35 DQA1-specific and 37 DQB1-specific probes of DNA from more than 10,000 subjects was used to stratify risk of CD in an at-risk U.S. population. DQ2 homozygosity (DQ2.5/DQ2.2+2.5) increased risk for CD, estimated by the rate of EMA positivity, compared with the entire sample population and other DQ genotypes. These data suggest a quantitative relationship between the type/proportion of DQ heterodimers and the risk of CD and identify potential immunotherapeutic targets." + }, + "questions": [ + { + "id": "ffb24890-9a88-447a-a265-c759879414d2", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 1424, + "text": "DQ2 homozygosity (DQ2.5/DQ2.2+2.5)" + } + ] + } + ] +} \ No newline at end of file diff --git a/9c046ee3-2e41-497c-a642-c0722e664e63.json b/9c046ee3-2e41-497c-a642-c0722e664e63.json new file mode 100644 index 0000000000000000000000000000000000000000..085a0a3700dd826208ac3f13fd40dc0d5cc1d4b6 --- /dev/null +++ b/9c046ee3-2e41-497c-a642-c0722e664e63.json @@ -0,0 +1,46 @@ +{ + "id": "9c046ee3-2e41-497c-a642-c0722e664e63", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "23084519", + "text": "BACKGROUND:\nMenarche and menopause mark the onset and cessation, respectively, of ovarian activity associated with reproduction, and affect breast cancer risk. Our aim was to assess the strengths of their effects and determine whether they depend on characteristics of the tumours or the affected women.\n\nMETHODS:\nIndividual data from 117 epidemiological studies, including 118 964 women with invasive breast cancer and 306 091 without the disease, none of whom had used menopausal hormone therapy, were included in the analyses. We calculated adjusted relative risks (RRs) associated with menarche and menopause for breast cancer overall, and by tumour histology and by oestrogen receptor expression.\n\nFINDINGS:\nBreast cancer risk increased by a factor of 1·050 (95% CI 1·044-1·057; p\u003c0·0001) for every year younger at menarche, and independently by a smaller amount (1·029, 1·025-1·032; p\u003c0·0001), for every year older at menopause. Premenopausal women had a greater risk of breast cancer than postmenopausal women of an identical age (RR at age 45-54 years 1·43, 1·33-1·52, p\u003c0·001). All three of these associations were attenuated by increasing adiposity among postmenopausal women, but did not vary materially by women's year of birth, ethnic origin, childbearing history, smoking, alcohol consumption, or hormonal contraceptive use. All three associations were stronger for lobular than for ductal tumours (p\u003c0·006 for each comparison). The effect of menopause in women of an identical age and trends by age at menopause were stronger for oestrogen receptor-positive disease than for oestrogen receptor-negative disease (p\u003c0·01 for both comparisons).\n\nINTERPRETATION:\nThe effects of menarche and menopause on breast cancer risk might not be acting merely by lengthening women's total number of reproductive years. Endogenous ovarian hormones are more relevant for oestrogen receptor-positive disease than for oestrogen receptor-negative disease and for lobular than for ductal tumours.\n\nFUNDING:\nCancer Research UK." + }, + "questions": [ + { + "id": "1e9216bc-0cf1-40ca-bcb7-c023fa113972", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 798, + "text": "every year younger at menarche" + }, + { + "answer_start": 904, + "text": "every year older at menopause" + }, + { + "answer_start": 935, + "text": "Premenopausal women" + }, + { + "answer_start": 1138, + "text": "increasing adiposity among postmenopausal women" + } + ] + } + ] +} \ No newline at end of file diff --git a/9c6c63b4-ec74-43a9-9dcf-408f109842f9.json b/9c6c63b4-ec74-43a9-9dcf-408f109842f9.json new file mode 100644 index 0000000000000000000000000000000000000000..c69d670c982e133b160e87f037c7518347a05a09 --- /dev/null +++ b/9c6c63b4-ec74-43a9-9dcf-408f109842f9.json @@ -0,0 +1,38 @@ +{ + "id": "9c6c63b4-ec74-43a9-9dcf-408f109842f9", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "9497251", + "text": "Celiac disease (CD), a malabsorption disorder of the small intestine, results from ingestion of gluten. The HLA risk factors involved in CD are well known but do not explain the entire genetic susceptibility. To determine the localization of other genetic risk factors, a systematic screening of the genome has been undertaken. The typing information of 281 markers on 110 affected sib pairs and their parents was used to test linkage. Systematic linkage analysis was first performed on 39 pairs in which both sibs had a symptomatic form of CD. Replication of the regions of interest was then carried out on 71 pairs in which one sib had a symptomatic form and the other a silent form of CD. In addition to the HLA loci, our study suggests that a risk factor in 5qter is involved in both forms of CD (symptomatic and silent). Furthermore, a factor on 11qter possibly differentiates the two forms. In contrast, none of the regions recently published was confirmed by the present screening." + }, + "questions": [ + { + "id": "7b8bcc5e-0d32-439c-b059-8a10c7e7c6ed", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 762, + "text": "5qter" + }, + { + "answer_start": 851, + "text": "11qter" + } + ] + } + ] +} \ No newline at end of file diff --git a/9c6e1933-ee35-4a9c-a2f8-dd6c453c2638.json b/9c6e1933-ee35-4a9c-a2f8-dd6c453c2638.json new file mode 100644 index 0000000000000000000000000000000000000000..0d99ace7c23636f5fc8327b0d2ef9bee70954ec4 --- /dev/null +++ b/9c6e1933-ee35-4a9c-a2f8-dd6c453c2638.json @@ -0,0 +1,42 @@ +{ + "id": "9c6e1933-ee35-4a9c-a2f8-dd6c453c2638", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "23975662", + "text": "This study aimed to conduct a systematic review to sum up evidence of the associations between different aspects of night shift work and female breast cancer using a dose-response meta-analysis approach. We systematicly searched all cohort and case-control studies published in English on MEDLINE, Embase, PSYCInfo, APC Journal Club and Global Health, from January 1971 to May 2013. We extracted effect measures (relative risk, RR; odd ratio, OR; or hazard ratio, HR) from individual studies to generate pooled results using meta-analysis approaches. A log-linear dose-response regression model was used to evaluate the relationship between various indicators of exposure to night shift work and breast cancer risk. Downs and Black scale was applied to assess the methodological quality of included studies. Ten studies were included in the meta-analysis. A pooled adjusted relative risk for the association between 'ever exposed to night shift work' and breast cancer was 1.19 [95% confidence interval (CI) 1.05-1.35]. Further meta-analyses on dose-response relationship showed that every 5-year increase of exposure to night shift work would correspondingly enhance the risk of breast cancer of the female by 3% (pooled RR = 1.03, 95% CI 1.01-1.05; Pheterogeneity \u003c 0.001). Our meta-analysis also suggested that an increase in 500-night shifts would result in a 13% (RR = 1.13, 95% CI 1.07-1.21; Pheterogeneity = 0.06) increase in breast cancer risk. This systematic review updated the evidence that a positive dose-response relationship is likely to present for breast cancer with increasing years of employment and cumulative shifts involved in the work." + }, + "questions": [ + { + "id": "017d3452-6ebd-45f4-af6f-96499c434762", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1584, + "text": "increasing years of employment and cumulative shifts involved in the work" + }, + { + "answer_start": 1084, + "text": "every 5-year increase of exposure to night shift work" + }, + { + "answer_start": 916, + "text": "'ever exposed to night shift work' and breast cancer" + } + ] + } + ] +} \ No newline at end of file diff --git a/9c82d864-2b43-42ec-af0a-f16b6b8e39bf.json b/9c82d864-2b43-42ec-af0a-f16b6b8e39bf.json new file mode 100644 index 0000000000000000000000000000000000000000..ace517cff38409707f4fdcbd73662c6473c614e9 --- /dev/null +++ b/9c82d864-2b43-42ec-af0a-f16b6b8e39bf.json @@ -0,0 +1,38 @@ +{ + "id": "9c82d864-2b43-42ec-af0a-f16b6b8e39bf", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "17290721", + "text": "OBJECTIVE:\nTo estimate the association between plasma lipoprotein-associated phospholipase A2 (Lp-PLA2) levels and cardiovascular disease (CVD).\n\nMETHODS:\nWe searched MEDLINE (January 1, 1985, through September 30, 2006), the Cochrane library (from inception through 2006), conference proceedings, and reference sections of obtained articles and contacted experts for unpublished studies. Eligible studies were cohorts with 1 year or more of follow-up or case-control designs that provided risk estimates for CVD according to blood levels of Lp-PLA2 that were unadjusted or adjusted for conventional CVD risk factors. We used random-effects meta-analysis to estimate the association between Lp-PLA2 and CVD risk and conducted preplanned subgroup analyses to identify risk-subgroup interactions that could explain between-study differences.\n\nRESULTS:\nWe found 14 eligible studies (N = 20,549 patients) that reported either Lp-PLA2 plasma activity (n = 5) or an immunoassay that measured the plasma concentration (n = 9). The meta-analytic estimate from the unadjusted odds ratio for the association between elevated Lp-PLA2 levels and CVD risk was 1.51 (95% confidence interval, 1.30-1.75) and from the odds ratio adjusted for conventional CVD risk factors was 1.60 (95% confidence interval, 1.36-1.89). Differences in study methods explained differences in results across studies.\n\nCONCLUSIONS:\nLipoprotein-associated phospholipase A2 is significantly associated with CVD. The risk estimate appears to be relatively unaffected by adjustment for conventional CVD risk factors. Measurement of Lp-PLA2 may be useful in CVD risk stratification. In addition, Lp-PLA2 may represent a potential therapeutic target for CVD risk reduction." + }, + "questions": [ + { + "id": "d8d6e0f2-7942-4ddc-8555-1ecc0402ef4f", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1395, + "text": "Lipoprotein-associated phospholipase A2" + }, + { + "answer_start": 1106, + "text": "elevated Lp-PLA2" + } + ] + } + ] +} \ No newline at end of file diff --git a/9c9810da-7b72-4946-addd-15d2e5509388.json b/9c9810da-7b72-4946-addd-15d2e5509388.json new file mode 100644 index 0000000000000000000000000000000000000000..7d694e79f1145a7af16e3fd45e108eef5de274f4 --- /dev/null +++ b/9c9810da-7b72-4946-addd-15d2e5509388.json @@ -0,0 +1,46 @@ +{ + "id": "9c9810da-7b72-4946-addd-15d2e5509388", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "21852111", + "text": "BACKGROUND:\nWorking outside normal daytime hours is increasing worldwide and is now one of the most widespread potential carcinogenic occupational exposures. There is sufficient evidence in experimental animals that light exposure during the biologic night increases tumour growth and limited epidemiologic evidence that night shift-work cause breast cancer. Existing studies had crude definitions of shift-work and did not discriminate between shift-work systems (e.g. permanent versus rotating or evening versus night).\n\nMETHODS:\nWe performed an interview based nested case-control study within a nationwide cohort of Danish nurses, including detailed information on lifetime shift-work and potential confounders. Cases of primary breast cancer (n=310) were identified from the nationwide Danish Cancer Registry. Four control nurses were selected for each case by incidence density sampling. Odds rations (ORs) and 95% confidence intervals (CIs) were estimated by conditional logistic regression, with adjustment for potential confounders.\n\nFINDINGS:\nOverall, nurses who worked rotating shifts after midnight had a significantly increased OR (1.8; CI 1.2-2.8) for breast cancer compared to nurses with permanent day work. No association was found in a small group of nurses with evening work and no night work (OR=0.9; 0.4-1.9). The subgroup of nurses with periods of permanent night shift in addition to rotating night and day shifts experienced an OR of 2.9 (1.1-8.0). For nurses working after midnight compared to nurses never ending work before midnight, OR in the third tertile of cumulative number of shifts was 2.2 (1.5-3.2). In an analysis of different rotating shift systems, the highest OR (2.6; 1.8-3.8) was observed for long-term day-night rotating shifts.\n\nINTERPRETATION:\nThe results provide further evidence that night shift-work may increase the risk for breast cancer and suggest that the largest impact on risk is associated with the most disruptive shifts.\n\nFUNDING:\nDanish Cancer Society and National Programme of Environmental Health Research." + }, + "questions": [ + { + "id": "c02305d1-f668-4823-9a89-9d9abb8b7449", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1062, + "text": "nurses who worked rotating shifts after midnight" + }, + { + "answer_start": 1347, + "text": "nurses with periods of permanent night shift in addition to rotating night and day shifts" + }, + { + "answer_start": 1477, + "text": "nurses working after midnight compared to nurses never ending work before midnight" + }, + { + "answer_start": 1830, + "text": "night shift-work" + } + ] + } + ] +} \ No newline at end of file diff --git a/9d064909-7a92-46de-9948-e58fd9f568f3.json b/9d064909-7a92-46de-9948-e58fd9f568f3.json new file mode 100644 index 0000000000000000000000000000000000000000..56b6ced11111f3fd80a93dc944148bbe4f18c45d --- /dev/null +++ b/9d064909-7a92-46de-9948-e58fd9f568f3.json @@ -0,0 +1,49 @@ +{ + "id": "9d064909-7a92-46de-9948-e58fd9f568f3", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "21674008", + "text": "BACKGROUND:\nThe evidence that red and processed meat influences colorectal carcinogenesis was judged convincing in the 2007 World Cancer Research Fund/American Institute of Cancer Research report. Since then, ten prospective studies have published new results. Here we update the evidence from prospective studies and explore whether there is a non-linear association of red and processed meats with colorectal cancer risk.\n\nMETHODS AND FINDINGS:\nRelevant prospective studies were identified in PubMed until March 2011. For each study, relative risks and 95% confidence intervals (CI) were extracted and pooled with a random-effects model, weighting for the inverse of the variance, in highest versus lowest intake comparison, and dose-response meta-analyses. Red and processed meats intake was associated with increased colorectal cancer risk. The summary relative risk (RR) of colorectal cancer for the highest versus the lowest intake was 1.22 (95% CI = 1.11-1.34) and the RR for every 100 g/day increase was 1.14 (95% CI = 1.04-1.24). Non-linear dose-response meta-analyses revealed that colorectal cancer risk increases approximately linearly with increasing intake of red and processed meats up to approximately 140 g/day, where the curve approaches its plateau. The associations were similar for colon and rectal cancer risk. When analyzed separately, colorectal cancer risk was related to intake of fresh red meat (RR(for 100 g/day increase) = 1.17, 95% CI = 1.05-1.31) and processed meat (RR (for 50 g/day increase) = 1.18, 95% CI = 1.10-1.28). Similar results were observed for colon cancer, but for rectal cancer, no significant associations were observed.\n\nCONCLUSIONS:\nHigh intake of red and processed meat is associated with significant increased risk of colorectal, colon and rectal cancers. The overall evidence of prospective studies supports limiting red and processed meat consumption as one of the dietary recommendations for the prevention of colorectal cancer." + }, + "questions": [ + { + "id": "a2b97e3a-842d-4b61-93f5-3ea31a1ca498", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1682, + "text": "High intake of red and processed meat" + }, + { + "answer_start": 1407, + "text": "fresh red meat" + }, + { + "answer_start": 1482, + "text": "processed meat" + }, + { + "answer_start": 760, + "text": "Red and processed meats" + } + ] + } + ] +} \ No newline at end of file diff --git a/9d62072a-d6d4-4bac-bfe4-7811f00de2df.json b/9d62072a-d6d4-4bac-bfe4-7811f00de2df.json new file mode 100644 index 0000000000000000000000000000000000000000..5728fefe4316836f7db255486dcf7efe23abee78 --- /dev/null +++ b/9d62072a-d6d4-4bac-bfe4-7811f00de2df.json @@ -0,0 +1,40 @@ +{ + "id": "9d62072a-d6d4-4bac-bfe4-7811f00de2df", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "11914989", + "text": "Chronic obstructive pulmonary disease (COPD) is a common, complex disease associated with substantial morbidity and mortality. COPD is defined by irreversible airflow obstruction; airflow obstruction is typically determined by reductions in quantitative spirometric indices, including forced expiratory volume at 1 s (FEV(1)) and the ratio of FEV(1) to forced vital capacity (FVC). To identify genetic determinants of quantitative spirometric phenotypes, an autosomal 10-cM genomewide scan of short tandem repeat (STR) polymorphic markers was performed in 72 pedigrees (585 individuals) ascertained through probands with severe early-onset COPD. Multipoint variance-component linkage analysis (using SOLAR) was performed for quantitative phenotypes, including FEV(1), FVC, and FEV(1)/FVC. In the initial genomewide scan, significant evidence for linkage to FEV(1)/FVC was demonstrated on chromosome 2q (LOD score 4.12 at 222 cM). Suggestive evidence was found for linkage to FEV(1)/FVC on chromosomes 1 (LOD score 1.92 at 120 cM) and 17 (LOD score 2.03 at 67 cM) and to FVC on chromosome 1 (LOD score 2.05 at 13 cM). The highest LOD score for FEV(1) in the initial genomewide scan was 1.53, on chromosome 12, at 36 cM. After inclusion of 12 additional STR markers on chromosome 12p, which had been previously genotyped in this population, suggestive evidence for linkage of FEV(1) (LOD score 2.43 at 37 cM) to this region was demonstrated. These observations provide both significant evidence for an early-onset COPD-susceptibility locus on chromosome 2 and suggestive evidence for linkage of spirometry-related phenotypes to several other genomic regions. The significant linkage of FEV(1)/FVC to chromosome 2q could reflect one or more genes influencing the development of airflow obstruction or dysanapsis." + }, + "questions": [ + { + "id": "6fbdebe0-7eff-494f-8467-e97c17d332ea", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 857, + "text": "chromosomes 12" + }, + { + "answer_start": 1698, + "text": "chromosome 2q" + } + ] + } + ] +} \ No newline at end of file diff --git a/9d89dd0a-366d-44ed-bc67-ec460c1a3e33.json b/9d89dd0a-366d-44ed-bc67-ec460c1a3e33.json new file mode 100644 index 0000000000000000000000000000000000000000..6e49bc1077ea95d85a6f857b98d55580b558597d --- /dev/null +++ b/9d89dd0a-366d-44ed-bc67-ec460c1a3e33.json @@ -0,0 +1,39 @@ +{ + "id": "9d89dd0a-366d-44ed-bc67-ec460c1a3e33", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "25030783", + "text": "BACKGROUND:\nSugar-sweetened soda consumption is consistently associated with an increased risk of several chronic inflammatory diseases such as type 2 diabetes and cardiovascular diseases. Whether it plays a role in the development of rheumatoid arthritis (RA), a common autoimmune inflammatory disease, remains unclear.\n\nOBJECTIVE:\nThe aim was to evaluate the association between sugar-sweetened soda consumption and risk of RA in US women.\n\nDESIGN:\nWe prospectively followed 79,570 women from the Nurses' Health Study (NHS; 1980-2008) and 107,330 women from the NHS II (1991-2009). Information on sugar-sweetened soda consumption (including regular cola, caffeine-free cola, and other sugar-sweetened carbonated soda) was obtained from a validated food-frequency questionnaire at baseline and approximately every 4 y during follow-up. Incident RA cases were validated by medical record review. Time-varying Cox proportional hazards regression models were used to calculate HRs after adjustment for confounders. Results from both cohorts were pooled by an inverse-variance-weighted, fixed-effects model.\n\nRESULTS:\nDuring 3,381,268 person-years of follow-up, 857 incident cases of RA were documented in the 2 cohorts. In the multivariable pooled analyses, we found that women who consumed ≥1 serving of sugar-sweetened soda/d had a 63% (HR: 1.63; 95% CI: 1.15, 2.30; P-trend = 0.004) increased risk of developing seropositive RA compared with those who consumed no sugar-sweetened soda or who consumed \u003c1 serving/mo. When we restricted analyses to those with later RA onset (after age 55 y) in the NHS, the association appeared to be stronger (HR: 2.64; 95% CI: 1.56, 4.46; P-trend \u003c 0.0001). No significant association was found for sugar-sweetened soda and seronegative RA. Diet soda consumption was not significantly associated with risk of RA in the 2 cohorts.\n\nCONCLUSION:\nRegular consumption of sugar-sweetened soda, but not diet soda, is associated with increased risk of seropositive RA in women, independent of other dietary and lifestyle factors." + }, + "questions": [ + { + "id": "dd0b7a85-3993-4ea2-8c42-63d615412191", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 1269, + "text": " women who consumed ≥1 serving of sugar-sweetened soda/d" + }, + { + "answer_start": 1878, + "text": "Regular consumption of sugar-sweetened soda, but not diet soda" + } + ] + } + ] +} \ No newline at end of file diff --git a/9dd2af61-d097-4f8c-8b83-055366b7e4a7.json b/9dd2af61-d097-4f8c-8b83-055366b7e4a7.json new file mode 100644 index 0000000000000000000000000000000000000000..decc60653c2218b483e39ffe07261dfbe62f0ff5 --- /dev/null +++ b/9dd2af61-d097-4f8c-8b83-055366b7e4a7.json @@ -0,0 +1,34 @@ +{ + "id": "9dd2af61-d097-4f8c-8b83-055366b7e4a7", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "20031795", + "text": "BACKGROUND:\nThe relationship of circulating levels of high-sensitivity C-reactive protein (CRP) with cardiovascular disease (CVD) risk, particularly with consideration of effects at intermediate levels of risk, has not been fully assessed.\n\nMETHODS AND RESULTS:\nAmong 3006 offspring participants in the Framingham Heart Study free of CVD (mean age, 46 years at baseline), there were 129 hard coronary heart disease (CHD) events and 286 total CVD events during 12 years of follow-up. Cox regression, discrimination with area under the receiver operating characteristic curve, and net reclassification improvement were used to assess the role of CRP on vascular risk. In an age-adjusted model that included both sexes, the hazard ratios for new hard CHD and total CVD were significantly associated with higher CRP levels. Similar analyses according to increasing homocysteine level showed significant protective associations for hard CHD but not for total CVD. In multivariable analyses that included age, sex, systolic blood pressure, total cholesterol, high-density lipoprotein cholesterol, diabetes mellitus, current smoking, hypertension treatment, and homocysteine, the log CRP level remained significantly related to development of hard CHD and total CVD and provided moderate improvement in the discrimination of events. The net reclassification improvement when CRP was added to traditional factors was 5.6% for total CVD (P=0.014) and 11.8% for hard CHD (P=0.009).\n\nCONCLUSIONS:\nCirculating levels of CRP help to estimate risk for initial cardiovascular events and may be used most effectively in persons at intermediate risk for vascular events, offering moderate improvement in reclassification of risk." + }, + "questions": [ + { + "id": "1609299a-5c6d-4473-845d-209f71535b5c", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1486, + "text": "Circulating levels of CRP" + } + ] + } + ] +} \ No newline at end of file diff --git a/9df59801-c19d-48c0-a13a-fd88ada49214.json b/9df59801-c19d-48c0-a13a-fd88ada49214.json new file mode 100644 index 0000000000000000000000000000000000000000..e9930968c71c6dd76c1c18da7e71a067886d6e45 --- /dev/null +++ b/9df59801-c19d-48c0-a13a-fd88ada49214.json @@ -0,0 +1,50 @@ +{ + "id": "9df59801-c19d-48c0-a13a-fd88ada49214", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "16845665", + "text": "BACKGROUND:\nThe familial risk of bladder cancer (BC) is not well understood and, to date, little attention has been paid to the joint effect of smoking and family history in modifying the risk of BC. The authors investigated the role of family history in association with the risk of BC.\n\nMETHODS:\nCase and control probands were identified as part of an on-going BC case-control study. The relative risk associated with a family history of BC was estimated.\n\nRESULTS:\nIn total, 713 cases and 658 controls were included. In a case-control analysis, compared with individuals who never smoked and who had no family history of BC, probands who had smoked and who also had a positive family history were at 5.31-fold increased risk of BC (P for interaction = .04). The 713 case probands and the 658 controls reported 5160 and 4816 first-degree relatives, respectively. Compared with never-smoking relatives who had probands diagnosed with BC at an older age (age \u003e65 years), ever-smoking relatives who had probands diagnosed at a younger age (ages 40-65 years) showed a 6.89-fold (95% confidence interval, from 2.25-fold to 21.12-fold) increased risk. Similar results were obtained for the joint effects of family history of BC and smoking. CONCLUSIONS. The current results indicated that a positive family history of BC may have interacted with smoking habits to increase the risk of BC in the study population." + }, + "questions": [ + { + "id": "fe06950b-6824-4e54-9ad4-c5aeca13ec7b", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 1287, + "text": "positive family history" + }, + { + "answer_start": 1342, + "text": "smoking habits" + }, + { + "answer_start": 971, + "text": "ever-smoking relatives who had probands diagnosed at a younger age (ages 40-65 years)" + }, + { + "answer_start": 1203, + "text": "family history of BC and smoking" + }, + { + "answer_start": 628, + "text": "probands who had smoked and who also had a positive family history" + } + ] + } + ] +} \ No newline at end of file diff --git a/9e26faf6-3fb3-4cd5-b5ad-01a277db4481.json b/9e26faf6-3fb3-4cd5-b5ad-01a277db4481.json new file mode 100644 index 0000000000000000000000000000000000000000..28a7369d9166c647cbb79bc8c18460ab8b7289c5 --- /dev/null +++ b/9e26faf6-3fb3-4cd5-b5ad-01a277db4481.json @@ -0,0 +1,43 @@ +{ + "id": "9e26faf6-3fb3-4cd5-b5ad-01a277db4481", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "16187269", + "text": "BACKGROUND:\nIt is well established that the incidence of nonmelanoma skin carcinoma is increased in renal transplantation recipients. However, existing studies are not in agreement over whether patients who undergo transplantation have an increased risk of melanoma. The objective of this study was to estimate the risk of melanoma among immunosuppressed renal transplantation recipients and to determine whether that risk is associated with patient and transplantation characteristics.\n\nMETHODS:\nThe authors studied 89,786 patients who underwent renal transplantation between 1988 and 1998 using the United States Renal Data System. Age standardized (to the United States 2000 population) incidence rates for melanoma were computed as diagnoses per 100,000 population and were compared with rates from the Surveillance, Epidemiology, and End Results (SEER) data. Incidence rates also were stratified to examine differences by age and gender.\n\nRESULTS:\nOf the 89,786 patients who underwent transplantation, 246 patients developed melanoma. The age-adjusted incidence rate of melanoma among renal transplantation recipients was 55.9 diagnoses per 100,000 population. This represented an increase in age-adjusted, standardized risk that was 3.6 times greater than the SEER population. Stratified analysis suggested that the risk of melanoma accelerated in male transplantation recipients as age increased, but the risk leveled off with age among female transplantation recipients. Finally, there was a trend for patients who experienced at least 1 acute rejection episode to develop melanoma (odds ratio = 1.34; P = 0.059).\n\nCONCLUSIONS:\nRenal transplantation recipients were nearly 3.6 times more likely to develop melanoma than the general population. Physicians who care for renal transplantation recipients should be vigilant in screening for melanoma." + }, + "questions": [ + { + "id": "3834a671-bb4a-491f-94a0-06a201d8bc81", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 1354, + "text": "male transplantation recipients as age increased" + }, + { + "answer_start": 1510, + "text": "patients who experienced at least 1 acute rejection episode" + }, + { + "answer_start": 1636, + "text": "Renal transplantation recipients" + } + ] + } + ] +} \ No newline at end of file diff --git a/9ead5aae-6d1e-45f2-a9d8-cb11615c5ea6.json b/9ead5aae-6d1e-45f2-a9d8-cb11615c5ea6.json new file mode 100644 index 0000000000000000000000000000000000000000..13e0cd1dc43d3a2737c5a8a81be269c82de8fd70 --- /dev/null +++ b/9ead5aae-6d1e-45f2-a9d8-cb11615c5ea6.json @@ -0,0 +1,37 @@ +{ + "id": "9ead5aae-6d1e-45f2-a9d8-cb11615c5ea6", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "32159744", + "text": "IMPORTANCE:\nAlthough bariatric surgery is effective against morbid obesity, the association of this surgery with the risk of colorectal cancer remains controversial.\n\nOBJECTIVE:\nTo assess whether bariatric surgery is associated with altered risk of colorectal cancer among individuals with obesity.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nThis retrospective, population-based, multicenter, cohort study based on French electronic health data included 1 045 348 individuals with obesity, aged 50 to 75 years, and free of colorectal cancer at baseline. All inpatients with obesity having data recorded during a hospital stay between 2009 and 2018 by the French national health insurance information system database were followed up for a mean (SD) of 5.3 (2.1) years for those who did not undergo bariatric surgery and 5.7 (2.2) years for those who underwent bariatric surgery. Two groups of patients comparable in terms of age, sex, body mass index, follow-up, comorbidities, and conditions who did or did not undergo surgery were also obtained by propensity score matching.\n\nEXPOSURES:\nBariatric surgery (n = 74 131), including adjustable gastric banding, sleeve gastrectomy, gastric bypass; or no bariatric surgery (n = 971 217).\n\nMAIN OUTCOMES AND MEASURES:\nPrimary outcome was incident colorectal cancer. Standardized incidence ratios were calculated using age-, sex-, and calendar year-matched colorectal cancer incidence among the general French population during the corresponding years. Secondary outcome was incident colorectal benign polyps.\n\nRESULTS:\nAmong a total of 1 045 348 patients, the mean (SD) age was 57.3 (5.5) years for the 74 131 patients in the surgical cohort vs 63.4 (7.0) years for the 971 217 patients in the nonsurgical cohort. The mean (SD) follow-up was 6.2 (2.1) years for patients who underwent adjustable gastric banding, 5.5 (2.1) years for patients who underwent sleeve gastrectomy, and 5.7 (2.2) years for patients who underwent gastric bypass. In total, 13 052 incident colorectal cancers (1.2%) and 63 649 colorectal benign polyps were diagnosed. The rate of colorectal cancer was 0.6% in the bariatric surgery cohort and 1.3% in the cohort without bariatric surgery. In the latter cohort, 9417 cases were expected vs 12 629 observed, a standardized incidence ratio of 1.34 (95% CI, 1.32-1.36). In the bariatric surgery cohort, 428 cases were expected and 423 observed, a standardized incidence ratio of 1.0 (95% CI, 0.90-1.09). Propensity score-matched hazard ratios in comparable operated vs nonoperated groups were 0.68 (95% CI, 0.60-0.77) for colorectal cancer and 0.56 (95% CI, 0.53-0.59) for colorectal benign polyp. There were fewer new diagnoses of colorectal cancer after gastric bypass (123 of 22 343 [0.5%]) and sleeve gastrectomy (185 of 35 328 [0.5%]) than after adjustable gastric banding (115 of 16 460 [0.7%]), and more colorectal benign polyps after adjustable gastric banding (775 of 15 647 [5.0%]) than after gastric bypass (639 of 20 863 [3.1%]) or sleeve gastrectomy (1005 of 32 680 [3.1%]).\n\nCONCLUSION AND RELEVANCE:\nThe results of this nationwide cohort study suggested that following bariatric surgery, patients with obesity share the same risk of colorectal cancer as the general population, whereas for patients with obesity who do not undergo bariatric surgery, the risk is 34% above that of the general population." + }, + "questions": [ + { + "id": "2b88cce0-b0a3-40e0-9fcf-7ca86bea8bfb", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 3264, + "text": "patients with obesity who do not undergo bariatric surgery" + } + ] + } + ] +} \ No newline at end of file diff --git a/9eb53eec-d0e3-4527-ac83-a445ffecec28.json b/9eb53eec-d0e3-4527-ac83-a445ffecec28.json new file mode 100644 index 0000000000000000000000000000000000000000..b0741388990a3ad3f4ecdd450b687a8288c762f8 --- /dev/null +++ b/9eb53eec-d0e3-4527-ac83-a445ffecec28.json @@ -0,0 +1,34 @@ +{ + "id": "9eb53eec-d0e3-4527-ac83-a445ffecec28", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "28379800", + "text": "BACKGROUND:\nBody-weight fluctuation is a risk factor for death and coronary events in patients without cardiovascular disease. It is not known whether variability in body weight affects outcomes in patients with coronary artery disease.\n\nMETHODS:\nWe determined intraindividual fluctuations in body weight from baseline weight and follow-up visits and performed a post hoc analysis of the Treating to New Targets trial, which involved assessment of the efficacy and safety of lowering low-density lipoprotein cholesterol levels with atorvastatin. The primary outcome was any coronary event (a composite of death from coronary heart disease, nonfatal myocardial infarction, resuscitated cardiac arrest, revascularization, or angina). Secondary outcomes were any cardiovascular event (a composite of any coronary event, a cerebrovascular event, peripheral vascular disease, or heart failure), death, myocardial infarction, or stroke.\n\nRESULTS:\nAmong 9509 participants, after adjustment for risk factors, baseline lipid levels, mean body weight, and weight change, each increase of 1 SD in body-weight variability (measured according to average successive variability and used as a time-dependent covariate) was associated with an increase in the risk of any coronary event (2091 events; hazard ratio, 1.04; 95% confidence interval [CI], 1.01 to 1.07; P=0.01), any cardiovascular event (2727 events; hazard ratio, 1.04; 95% CI, 1.02 to 1.07; P\u003c0.001), and death (487 events; hazard ratio,1.09; 95% CI, 1.07 to 1.12; P\u003c0.001). Among patients in the quintile with the highest variation in body weight, the risk of a coronary event was 64% higher, the risk of a cardiovascular event 85% higher, death 124% higher, myocardial infarction 117% higher, and stroke 136% higher than it was among those in the quintile with the lowest variation in body weight in adjusted models.\n\nCONCLUSIONS:\nAmong participants with coronary artery disease, fluctuation in body weight was associated with higher mortality and a higher rate of cardiovascular events independent of traditional cardiovascular risk factors. (Funded by Pfizer; ClinicalTrials.gov number, NCT00327691 .)." + }, + "questions": [ + { + "id": "85781ca8-7dc5-43ae-8e49-aafe1ce65243", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1929, + "text": "fluctuation in body weight" + } + ] + } + ] +} \ No newline at end of file diff --git a/9f310015-2b7b-498d-be55-a6ff2ff69f28.json b/9f310015-2b7b-498d-be55-a6ff2ff69f28.json new file mode 100644 index 0000000000000000000000000000000000000000..121a5f961e74605331fa4888584f4a90e877f2f8 --- /dev/null +++ b/9f310015-2b7b-498d-be55-a6ff2ff69f28.json @@ -0,0 +1,42 @@ +{ + "id": "9f310015-2b7b-498d-be55-a6ff2ff69f28", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "11238268", + "text": "BACKGROUND:\nWe examined the relative importance of diastolic (DBP), systolic (SBP) and pulse pressure (PP) as predictors of coronary heart disease (CHD) risk in different age groups of Framingham Heart Study participants.\n\nMETHODS AND RESULTS:\nWe studied 3060 men and 3479 women between 20 and 79 years of age who were free of CHD and were not on antihypertensive drug therapy at baseline. Cox regression adjusted for age, sex, and other risk factors was used to assess the relations of BP indexes to CHD risk over a 20-year follow-up. In the group \u003c50 years of age, DBP was the strongest predictor of CHD risk (hazard ratio [HR] per 10 mm Hg increment, 1.34; 95% CI, 1.18 to 1.51) rather than SBP (HR, 1.14; 95% CI, 1.06 to 1.24) or PP (HR, 1.02; 95% CI, 0.89 to 1.17). In the group 50 to 59 years of age, risks were comparable for all 3 BP indexes. In the older age group, the strongest predictor of CHD risk was PP (HR, 1.24; 95% CI, 1.16 to 1.33). When both SBP and DBP were considered jointly, the former was directly and the latter was inversely related to CHD risk in the oldest age group\n\nCONCLUSIONS:\nWith increasing age, there was a gradual shift from DBP to SBP and then to PP as predictors of CHD risk. In patients \u003c50 years of age, DBP was the strongest predictor. Age 50 to 59 years was a transition period when all 3 BP indexes were comparable predictors, and from 60 years of age on, DBP was negatively related to CHD risk so that PP became superior to SBP." + }, + "questions": [ + { + "id": "97c26a6b-a481-4593-bffd-ad221d3f9edc", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1245, + "text": "DBP" + }, + { + "answer_start": 535, + "text": " In the group \u003c50 years of age, DBP was the strongest predictor" + }, + { + "answer_start": 851, + "text": "In the older age group, the strongest predictor of CHD risk was PP" + } + ] + } + ] +} \ No newline at end of file diff --git a/9fad5d7e-3672-4f7f-a410-eb1d8e74f843.json b/9fad5d7e-3672-4f7f-a410-eb1d8e74f843.json new file mode 100644 index 0000000000000000000000000000000000000000..778ba36e55449dc6981f665a2461acf19f482838 --- /dev/null +++ b/9fad5d7e-3672-4f7f-a410-eb1d8e74f843.json @@ -0,0 +1,34 @@ +{ + "id": "9fad5d7e-3672-4f7f-a410-eb1d8e74f843", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "20031199", + "text": "BACKGROUND:\nAssociations of C-reactive protein (CRP) concentration with risk of major diseases can best be assessed by long-term prospective follow-up of large numbers of people. We assessed the associations of CRP concentration with risk of vascular and non-vascular outcomes under different circumstances.\n\nMETHODS:\nWe meta-analysed individual records of 160 309 people without a history of vascular disease (ie, 1.31 million person-years at risk, 27 769 fatal or non-fatal disease outcomes) from 54 long-term prospective studies. Within-study regression analyses were adjusted for within-person variation in risk factor levels.\n\nRESULTS:\nLog(e) CRP concentration was linearly associated with several conventional risk factors and inflammatory markers, and nearly log-linearly with the risk of ischaemic vascular disease and non-vascular mortality. Risk ratios (RRs) for coronary heart disease per 1-SD higher log(e) CRP concentration (three-fold higher) were 1.63 (95% CI 1.51-1.76) when initially adjusted for age and sex only, and 1.37 (1.27-1.48) when adjusted further for conventional risk factors; 1.44 (1.32-1.57) and 1.27 (1.15-1.40) for ischaemic stroke; 1.71 (1.53-1.91) and 1.55 (1.37-1.76) for vascular mortality; and 1.55 (1.41-1.69) and 1.54 (1.40-1.68) for non-vascular mortality. RRs were largely unchanged after exclusion of smokers or initial follow-up. After further adjustment for fibrinogen, the corresponding RRs were 1.23 (1.07-1.42) for coronary heart disease; 1.32 (1.18-1.49) for ischaemic stroke; 1.34 (1.18-1.52) for vascular mortality; and 1.34 (1.20-1.50) for non-vascular mortality.\n\nINTERPRETATION:\nCRP concentration has continuous associations with the risk of coronary heart disease, ischaemic stroke, vascular mortality, and death from several cancers and lung disease that are each of broadly similar size. The relevance of CRP to such a range of disorders is unclear. Associations with ischaemic vascular disease depend considerably on conventional risk factors and other markers of inflammation.\n\nFUNDING:\nBritish Heart Foundation, UK Medical Research Council, BUPA Foundation, and GlaxoSmithKline." + }, + "questions": [ + { + "id": "137ce794-7879-4e41-bf47-5d0d42be7849", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1633, + "text": "CRP concentration" + } + ] + } + ] +} \ No newline at end of file diff --git a/9fbc7840-62d4-4413-aafe-06a139a192e7.json b/9fbc7840-62d4-4413-aafe-06a139a192e7.json new file mode 100644 index 0000000000000000000000000000000000000000..cb67f49fec84f19dda17d781dc0329e080078223 --- /dev/null +++ b/9fbc7840-62d4-4413-aafe-06a139a192e7.json @@ -0,0 +1,35 @@ +{ + "id": "9fbc7840-62d4-4413-aafe-06a139a192e7", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "17919705", + "text": "In the 1960s, the prevalence of asthma and allergic diseases began to increase worldwide. Currently, the burden of the disease is more than 300 million people affected. We hypothesize that as populations grow more prosperous, more time is spent indoors, and there is less exposure to sunlight, leading to decreased cutaneous vitamin D production. Coupled with inadequate intake from foods and supplements, this then leads to vitamin D deficiency, particularly in pregnant women, resulting in more asthma and allergy in their offspring. Vitamin D has been linked to immune system and lung development in utero, and our epidemiologic studies show that higher vitamin D intake by pregnant mothers reduces asthma risk by as much as 40% in children 3 to 5 years old. Vitamin D deficiency has been associated with obesity, African American race (particularly in urban, inner-city settings), and recent immigrants to westernized countries, thus reflecting the epidemiologic patterns observed in the asthma epidemic. Providing adequate vitamin D supplementation in pregnancy may lead to significant decreases in asthma incidence in young children." + }, + "questions": [ + { + "id": "8b5d047b-a111-4929-aed9-0f9a6fd8875a", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 425, + "text": "vitamin D deficiency, particularly in pregnant women" + } + ] + } + ] +} \ No newline at end of file diff --git a/a0533936-1808-41cd-b3a2-33713a93a670.json b/a0533936-1808-41cd-b3a2-33713a93a670.json new file mode 100644 index 0000000000000000000000000000000000000000..b170f53b491c5f5b7db0f324a2234e7e321597ef --- /dev/null +++ b/a0533936-1808-41cd-b3a2-33713a93a670.json @@ -0,0 +1,34 @@ +{ + "id": "a0533936-1808-41cd-b3a2-33713a93a670", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "9610529", + "text": "BACKGROUND:\nC-reactive protein (CRP) is a sensitive marker of inflammation, and elevated levels have been associated with future risk of myocardial infarction (MI). However, whether measurement of CRP adds to the predictive value of total cholesterol (TC) and HDL cholesterol (HDL-C) in determining risk is uncertain.\n\nMETHODS AND RESULTS:\nAmong 14916 apparently healthy men participating in the Physicians' Health Study, baseline levels of CRP, TC, and HDL-C were measured among 245 study subjects who subsequently developed a first MI (cases) and among 372 subjects who remained free of cardiovascular disease during an average follow-up period of 9 years (controls). In univariate analyses, high baseline levels of CRP, TC, and TC:HDL-C ratio were each associated with significantly increased risks of future MI (all P values \u003c0.001). In multivariate analyses, models incorporating CRP and lipid parameters provided a significantly better method to predict risk than did models using lipids alone (all likelihood ratio test P values \u003c0.003). For example, relative risks of future MI among those with high levels of both CRP and TC (RR=5.0, P=0.0001) were greater than the product of the individual risks associated with isolated elevations of either CRP (RR=1.5) or TC (RR=2.3). In stratified analyses, baseline CRP level was predictive of risk for those with low as well as high levels of TC and the TC:HDL-C ratio. These findings were virtually identical in analyses limited to nonsmokers and after control for other cardiovascular risk factors.\n\nCONCLUSIONS:\nIn prospective data from a large cohort of apparently healthy men, baseline CRP level added to the predictive value of lipid parameters in determining risk of first MI." + }, + "questions": [ + { + "id": "ffa5440b-ada7-4fc4-afe6-5103ec231066", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1103, + "text": "high levels of both CRP and TC" + } + ] + } + ] +} \ No newline at end of file diff --git a/a0d033e6-8e56-4676-9b76-42b1634dc56f.json b/a0d033e6-8e56-4676-9b76-42b1634dc56f.json new file mode 100644 index 0000000000000000000000000000000000000000..7823d1bd050f45a7dd33deec5ea7df706c1fd429 --- /dev/null +++ b/a0d033e6-8e56-4676-9b76-42b1634dc56f.json @@ -0,0 +1,39 @@ +{ + "id": "a0d033e6-8e56-4676-9b76-42b1634dc56f", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "7551368", + "text": "We prospectively evaluated the association of hormone replacement therapy and asthma incidence in a cohort of pre- and postmenopausal women 34 to 68 yr of age. During 582, 135 person-years of follow-up between 1980 and 1990, 726 new cases of asthma were documented. Postmenopausal women who were never users of replacement hormones had a significantly lower age-adjusted risk of asthma than premenopausal women (relative risk = 0.65; 95% confidence interval [CI] = 0.46 to 0.92). Among naturally menopausal women, the age-adjusted relative risk of asthma for ever use of postmenopausal hormones was 1.49 (95% CI = 1.10 to 2.00); for current use of hormones (conjugated estrogens with or without progesterone), 1.50 (95% CI = 0.98 to 2.30); and for past use, 1.52 (95% CI = 1.08 to 2.13), compared with never use of hormones. Ever users of 10 or more years' duration had twice the age-adjusted risk of asthma compared with women who never used postmenopausal hormones (95% CI = 1.39 to 2.87). Among current users of conjugated estrogens, there was a positive dose-response demonstrated between daily dose and asthma risk (p for trend = 0.007). While confirmatory studies are warranted, these data suggest that estrogen plays a role in the pathophysiology of asthma and that long-term use and/or high doses of postmenopausal hormone therapy increase subsequent risk of asthma." + }, + "questions": [ + { + "id": "6924069b-a69d-4df6-bf8f-583db703235f", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1273, + "text": "long-term use and/or high doses of postmenopausal hormone therapy" + }, + { + "answer_start": 559, + "text": "ever use of postmenopausal hormones" + } + ] + } + ] +} \ No newline at end of file diff --git a/a123a4d9-d544-4606-a9f4-9e9633925c87.json b/a123a4d9-d544-4606-a9f4-9e9633925c87.json new file mode 100644 index 0000000000000000000000000000000000000000..0d6726903600c6cbc01a8a4c08cbf1d71c8d4b69 --- /dev/null +++ b/a123a4d9-d544-4606-a9f4-9e9633925c87.json @@ -0,0 +1,50 @@ +{ + "id": "a123a4d9-d544-4606-a9f4-9e9633925c87", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "26190088", + "text": "OBJECTIVE:\nTo identify the impact of smoking intensity on tumor characteristics at the time of initial bladder cancer diagnosis.\n\nMETHODS:\nWe retrospectively reviewed our institution's prospective database of patients diagnosed with bladder cancer from 1987 to 2009. Only patients with urothelial cell carcinoma and recorded tobacco history were included. Patients were stratified by tobacco history into nonsmokers, light smokers (≤ 30 pack-years), and heavy smokers (\u003e 30 pack-years). An additional analysis was performed looking at patients meeting National Lung Cancer Screening Trial (NLCST) criteria (55- to 74-year-old patients with ≥ 30 pack-years smoking history and \u003c 15 years since smoking cessation). Clinicopathologic characteristics of the initial bladder tumor at time of diagnosis were analyzed.\n\nRESULTS:\nWe identified 197 (26.6%) nonsmokers, 251 (33.9%) light smokers, and 292 (39.5%) heavy smokers. Males were more likely to be heavy smokers (44.5% vs 23.6%, P ≤ .01). Compared with nonsmokers and light smokers, the initial tumors in heavy smokers were more likely to be high grade with a more advanced clinical stage. Heavy smokers were more likely to present with muscle-invasive bladder cancer (MIBC) at initial diagnosis. When compared to nonsmokers, the odds ratio for presenting with MIBC was 1.18 (95% confidence interval = 0.68-2.1) for light smokers and 1.38 (95% confidence interval = 1.06-1.8) for heavy smokers. Of 793 patients with adequate information for analysis, 184 (23.2%) met NLCST criteria. Those meeting NLCST criteria were most likely to be male, to present with gross hematuria, and to have initial tumors that were high grade and muscle invasive. NLCST criteria eligibility remained associated with MIBC on multivariate analysis.\n\nCONCLUSION:\nHeavy smokers and patients meeting NLCST criteria are more likely to have high-grade tumors with detrusor muscle invasion at initial presentation." + }, + "questions": [ + { + "id": "8315e8ac-2fbe-4b8e-8bce-2a0da7b0e8ef", + "text": "What are the risk factors of Bladder Cancer?", + "answers": [ + { + "answer_start": 1788, + "text": "Heavy smokers" + }, + { + "answer_start": 1806, + "text": "patients meeting NLCST criteria" + }, + { + "answer_start": 552, + "text": "National Lung Cancer Screening Trial (NLCST) criteria (55- to 74-year-old patients with ≥ 30 pack-years smoking history and \u003c 15 years since smoking cessation)" + }, + { + "answer_start": 1365, + "text": "light smokers" + }, + { + "answer_start": 1429, + "text": "heavy smokers" + } + ] + } + ] +} \ No newline at end of file diff --git a/a22c76b1-1cfb-4c07-88d2-0e4e47184500.json b/a22c76b1-1cfb-4c07-88d2-0e4e47184500.json new file mode 100644 index 0000000000000000000000000000000000000000..10ac82c004e71c75ccf9ccca7b246f52aff65fc0 --- /dev/null +++ b/a22c76b1-1cfb-4c07-88d2-0e4e47184500.json @@ -0,0 +1,46 @@ +{ + "id": "a22c76b1-1cfb-4c07-88d2-0e4e47184500", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "16710672", + "text": "AIMS/HYPOTHESIS:\nWe examined sex-specific associations between cigarette smoking and incident type 2 diabetes mellitus in Germany.\n\nSUBJECTS, MATERIALS AND METHODS:\nThe study was based on 5,470 men and 5,422 women (aged 25-74 years) without diabetes who participated in one of the three population-based MONICA Augsburg surveys between 1984 and 1995. Incident cases of type 2 diabetes were assessed using follow-up questionnaires. Hazard ratios (HRs) were estimated from Cox proportional hazard models.\n\nRESULTS:\nUp to 31 December 2002 a total of 409 cases of incident type 2 diabetes among men and 263 among women were registered. The number of cigarettes and the nicotine and tar consumption per day were associated with a significantly increased risk of type 2 diabetes among men, but not among women; this could be due to the low power of the study in women. After multivariable adjustment, the HRs for type 2 diabetes compared with never-smokers were 1.48, 2.03 and 2.10 for men smoking 1 to 14, 15 to 19 and \u003e or =20 cigarettes/day (p for trend \u003c0.0001) and 1.25, 1.34 and 1.37 for women smoking 1 to 9, 10 to 19 and \u003e or =20 cigarettes/day (p for trend 0.0985). Compared with never-smokers, the HRs for increasing tar intake in men (1-167, 168-259 and \u003e or =260 mg/day) were 1.45, 2.32 and 2.07 (p for trend \u003c0.0001); the respective HRs in women (1-89, 90-194 and \u003e or =195 mg/day) were 1.18, 1.57 and 1.24 (p for trend 0.1159).\n\nCONCLUSIONS/INTERPRETATION:\nCigarette smoking is an important modifiable risk factor of type 2 diabetes particularly in men from the general population." + }, + "questions": [ + { + "id": "cbe26ab1-d896-4e4b-a398-352aa2cea09e", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1465, + "text": "Cigarette smoking" + }, + { + "answer_start": 632, + "text": "The number of cigarettes and the nicotine and tar consumption per day" + }, + { + "answer_start": 980, + "text": "men smoking 1 to 14, 15 to 19 and \u003e or =20 cigarettes/day" + }, + { + "answer_start": 1088, + "text": "women smoking 1 to 9, 10 to 19 and \u003e or =20 cigarettes/day" + } + ] + } + ] +} \ No newline at end of file diff --git a/a28cfc44-a181-4961-ac12-3e45a0a9f54e.json b/a28cfc44-a181-4961-ac12-3e45a0a9f54e.json new file mode 100644 index 0000000000000000000000000000000000000000..19bf75abcb1e42421767e6f08dd0f564d1c664ea --- /dev/null +++ b/a28cfc44-a181-4961-ac12-3e45a0a9f54e.json @@ -0,0 +1,34 @@ +{ + "id": "a28cfc44-a181-4961-ac12-3e45a0a9f54e", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "14534877", + "text": "BACKGROUND:\nContralateral, metachronous upper urinary tract (UUT) tumors after primary transitional cell carcinoma (TCC) of the UUT are reported rarely, and to the authors' knowledge the risk factors have not been determined to date. In addition, few reports have described the characteristics of recurrent bladder tumors and contralateral UUT tumors and any relation between theses tumor types.\n\nMETHODS:\nStatistical analysis of data from 223 patients with documented primary UUT-TCC was undertaken. After excluding bilateral involvement and distant metastases, 12 variables were analyzed by multivariate analysis in 189 patients to determine the risk factors for recurrent urothelial tumors.\n\nRESULTS:\nThe incidence rates of recurrent bladder tumors and contralateral UUT tumors were 31.2% and 5.8%, respectively. Multiplicity was determined as a risk factor for recurrent bladder tumors. Renal insufficiency, uremia, and concurrent bladder tumors significantly predisposed patients to develop contralateral UUT tumors after primary UUT-TCC. The time intervals and stage distributions differed significantly between recurrent bladder tumors and contralateral UTT tumors. Patients who had recurrent bladder tumors had earlier stage tumors and had a shorter time to recur compared with patients who had contralateral, metachronous UUT tumors.\n\nCONCLUSIONS:\nFor patients with primary UUT-TCC, regular follow-up by cystoscopy is necessary to detect recurrent bladder tumors. Intravenous urography or retrograde pyelography should be performed for patients who have a high risk of developing contralateral UUT tumors." + }, + "questions": [ + { + "id": "caca559d-cb2f-4ba3-a00a-b954bd0aca53", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 1361, + "text": "patients with primary UUT-TCC" + } + ] + } + ] +} \ No newline at end of file diff --git a/a35cc4f2-5d65-454a-afbc-c881795f2ae9.json b/a35cc4f2-5d65-454a-afbc-c881795f2ae9.json new file mode 100644 index 0000000000000000000000000000000000000000..7813ff3e03d52bc07cb0e039e4946e2bd394b433 --- /dev/null +++ b/a35cc4f2-5d65-454a-afbc-c881795f2ae9.json @@ -0,0 +1,34 @@ +{ + "id": "a35cc4f2-5d65-454a-afbc-c881795f2ae9", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "27840181", + "text": "BACKGROUND \u0026 AIMS:\nLittle is known about the pathogenic mechanisms of gluten immunogenicity in patients with celiac disease. We studied temporal associations between infections and the development of celiac disease autoimmunity, and examined effects of HLA alleles, rotavirus vaccination status, and infant feeding.\n\nMETHODS:\nWe monitored 6327 children in the United States and Europe carrying HLA risk genotypes for celiac disease from 1 to 4 years of age for presence of tissue transglutaminase autoantibodies (the definition of celiac disease autoimmunity), until March 31, 2015. Parental reports of gastrointestinal and respiratory infections were collected every third month from birth. We analyzed time-varying relationships among reported infections, rotavirus vaccination status, time to first introduction of gluten, breastfeeding, and risk of celiac disease autoimmunity using proportional hazard models.\n\nRESULTS:\nWe identified 13,881 gastrointestinal infectious episodes (GIE) and 79,816 respiratory infectious episodes. During the follow-up period, 732 of 6327 (11.6%) children developed celiac disease autoimmunity. A GIE increased the risk of celiac disease autoimmunity within the following 3 months by 33% (hazard ratio [HR], 1.33; 95% confidence interval [CI], 1.11-1.59). This risk increased 2-fold among children born in winter and introduced to gluten before age 6 months (HR, 2.08; 95% CI, 1.46-2.98), and increased 10-fold among children without HLA-DQ2 alleles and breastfed for fewer than 4 months (HR, 9.76; 95% CI, 3.87-24.8). Risk of celiac disease autoimmunity was reduced in children vaccinated against rotavirus and introduced to gluten before age 6 months (HR, 0.57; 95% CI, 0.36-0.88).\n\nCONCLUSIONS:\nGastrointestinal infections increase the risk of celiac disease autoimmunity in children with genetic susceptibility to this autoimmune disorder. The risk is modified by HLA genotype, infant gluten consumption, breastfeeding, and rotavirus vaccination, indicating complex interactions among infections, genetic factors, and diet in the etiology of celiac disease in early childhood." + }, + "questions": [ + { + "id": "ccf6a3ad-4e16-44f2-bece-b5986beade87", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 1733, + "text": "Gastrointestinal infections" + } + ] + } + ] +} \ No newline at end of file diff --git a/a35ce177-bc7a-4ffc-97e3-902848468ca9.json b/a35ce177-bc7a-4ffc-97e3-902848468ca9.json new file mode 100644 index 0000000000000000000000000000000000000000..cb540f0094e63b4efd910cd51f94c6a2060d4a36 --- /dev/null +++ b/a35ce177-bc7a-4ffc-97e3-902848468ca9.json @@ -0,0 +1,38 @@ +{ + "id": "a35ce177-bc7a-4ffc-97e3-902848468ca9", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "26815017", + "text": "BACKGROUND:\nThe European Society for Paediatric Gastroenterology, Hepatology and Nutrition recommended in 2008, based on observational data, to avoid both early (\u003c4 months) and late (≥7 months) introduction of gluten and to introduce gluten while the infant is still being breast-fed. New evidence prompted ESPGHAN to revise these recommendations.\n\nOBJECTIVE:\nTo provide updated recommendations regarding gluten introduction in infants and the risk of developing coeliac disease (CD) during childhood.\n\nSUMMARY:\nThe risk of inducing CD through a gluten-containing diet exclusively applies to persons carrying at least one of the CD risk alleles. Because genetic risk alleles are generally not known in an infant at the time of solid food introduction, the following recommendations apply to all infants, although they are derived from studying families with first-degree relatives with CD. Although breast-feeding should be promoted for its other well-established health benefits, neither any breast-feeding nor breast-feeding during gluten introduction has been shown to reduce the risk of CD. Gluten may be introduced into the infant's diet anytime between 4 and 12 completed months of age. In children at high risk for CD, earlier introduction of gluten (4 vs 6 months or 6 vs 12 months) is associated with earlier development of CD autoimmunity (defined as positive serology) and CD, but the cumulative incidence of each in later childhood is similar. Based on observational data pointing to the association between the amount of gluten intake and risk of CD, consumption of large quantities of gluten should be avoided during the first weeks after gluten introduction and during infancy. The optimal amounts of gluten to be introduced at weaning, however, have not been established." + }, + "questions": [ + { + "id": "99b63ef9-5a3f-4a80-909f-07b463d2f1aa", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 1192, + "text": " In children at high risk for CD, earlier introduction of gluten (4 vs 6 months or 6 vs 12 months)" + }, + { + "answer_start": 1564, + "text": "consumption of large quantities of gluten should be avoided during the first weeks after gluten introduction and during infancy" + } + ] + } + ] +} \ No newline at end of file diff --git a/a3aee851-c971-44f8-8d15-e77f5942efff.json b/a3aee851-c971-44f8-8d15-e77f5942efff.json new file mode 100644 index 0000000000000000000000000000000000000000..b9fbf2943d82ff6f276b134ab79f3f9ab7d8153b --- /dev/null +++ b/a3aee851-c971-44f8-8d15-e77f5942efff.json @@ -0,0 +1,34 @@ +{ + "id": "a3aee851-c971-44f8-8d15-e77f5942efff", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "9727541", + "text": "BACKGROUND:\nC-reactive protein (CRP) predicts risk of myocardial infarction (MI) and stroke among apparently healthy men, but in women, virtually no data are available.\n\nMETHODS AND RESULTS:\nCRP was measured in baseline blood samples from 122 apparently healthy participants in the Women's Health Study who subsequently suffered a first cardiovascular event and from 244 age- and smoking-matched control subjects who remained free of cardiovascular disease during a 3-year follow-up period. Women who developed cardiovascular events had higher baseline CRP levels than control subjects (P=0.0001), such that those with the highest levels at baseline had a 5-fold increase in risk of any vascular event (RR=4.8; 95% CI, 2.3 to 10.1; P=0.0001) and a 7-fold increase in risk of MI or stroke (RR=7.3; 95% CI, 2.7 to 19.9; P=0.0001). Risk estimates were independent of other risk factors, and prediction models that included CRP provided a better method to predict risk than models that excluded CRP (all P values \u003c0.01). In stratified analyses, CRP was a predictor among subgroups of women with low as well as high risk as defined by other cardiovascular risk factors.\n\nCONCLUSIONS:\nIn these prospective data among women, CRP is a strong independent risk factor for cardiovascular disease that adds to the predictive value of risk models based on usual factors alone. (Circulation. 1998;98:731-733.)" + }, + "questions": [ + { + "id": "6d08ce43-d620-47a9-aae5-58ab57f12404", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 537, + "text": "higher baseline CRP levels" + } + ] + } + ] +} \ No newline at end of file diff --git a/a416a50e-a170-473b-a52e-3733f3e80fa5.json b/a416a50e-a170-473b-a52e-3733f3e80fa5.json new file mode 100644 index 0000000000000000000000000000000000000000..1e062851604b2924e810406f223c3074447c13c7 --- /dev/null +++ b/a416a50e-a170-473b-a52e-3733f3e80fa5.json @@ -0,0 +1,39 @@ +{ + "id": "a416a50e-a170-473b-a52e-3733f3e80fa5", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "16963691", + "text": "STUDY OBJECTIVE:\nTo determine the modifying effects of sex and allergy history on the association between body mass index (BMI) and asthma prevalence.\n\nDESIGN:\nCross-sectional study of 86,144 Canadians who were 20 to 64 years of age in 2000-2001.\n\nSETTING:\nA national survey.\n\nMEASUREMENTS AND ANALYSIS:\nSelf-reported asthma, allergy history, height, and weight. Logistic regression analysis was used to detect effect modification and to adjust for covariates. Population weight and design effects associated with complex survey design were taken into consideration.\n\nRESULTS:\nThe adjusted odds ratios (ORs) for obesity associated with asthma was 1.85 (95% confidence interval [CI], 1.65 to 2.07) for women and 1.21 (95% CI, 1.05 to 1.40) for men. One unit of increased BMI was associated with an approximate 6% increase in asthma risk in women, and 3% in men. A stronger association between obesity and asthma was observed in nonallergic women than in allergic women, with the adjusted ORs being 2.53 (95% CI, 2.11 to 3.04) and 1.57 (95% CI, 1.36 to 1.82), respectively. For men, the corresponding ORs were 1.30 (95% CI, 1.05 to 1.62) and 1.18 (95% CI, 0.98 to 1.53), respectively.\n\nCONCLUSIONS:\nObesity is likely to have a larger effect on nonallergic asthma. The greater prevalence of nonallergic asthma in women may explain the stronger obesity-asthma association seen in women compared with men and children who have a greater prevalence of allergic asthma." + }, + "questions": [ + { + "id": "195deb2a-3035-4c4f-a36d-a1a5abca9d05", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 748, + "text": "One unit of increased BMI" + }, + { + "answer_start": 1197, + "text": "Obesity" + } + ] + } + ] +} \ No newline at end of file diff --git a/a46587a7-8bff-4161-9faf-f9a7ee28a010.json b/a46587a7-8bff-4161-9faf-f9a7ee28a010.json new file mode 100644 index 0000000000000000000000000000000000000000..9d87fd555520e0b9d8e3a18ad379068f6805cec8 --- /dev/null +++ b/a46587a7-8bff-4161-9faf-f9a7ee28a010.json @@ -0,0 +1,42 @@ +{ + "id": "a46587a7-8bff-4161-9faf-f9a7ee28a010", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "10738259", + "text": "The primary risk factor for bladder cancer is cigarette smoking. Using a combined analysis of 11 case-control studies, we have accurately measured the relationship between cigarette smoking and bladder cancer in men. Available smoking information on 2,600 male bladder cancer cases and 5,524 male controls included duration of smoking habit, number of cigarettes smoked per day and time since cessation of smoking habit for ex-smokers. There was a linear increasing risk of bladder cancer with increasing duration of smoking, ranging from an odds ratio (OR) of 1.96 after 20 years of smoking (95% confidence interval [CI] 1.48-2.61) to 5.57 after 60 years (CI 4.18-7.44). A dose relationship was observed between number of cigarettes smoked per day and bladder cancer up to a threshold limit of 15-20 cigarettes per day, OR = 4.50 (CI 3.81-5. 33), after which no increased risk was observed. An immediate decrease in risk of bladder cancer was observed for those who gave up smoking. This decrease was over 30% after 1-4 years, OR = 0.65 (0. 53-0.79), and was over 60% after 25 years of cessation, OR = 0.37 (0. 30-0.45). However, even after 25 years, the decrease in risk did not reach the level of the never-smokers, OR = 0.20. (0.17-0.24). The proportion of bladder cancer cases attributable to ever-smoking was 0.66 (0.61-0.70) for all men and 0.73 (0.66-0.79) for men younger than 60. These estimates are higher than previously calculated." + }, + "questions": [ + { + "id": "99eb0746-358c-49d3-97cb-a18b3bfea15a", + "text": "What are the risk factors of Bladder Cancer?", + "answers": [ + { + "answer_start": 494, + "text": "increasing duration of smoking" + }, + { + "answer_start": 957, + "text": "those who gave up smoking" + }, + { + "answer_start": 1298, + "text": "ever-smoking" + } + ] + } + ] +} \ No newline at end of file diff --git a/a4a3dc28-ce1c-4522-b438-0acf75cee2a9.json b/a4a3dc28-ce1c-4522-b438-0acf75cee2a9.json new file mode 100644 index 0000000000000000000000000000000000000000..719fd2a0948a8159e2571ac6ed8981e62c63e9a9 --- /dev/null +++ b/a4a3dc28-ce1c-4522-b438-0acf75cee2a9.json @@ -0,0 +1,35 @@ +{ + "id": "a4a3dc28-ce1c-4522-b438-0acf75cee2a9", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "26818409", + "text": "IMPORTANCE:\nIn the United States and Minnesota, melanoma incidence is rising more steeply among women than men younger than 50 years. To our knowledge, no study has examined age- and sex-specific associations between indoor tanning and melanoma to determine if these trends could be due to greater indoor tanning use among younger women.\n\nOBJECTIVE:\nTo examine associations between indoor tanning and melanoma among men and women younger than 50 years.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nPopulation-based case-control study conducted in Minnesota of 681 patients (465 [68.3%] women) diagnosed as having melanoma between 2004 and 2007, and 654 controls (446 [68.2%] women), ages 25 to 49 years.\n\nEXPOSURE:\nIndoor tanning, defined as any use, first age of use, and total sessions.\n\nMAIN OUTCOMES AND MEASURES:\nCrude and adjusted odds ratios (ORs) and 95% CIs were calculated for melanoma in relation to indoor tanning exposure for men and women by diagnosis or reference age (\u003c30, 30-39, 40-49 years). Sex-specific associations for indoor tanning and melanoma by anatomic site were examined.\n\nRESULTS:\nCompared with women aged 40 to 49 years, women younger than 40 years initiated indoor tanning at a younger age (16 vs 25 years, P \u003c .001) and reported more frequent indoor tanning (median number of sessions, 100 vs 40, P \u003c .001). Women younger than 30 years were 6 times more likely to be in the case than the control group if they tanned indoors (crude OR, 6.0; 95% CI, 1.3-28.5). Odds ratios were also significantly elevated among women, ages 30 to 49 years (adjusted OR, 3.5; 95% CI, 1.2-9.7 for women 30-39 years; adjusted OR, 2.3; 95% CI, 1.4-3.6 for women 40-49 years); a dose response was observed among women regardless of age. Among men, results by age were inconsistent. The strongest OR for indoor tanning by anatomic site was for melanomas arising on the trunk of women (adjusted OR, 3.7; 95% CI, 1.9-7.2).\n\nCONCLUSIONS AND RELEVANCE:\nIndoor tanning is a likely factor for the steeper increase in melanoma rates in the United States among younger women compared with men, given the timing of when women initiated indoor tanning relative to diagnosis. The melanoma epidemic can be expected to continue unless indoor tanning is restricted and reduced." + }, + "questions": [ + { + "id": "a125bd2f-e064-49d7-ab04-e513acb1edb7", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 1948, + "text": "Indoor tanning" + } + ] + } + ] +} \ No newline at end of file diff --git a/a4de1c50-1e4e-4a4a-8abc-862ba4ec244b.json b/a4de1c50-1e4e-4a4a-8abc-862ba4ec244b.json new file mode 100644 index 0000000000000000000000000000000000000000..a3fe6a644b3e504abfdc3ee246e4fc34eeb28441 --- /dev/null +++ b/a4de1c50-1e4e-4a4a-8abc-862ba4ec244b.json @@ -0,0 +1,42 @@ +{ + "id": "a4de1c50-1e4e-4a4a-8abc-862ba4ec244b", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "10709885", + "text": "Coeliac disease has emerged as a public health problem. The aim of the present study was to analyse trends in the occurrence of symptomatic coeliac disease in Swedish children from 1973 to 1997, and to explore any temporal relationship to changes in infant dietary patterns. We established a population-based prospective incidence register of coeliac disease in 1991, and, in addition, retrospective data from 1973 were collected. A total of 2151 cases fulfilled the diagnostic criteria. Furthermore. We collected national data on a yearly basis on duration of breastfeeding, intake of gluten-containing cereals and recommendations on when and how to introduce gluten into the diet of infants. From 1985 to 1987 the annual incidence rate in children below 2 y of age increased fourfold to 200-240 cases per 100000 person years, followed from 1995 by a sharp decline to the previous level of 50-60 cases per 100000 person years. This epidemic pattern is quite unique for a chronic disease of immunological pathogenesis, suggesting that prevention could be possible. The ecological observations made in this study are compatible with the epidemic being the result, at least in part, of a change in and an interplay among three factors within the area of infant feeding, i.e. amount of gluten given, age at introduction of gluten, and whether breastfeeding was ongoing or not when gluten was introduced. Other factor(s) may also have contributed, and the search for these should be intensified." + }, + "questions": [ + { + "id": "3a9f679d-9ff9-4df8-a4c5-a7386975ce4a", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 1273, + "text": "amount of gluten given" + }, + { + "answer_start": 1297, + "text": "age at introduction of gluten" + }, + { + "answer_start": 1332, + "text": "whether breastfeeding was ongoing or not when gluten was introduced" + } + ] + } + ] +} \ No newline at end of file diff --git a/a4fee198-1e97-462c-aed7-916fb13595d6.json b/a4fee198-1e97-462c-aed7-916fb13595d6.json new file mode 100644 index 0000000000000000000000000000000000000000..fbc79024d8f3ad0369f060c79279f19c59256896 --- /dev/null +++ b/a4fee198-1e97-462c-aed7-916fb13595d6.json @@ -0,0 +1,37 @@ +{ + "id": "a4fee198-1e97-462c-aed7-916fb13595d6", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "17919484", + "text": "BACKGROUND \u0026 AIMS:\nThe risk of developing colorectal neoplasia is not well established among family members of individuals with large adenomas, and screening strategies remain under debate in this population. This study aimed at quantifying the risk of colorectal adenomas and cancers using colonoscopic screening in first-degree relatives of patients with large adenomas.\n\nMETHODS:\nThis case-control study was performed in 18 endoscopic units of French nonuniversity hospitals. A colonoscopy was offered to first-degree relatives of 306 index cases with adenomas \u003e or =10 mm if they were alive, aged 40-75 years, and could be contacted by the index case. Among them, 168 were examined and matched for age, sex, and geographical area with 2 controls (n = 307). Controls were randomly selected from 1362 consecutive patients aged 40-75 years having undergone a colonoscopy for minor symptoms.\n\nRESULTS:\nThe prevalence of large adenomas and cancers was 8.4% and 4.2%, in relatives and controls, respectively. Odds ratios (ORs) associated with a history of large adenomas in relatives were 2.27 (95% confidence interval [CI], 1.01-5.09) for cancers or large adenomas, 1.21 (95% CI, 0.68-2.15) for small adenomas, and 1.56 (95% CI, 0.96-2.53) for all colorectal neoplasia. The risk of large adenomas and cancers was higher in relatives of index cases younger than 60 years (OR, 3.82; 95% CI, 0.92-15.87) and when the index case had large distal adenomas (OR, 3.14; 95% CI, 1.27-7.73).\n\nCONCLUSIONS:\nFirst-degree relatives of patients with large adenomas are at increased risk of developing colorectal cancers or large adenomas. This result has implications for screening in this high-risk population." + }, + "questions": [ + { + "id": "b7057d90-cfb4-4c21-b475-3e08c287f708", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1495, + "text": "First-degree relatives of patients with large adenomas" + } + ] + } + ] +} \ No newline at end of file diff --git a/a51cf4e3-3d23-43f2-9efc-4700b475374b.json b/a51cf4e3-3d23-43f2-9efc-4700b475374b.json new file mode 100644 index 0000000000000000000000000000000000000000..7749f0b3651a31b037741a297c20bd1dce6dbda6 --- /dev/null +++ b/a51cf4e3-3d23-43f2-9efc-4700b475374b.json @@ -0,0 +1,39 @@ +{ + "id": "a51cf4e3-3d23-43f2-9efc-4700b475374b", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "17889931", + "text": "BACKGROUND:\nThe percentage of asthma cases attributable to atopy is the subject of debate.\n\nOBJECTIVES:\nThe objectives were to estimate the percentage of asthma cases in the US population attributable to atopy and to examine associations between allergen-specific skin tests and asthma.\n\nMETHODS:\nData were obtained from the Third National Health and Nutrition Examination Survey, in which subjects age 6 to 59 years were skin tested with 10 allergens. Atopy was defined as at least 1 positive allergen-specific test. Doctor-diagnosed current asthma was assessed by questionnaire.\n\nRESULTS:\nIn the United States, 56.3% of the asthma cases were attributable to atopy, and that percentage was greater among males than females, among persons in the highest education category than in lower education categories, and among persons living in highly populated metropolitan areas than in all other areas. Each allergen-specific test was strongly associated with asthma before adjustment (odds ratios varied from 2.1 to 4.5); however, after adjustment by all the allergens, only tests to cat, Alternaria, white oak, and perennial rye were independently associated with asthma. Perennial rye was inversely associated with asthma. Of the 10 allergens, a positive response to cat accounted for the highest percentage of asthma cases (29.3%).\n\nCONCLUSION:\nAbout half of the current asthma cases in the US population represented by the Third National Health and Nutrition Examination Survey were attributable to atopy. Some allergen-specific skin tests were not independently associated with asthma.\n\nCLINICAL IMPLICATIONS:\nIf atopy could be prevented or reversed, or its effect on asthma blocked, then a large percentage of asthma cases in the US population could be prevented." + }, + "questions": [ + { + "id": "fd28f707-2d9b-461a-8927-0a9feb6d924d", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1071, + "text": "tests to cat, Alternaria, white oak, and perennial rye" + }, + { + "answer_start": 1614, + "text": "atopy" + } + ] + } + ] +} \ No newline at end of file diff --git a/a54fe76c-14ab-48dc-9f11-3e748ca6ac94.json b/a54fe76c-14ab-48dc-9f11-3e748ca6ac94.json new file mode 100644 index 0000000000000000000000000000000000000000..65e9a9229380e9d57aa3853b7f8231b659a279be --- /dev/null +++ b/a54fe76c-14ab-48dc-9f11-3e748ca6ac94.json @@ -0,0 +1,43 @@ +{ + "id": "a54fe76c-14ab-48dc-9f11-3e748ca6ac94", + "disease": { + "id": "H00056", + "names": [ + "Alzheimer disease", + "Dementia due to Alzheimer disease" + ], + "dbLinks": { + "icd10": [ + "G30" + ], + "mesh": [ + "D000544" + ] + }, + "category": "Neurodegenerative disease" + }, + "article": { + "id": "25208536", + "text": "OBJECTIVES:\nTo investigate the relation between the risk of Alzheimer's disease and exposure to benzodiazepines started at least five years before, considering both the dose-response relation and prodromes (anxiety, depression, insomnia) possibly linked with treatment.\n\nDESIGN:\nCase-control study.\n\nSETTING:\nThe Quebec health insurance program database (RAMQ).\n\nPARTICIPANTS:\n1796 people with a first diagnosis of Alzheimer's disease and followed up for at least six years before were matched with 7184 controls on sex, age group, and duration of follow-up. Both groups were randomly sampled from older people (age \u003e66) living in the community in 2000-09.\n\nMAIN OUTCOME MEASURE:\nThe association between Alzheimer's disease and benzodiazepine use started at least five years before diagnosis was assessed by using multivariable conditional logistic regression. Ever exposure to benzodiazepines was first considered and then categorised according to the cumulative dose expressed as prescribed daily doses (1-90, 91-180, \u003e180) and the drug elimination half life.\n\nRESULTS:\nBenzodiazepine ever use was associated with an increased risk of Alzheimer's disease (adjusted odds ratio 1.51, 95% confidence interval 1.36 to 1.69; further adjustment on anxiety, depression, and insomnia did not markedly alter this result: 1.43, 1.28 to 1.60). No association was found for a cumulative dose \u003c91 prescribed daily doses. The strength of association increased with exposure density (1.32 (1.01 to 1.74) for 91-180 prescribed daily doses and 1.84 (1.62 to 2.08) for \u003e180 prescribed daily doses) and with the drug half life (1.43 (1.27 to 1.61) for short acting drugs and 1.70 (1.46 to 1.98) for long acting ones).\n\nCONCLUSION:\nBenzodiazepine use is associated with an increased risk of Alzheimer's disease. The stronger association observed for long term exposures reinforces the suspicion of a possible direct association, even if benzodiazepine use might also be an early marker of a condition associated with an increased risk of dementia. Unwarranted long term use of these drugs should be considered as a public health concern." + }, + "questions": [ + { + "id": "772cfbcb-1f71-4004-96e1-5cff2072305a", + "text": "What are the risk factors of Alzheimer disease?", + "answers": [ + { + "answer_start": 1072, + "text": "Benzodiazepine ever use" + }, + { + "answer_start": 1714, + "text": "Benzodiazepine use" + }, + { + "answer_start": 1832, + "text": "long term exposures" + } + ] + } + ] +} \ No newline at end of file diff --git a/a56ccf2d-e8b4-41a9-a23e-474a8b9404e8.json b/a56ccf2d-e8b4-41a9-a23e-474a8b9404e8.json new file mode 100644 index 0000000000000000000000000000000000000000..a1f16c3f9e1fda1cbb049c536bc2cd6c27bcbed9 --- /dev/null +++ b/a56ccf2d-e8b4-41a9-a23e-474a8b9404e8.json @@ -0,0 +1,35 @@ +{ + "id": "a56ccf2d-e8b4-41a9-a23e-474a8b9404e8", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "15767329", + "text": "BACKGROUND:\nA number of studies have been conducted evaluating the risk of cutaneous malignant melanoma after exposure to sunlamps and/or sunbeds. The proportion of subjects in the individual studies who have reported exposure has, in general, been modest, and the resulting risk estimates for melanoma have been unstable with wide 95% confidence intervals (95% CI). The inconclusive results seen in individual studies have resulted in confusion as to the carcinogenicity of these devices.\n\nMETHODS:\nWe conducted a systematic review and meta-analysis of these studies. A review of the literature from Jan 1, 1984 to April 2004 using MEDLINE identified 12 case-control studies and 1 cohort study which quantitatively evaluated the use of sunlamps and/or sunbeds and subsequent melanoma. After applying exclusion/inclusion criteria, 9 case-control and 1 cohort study provided data for the analysis. Summary odds ratios (OR) and 95% CIs for sunlamp/sunbed use and subsequent melanoma were calculated using a random-effect model.\n\nRESULTS:\nTen studies provided data for assessment of melanoma risk among subjects who reported \"ever\" being exposed compared with those \"never\" exposed. A positive association was found between exposure and risk (summary OR, 1.25; 95% CI, 1.05-1.49). Significant heterogeneity between studies was present. Evaluation of the metrics \"first exposure as a young adult\" (5 studies) and \"longest duration or highest frequency of exposure\" (6 studies) also yielded significantly elevated risk estimates (summary OR, 1.69; 95% CI, 1.32-2.18, and 1.61; 95% CI, 1.21-2.12, respectively, with no heterogeneity in either analysis).\n\nCONCLUSIONS:\nResults indicate a significantly increased risk of cutaneous melanoma subsequent to sunbed/sunlamp exposure." + }, + "questions": [ + { + "id": "14b8619f-b42e-452e-8a70-73067def0564", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 1746, + "text": "sunbed/sunlamp exposure" + } + ] + } + ] +} \ No newline at end of file diff --git a/a5f80d4b-a25b-4b1f-8196-25203b94edd5.json b/a5f80d4b-a25b-4b1f-8196-25203b94edd5.json new file mode 100644 index 0000000000000000000000000000000000000000..a365b75b4b9cc194d5b1e4562a96388c8ad55abb --- /dev/null +++ b/a5f80d4b-a25b-4b1f-8196-25203b94edd5.json @@ -0,0 +1,39 @@ +{ + "id": "a5f80d4b-a25b-4b1f-8196-25203b94edd5", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "12084840", + "text": "Genetic factors cannot explain the recent rapid increase in the incidence of atopic diseases. The phenomenon has been explained by environmental factors, and there are data for and against the hypothesis that a decline in the pressure of microbial stimulation early in life could be behind the allergy epidemic. Changes have also occurred in maternity care, among them a rise in the caesarean section rate, which could diminish initial microbial exposure and thereby alter T helper 1 cell/T helper-2 cell development and affect the risk of developing atopy. In this study, we sought to establish whether mode of delivery does influence the development of atopic asthma. Finnish 1987 Medical Birth Register (n = 59,927 live births) information was linked between several national health registers to obtain information on asthma and mode of delivery in children registered. The data were adjusted for maternal age, previous deliveries, child's sex, and birth size. Atopy was evaluated in the second study (Turku Birth Cohort), which involved 219 children born by vaginal delivery (n = 106) or caesarean section (n = 113); history of atopic symptoms was established by questionnaire and a clinical examination was conducted, including skin prick testing and determination of total and allergen-specific IgE in serum. The register study showed the cumulative incidence of asthma at the age of seven to be significantly higher in children born by caesarean section (4.2%) than in those vaginally delivered (3.3%), the adjusted odds ratio (OR) for confounding variables being 1.21 (1.08-1.36), p \u003c 0.01. In the second study, significantly more positive allergy tests were reported in questionnaires in the caesarean (22%) than in the vaginal delivery group (11%), OR 2.22 (1.06-4.64), p \u003c 0.01, and a trend toward more positive skin prick reactions was documented at clinical examination; 41% versus 29%, OR 1.31 (0.65-2.65), p = 0.11. In conclusion, these results suggest that caesarean section delivery may be associated with an increased prevalence of atopic asthma." + }, + "questions": [ + { + "id": "52a82437-b56e-461f-8c73-317a575eac3e", + "text": "What are the risk factors of Asthma? ", + "answers": [ + { + "answer_start": 1443, + "text": "caesarean section" + }, + { + "answer_start": 1973, + "text": "caesarean section delivery" + } + ] + } + ] +} \ No newline at end of file diff --git a/a6a30930-a33d-4630-a4c1-3bf17aff6fcb.json b/a6a30930-a33d-4630-a4c1-3bf17aff6fcb.json new file mode 100644 index 0000000000000000000000000000000000000000..e0f0053b0a9dff1a1c352a8aceff79d1d9c0ac7e --- /dev/null +++ b/a6a30930-a33d-4630-a4c1-3bf17aff6fcb.json @@ -0,0 +1,39 @@ +{ + "id": "a6a30930-a33d-4630-a4c1-3bf17aff6fcb", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "31806712", + "text": "RATIONALE:\nThere is growing evidence that air pollution may contribute to the development of childhood asthma and other allergic diseases. In this follow-up of the Toronto Child Health Evaluation Questionnaire (T-CHEQ) study, we examined associations between early life exposures to air pollution and incidence of asthma, allergic rhinitis and eczema from birth through adolescence.\n\nMETHODS:\n1286 T-CHEQ participants were followed from birth until outcome (March 31, 2016) or loss to follow-up, with a mean of 17 years of follow-up. Concentrations of nitrogen dioxide (NO), ozone (O) and particulate matter with a 50% cut-off aerodynamic diameter of 2.5 µm (PM) from January 1, 1999 to December 31, 2012 were assigned to participants based on their postal codes at birth using ground observations, chemical/meteorological models, remote sensing and land-use regression models. Study outcomes included incidence of physician-diagnosed asthma, allergic rhinitis and eczema. Cox proportional hazard regression models were used to estimate hazard ratios per interquartile range of exposures and outcomes, adjusting for potential confounders.\n\nRESULTS:\nHazard ratios of 1.17 (95% CI 1.05-1.31) for asthma and 1.07 (95% CI 0.99-1.15) for eczema were observed for total oxidants (O and NO) at birth. No significant increase in risk was found for PM.\n\nCONCLUSIONS:\nExposures to oxidant air pollutants (O and NO) but not PM were associated with an increased risk of incident asthma and eczema in children. This suggests that improving air quality may contribute to the prevention of asthma and other allergic disease in childhood and adolescence." + }, + "questions": [ + { + "id": "8c6fe6db-6cea-4a88-8717-15382518328a", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1258, + "text": "total oxidants (O and NO) at birth" + }, + { + "answer_start": 1358, + "text": "Exposures to oxidant air pollutants (O and NO)" + } + ] + } + ] +} \ No newline at end of file diff --git a/a6d1ad9e-659b-4e2e-b4e4-7da53f3b2daa.json b/a6d1ad9e-659b-4e2e-b4e4-7da53f3b2daa.json new file mode 100644 index 0000000000000000000000000000000000000000..4bcdf18385fa95baf8d218fc792ef5a9aa539b6e --- /dev/null +++ b/a6d1ad9e-659b-4e2e-b4e4-7da53f3b2daa.json @@ -0,0 +1,54 @@ +{ + "id": "a6d1ad9e-659b-4e2e-b4e4-7da53f3b2daa", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "23449445", + "text": "BACKGROUND:\nThe relationship between active cigarette smoking and breast cancer risk remains controversial because of unresolved issues of confounding and dose response.\n\nMETHODS:\nTo investigate these issues further, we analyzed data from 73 388 women in the American Cancer Society's Cancer Prevention Study II (CPS-II) Nutrition Cohort. Analyses were based on 3721 invasive breast cancer case patients identified during a median follow-up of 13.8 years. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated from multivariable-adjusted Cox proportional hazard regression models. P values were two-sided. We also conducted meta-analyses of our results with those published from 14 other cohort studies.\n\nRESULTS:\nIn CPS-II, incidence was higher in current (HR = 1.24, 95% CI = 1.07 to 1.42) and former smokers (HR =1.13, 95% CI = 1.06 to 1.21) than in never smokers. Women who initiated smoking before menarche (HR = 1.61, 95% CI = 1.10 to 2.34) or after menarche but 11 or more years before first birth (HR = 1.45, 95% CI = 1.21 to 1.74) had higher risk (P trend = .03). No relationships were observed with other smoking parameters. Alcohol consumption did not confound associations with smoking status, although neither current nor former smoking were associated with risk among never drinkers (P interaction = .11). In meta-analyses, current (HR = 1.12, 95% CI = 1.08 to 1.16) and former smoking (HR = 1.09, 95% CI = 1.04 to 1.15) were weakly associated with risk; a stronger association (HR = 1.21, 95% CI = 1.14 to 1.28) was observed in women who initiated smoking before first birth.\n\nCONCLUSIONS:\nThese results support the hypothesis that active smoking is associated with increased breast cancer risk for women who initiate smoking before first birth and suggest that smoking might play a role in breast cancer initiation." + }, + "questions": [ + { + "id": "177ae03d-2ae8-467d-a13a-3f485a9bb400", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 765, + "text": "current (HR = 1.24, 95% CI = 1.07 to 1.42) and former smokers" + }, + { + "answer_start": 812, + "text": "former smokers" + }, + { + "answer_start": 883, + "text": " Women who initiated smoking before menarche" + }, + { + "answer_start": 966, + "text": "after menarche but 11 or more years before first birth" + }, + { + "answer_start": 1559, + "text": "women who initiated smoking before first birth" + }, + { + "answer_start": 1663, + "text": "active smoking" + } + ] + } + ] +} \ No newline at end of file diff --git a/a710a0f1-7ec5-4bb9-b165-6a60579357e2.json b/a710a0f1-7ec5-4bb9-b165-6a60579357e2.json new file mode 100644 index 0000000000000000000000000000000000000000..aa73b9a2c3f5f4d7a63532f30e7d7c1a75a07d8b --- /dev/null +++ b/a710a0f1-7ec5-4bb9-b165-6a60579357e2.json @@ -0,0 +1,39 @@ +{ + "id": "a710a0f1-7ec5-4bb9-b165-6a60579357e2", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "15894679", + "text": "It has been hypothesized that cutaneous melanoma at different anatomic sites develops through divergent pathways. We examined this hypothesis prospectively. We followed 152,949 women and 25,204 men free of cancer at baseline for up to 14 years in three large prospective studies. We examined risk factors for melanoma by anatomic location (head or neck, trunk, upper extremity, and lower extremity). Polytomous logistic regression was used to test the difference among risk factors by location of melanoma. A total of 511 incident cases of invasive melanoma (49 head or neck, 188 trunk, 98 upper extremity, and 176 lower extremity) were included in the analysis. Compared with females, males had a higher risk of developing melanoma on the head or neck and trunk. History of severe and painful sunburn was most strongly related to melanoma of upper extremity; individuals with \u003e10 burns had a 6.86-fold (95% confidence interval, 2.62-18.00) higher risk of melanoma of upper extremity compared with those with no burns (P for trend \u003c 0.0001; P for difference by body site = 0.04). Number of moles was most strongly related to melanoma of the trunk; the multivariate relative risk for having \u003e10 moles was 4.67 (95% confidence interval, 3.07-7.11) compared with having no moles (P for trend \u003c 0.0001; P for difference by body site = 0.04). Age, family history of melanoma, and hair color did not statistically differ by anatomic site of the cancer. These data support divergent etiologic pathways of melanoma development by anatomic sites." + }, + "questions": [ + { + "id": "f3bef43c-fdc1-4831-927f-380f047cd4c1", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 1080, + "text": "Number of moles" + }, + { + "answer_start": 764, + "text": "History of severe and painful sunburn" + } + ] + } + ] +} \ No newline at end of file diff --git a/a762214e-2692-4f73-91fa-e77813b144c2.json b/a762214e-2692-4f73-91fa-e77813b144c2.json new file mode 100644 index 0000000000000000000000000000000000000000..d66495ac3d790def547ddcda52ad9e62316e84d8 --- /dev/null +++ b/a762214e-2692-4f73-91fa-e77813b144c2.json @@ -0,0 +1,34 @@ +{ + "id": "a762214e-2692-4f73-91fa-e77813b144c2", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "32105187", + "text": "PURPOSE:\nStudies exploring the association of cigarette smoking and long-term survival outcomes following radical cystectomy have yielded mixed results. We performed a systematic review and meta-analysis to investigate the impact of tobacco smoking exposure, duration, intensity and cessation on response to neoadjuvant chemotherapy and long-term survival outcomes in patients undergoing radical cystectomy for bladder cancer.\n\nMATERIALS AND METHODS:\nWe systematically searched PubMed®, MEDLINE®, Embase® and Cochrane® Library databases for original articles published before April 2019. Primary end points were neoadjuvant chemotherapy response, overall and cancer specific mortality, and recurrence-free survival after radical cystectomy. Observational studies reporting Cox proportional hazards regression or logistic regression analysis were independently screened. Available multivariable hazard ratios and corresponding 95% CIs were included in the quantitative analysis. Sensitivity analyses were performed as appropriate. A risk of bias assessment was completed for nonrandomized studies.\n\nRESULTS:\nOur electronic search identified a total of 649 articles. After a detailed review we selected 17 studies that addressed the impact of smoking status on survival outcomes in 13,777 patients after radical cystectomy for bladder cancer. Pooled meta-analysis revealed that active smokers have an increased risk of overall mortality (HR 1.21, 95% CI 1.08-1.36; p=0.001, I=0%), cancer specific mortality (HR 1.24, 95% CI 1.13-1.36; p \u003c0.00001, I=0%) and bladder cancer recurrence (HR 1.24, 95% CI 1.12-1.38; p \u003c0.0001, I=3%). Sensitivity analyses evaluating only patients who underwent neoadjuvant chemotherapy followed by radical cystectomy showed an advantage of non/never smokers in terms of neoadjuvant chemotherapy complete response rate (HR 0.47, 95% CI 0.29-0.75; p=0.001, I=0%).\n\nCONCLUSIONS:\nSmoking status is associated with lower neoadjuvant chemotherapy response rates and higher overall and cancer specific mortality as well as bladder cancer recurrence after radical cystectomy. Appropriate preoperative counseling, together with tightened followup, may have a pivotal role in improving the smoking-related long-term survival outcomes in patients with bladder cancer." + }, + "questions": [ + { + "id": "08fca26f-3e06-46cc-9d18-5dc5b14287c0", + "text": "What are the risk factors of Bladder Cancer?", + "answers": [ + { + "answer_start": 1376, + "text": "active smokers" + } + ] + } + ] +} \ No newline at end of file diff --git a/a7699d12-d50e-4fe9-a8e6-ec5e56cfee6d.json b/a7699d12-d50e-4fe9-a8e6-ec5e56cfee6d.json new file mode 100644 index 0000000000000000000000000000000000000000..66214b3694dc5947b60f59da2055d7cb06341d93 --- /dev/null +++ b/a7699d12-d50e-4fe9-a8e6-ec5e56cfee6d.json @@ -0,0 +1,53 @@ +{ + "id": "a7699d12-d50e-4fe9-a8e6-ec5e56cfee6d", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "33947661", + "text": "OBJECTIVE:\nTo assess the risk of colorectal cancer (CRC) in first degree relatives (parents and full siblings) of patients with precursor lesions (polyps) for CRC.\n\nDESIGN:\nCase-control study.\n\nSETTING:\nLinkage to the multi-generation register and gastrointestinal ESPRESSO (Epidemiology Strengthened by histoPathology Reports in Sweden) histopathology cohort in Sweden.\n\nPARTICIPANTS:\n68 060 patients with CRC and 333 753 matched controls.\n\nMAIN OUTCOME MEASURES:\nMultivariable adjusted odds ratios of CRC according to the number of first degree relatives with a colorectal polyp and the histology of polyps and age at diagnosis in first degree relatives. Subgroup analysis was also performed according to age at CRC diagnosis and evaluated the joint association of family history of colorectal polyps and family history of CRC.\n\nRESULTS:\nAfter adjusting for family history of CRC and other covariates, having a first degree relative with a colorectal polyp (8.4% (5742/68 060) in cases and 5.7% (18 860/333 753) in controls) was associated with a higher risk of CRC (odds ratio 1.40, 95% confidence interval 1.35 to 1.45). The odds ratios ranged from 1.23 for those with hyperplastic polyps to 1.44 for those with tubulovillous adenomas. To better put this risk in perspective, the age specific absolute risk of colon and rectal cancers was estimated according to family history of polyps based on the 2018 national CRC incidence in Sweden. For example, the absolute risk of colon cancer in individuals aged 60-64 years with and without a family history of colorectal polyp was, respectively, 94.3 and 67.9 per 100 000 for men and 89.1 and 64.1 per 100 000 for women. The association between family history of polyps and CRC risk was strengthened by the increasing number of first degree relatives with polyps (≥2 first degree relatives: 1.70, 1.52 to 1.90, P\u003c0.001 for trend) and decreasing age at polyp diagnosis (\u003c50 years: 1.77, 1.57 to 1.99, P\u003c0.001 for trend). A particularly strong association was found for early onset CRC diagnosed before age 50 years (≥2 first degree relatives: 3.34, 2.05 to 5.43, P=0.002 for heterogeneity by age of CRC diagnosis). In the joint analysis, the odds ratio of CRC for individuals with two or more first degree relatives with polyps but no CRC was 1.79 (1.52 to 2.10), with one first degree relative with CRC but no polyps was 1.70 (1.65 to 1.76), and with two or more first degree relatives with both polyps and CRC was 5.00 (3.77 to 6.63) (P\u003c0.001 for interaction).\n\nCONCLUSIONS:\nAfter adjusting for family history of CRC, the siblings and children of patients with colorectal polyps are still at higher risk of CRC, particularly early onset CRC. Early screening for CRC might be considered for first degree relatives of patients with polyps." + }, + "questions": [ + { + "id": "644e7033-a246-403c-b710-290daaae6614", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 904, + "text": "having a first degree relative with a colorectal polyp" + }, + { + "answer_start": 2572, + "text": "siblings and children of patients with colorectal polyps" + }, + { + "answer_start": 2212, + "text": "individuals with two or more first degree relatives with polyps but no CRC" + }, + { + "answer_start": 2317, + "text": "one first degree relative with CRC but no polyps" + }, + { + "answer_start": 2400, + "text": "two or more first degree relatives with both polyps and CRC" + } + ] + } + ] +} \ No newline at end of file diff --git a/a77a4633-62fb-49be-ad77-5b5de2cb0d07.json b/a77a4633-62fb-49be-ad77-5b5de2cb0d07.json new file mode 100644 index 0000000000000000000000000000000000000000..e53de14a84b669466d9994827bf0b92d16504fe3 --- /dev/null +++ b/a77a4633-62fb-49be-ad77-5b5de2cb0d07.json @@ -0,0 +1,46 @@ +{ + "id": "a77a4633-62fb-49be-ad77-5b5de2cb0d07", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "11887115", + "text": "OBJECTIVES:\nTo evaluate whether the risk of bladder cancer is greater in individuals with spinal cord injury (SCI) than in the general population and whether indwelling catheter (IDC) use is a significant independent risk factor for bladder cancer.\n\nDESIGN:\nHistorical cohort study in which subjects with SCI were stratified according to bladder management method and followed for the development of bladder cancer.\n\nSETTING:\nA large rehabilitation hospital in the Spinal Cord Injury Model Systems.\n\nPARTICIPANTS:\nA total of 3670 patients with SCI who were evaluated for bladder cancer on at least 1 occasion by cystoscopy over a period of 1 to 47 years.\n\nINTERVENTIONS:\nNot applicable.\n\nMAIN OUTCOME MEASURES:\nBladder cancer occurring after SCI determined by diagnosis at our facility, by subject report, or by report of next of kin.\n\nRESULTS:\nTwenty-one cases of bladder cancer were found in the 3670 study participants. The risk of bladder cancer for subjects with SCI using IDC is 77 per 100,000 person-years, corresponding to an age- and gender-adjusted standardized morbidity ratio (SMR) of 25.4 (95% confidence interval [CI], 14.0--41.9) when compared with the general population. After controlling for age at injury, gender, level and completeness of SCI, history of bladder calculi, and smoking, those using solely IDC had a significantly greater risk of bladder cancer (relative risk [RR] = 4.9; 95% CI, 1.3--13.8) than those using nonindwelling methods. Mortality caused by bladder cancer in individuals with SCI was significantly greater than that of the US population (SMR = 70.6; 95% CI, 36.9--123.3).\n\nCONCLUSIONS:\nBladder cancer risk and mortality are heightened in SCI compared with the general population. IDC is a significant independent risk factor for the increased risk of and mortality caused by bladder cancer in the SCI population." + }, + "questions": [ + { + "id": "67b99d46-40c2-4c43-b2a5-e1d00e1d3711", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 1305, + "text": "those using solely IDC" + }, + { + "answer_start": 158, + "text": "indwelling catheter (IDC)" + }, + { + "answer_start": 1682, + "text": "SCI" + }, + { + "answer_start": 90, + "text": "spinal cord injury (SCI)" + } + ] + } + ] +} \ No newline at end of file diff --git a/a822ef3e-877b-4580-82d1-c4261f95c020.json b/a822ef3e-877b-4580-82d1-c4261f95c020.json new file mode 100644 index 0000000000000000000000000000000000000000..a69d7c7b8c9a9e1022f2490154588be31a60c57e --- /dev/null +++ b/a822ef3e-877b-4580-82d1-c4261f95c020.json @@ -0,0 +1,46 @@ +{ + "id": "a822ef3e-877b-4580-82d1-c4261f95c020", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "30903422", + "text": "BACKGROUND:\nThe impact of different radiotherapy modalities on the development and characteristics of second primary bladder cancers (BCa) and BCa-specific mortality (BCa-SM) remains unclear. Thus, we evaluated the incidence and biological behavior of subsequent BCa and related survival in patients who underwent radiation therapy for prostate cancer (PCa).\n\nMETHODS:\nA total of 530,581 patients in the surveillance, epidemiology, and end results database with localized PCa between 1988 and 2013 were identified. PCa treatments included radical prostatectomy (RP), external beam radiotherapy (EBRT), radioactive implants (RI), and combined EBRT and RI (EBRI). A multivariable competing risk analysis based on a proportional sub distribution hazards model was used to determine the impact of different radiotherapy modalities on BCa incidence and specific mortality.\n\nRESULTS:\nIncidence of BCa was significantly high in patients treated with EBRT, RI, and EBRI vs. RP [sub distribution hazard ratio (SHR) 1.41, P \u003c 0.001; SHR 1.58, P \u003c 0.001; SHR 1.56, P \u003c 0.001, respectively]. BCa following EBRT, RI, and EBRI were more commonly non-urothelial (3.3%, 2.9%, 3.3%, respectively, versus 1.2%) and T4 (3.5%, 6.1%, 5.0%, respectively, versus 1.6%) compared with RP. RI associated with a higher rate of BCa metastasis than RP (2.6% vs. 1.1%). Prior EBRT, RI, and EBRI increased BCa-SM (SHR 1.44, P = 0.001; SHR 1.21, P = 0.047; and SHR 1.42, P = 0.032, respectively).\n\nCONCLUSIONS:\nPatients receiving radiotherapy for PCa have a higher risk of BCa. BCa after EBRT, RI, and EBRI is more likely to be non-urothelial, stage T4, and with increased BCa-SM. Prior RI associated with a higher rate of BCa metastasis." + }, + "questions": [ + { + "id": "5be04ffe-9537-46cd-9f32-b9f46dcebb5c", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 1479, + "text": "Patients receiving radiotherapy for PCa" + }, + { + "answer_start": 336, + "text": "prostate cancer (PCa)" + }, + { + "answer_start": 921, + "text": "patients treated with EBRT, RI, and EBRI" + }, + { + "answer_start": 567, + "text": "external beam radiotherapy (EBRT), radioactive implants (RI), and combined EBRT and RI (EBRI" + } + ] + } + ] +} \ No newline at end of file diff --git a/a88a7345-b19e-43cc-a765-3d71d23da0c7.json b/a88a7345-b19e-43cc-a765-3d71d23da0c7.json new file mode 100644 index 0000000000000000000000000000000000000000..985dea217585deba2ed0ea9912a75872452b2a23 --- /dev/null +++ b/a88a7345-b19e-43cc-a765-3d71d23da0c7.json @@ -0,0 +1,47 @@ +{ + "id": "a88a7345-b19e-43cc-a765-3d71d23da0c7", + "disease": { + "id": "H00056", + "names": [ + "Alzheimer disease", + "Dementia due to Alzheimer disease" + ], + "dbLinks": { + "icd10": [ + "G30" + ], + "mesh": [ + "D000544" + ] + }, + "category": "Neurodegenerative disease" + }, + "article": { + "id": "20817608", + "text": "Converging evidence from clinical and pathological studies indicate the presence of important relationships between the ongoing deterioration of brain lipid homeostasis, vascular changes and the pathophysiology of sporadic Alzheimer's disease (AD). These associations include the recognition of cholesterol transporters apolipoprotein E (APOE), APOC1 and APOJ as major genetic risk factors for common AD and observations associating risk factors for cardiovascular disease such as high midlife plasma cholesterol, diabetes, stroke, obesity and hypertension to dementia. Moreover, recent clinical findings lend support to the notion that progressive deterioration of cholesterol homeostasis in AD is a central player in the disease pathophysiology and is, therefore, a potential therapeutic target for disease prevention." + }, + "questions": [ + { + "id": "59e43871-4827-4963-bafc-a13daa921377", + "text": "What are the risk factors of Alzheimer disease?", + "answers": [ + { + "answer_start": 295, + "text": "cholesterol transporters apolipoprotein E (APOE)" + }, + { + "answer_start": 345, + "text": "APOC1" + }, + { + "answer_start": 355, + "text": "APOJ" + }, + { + "answer_start": 637, + "text": "progressive deterioration of cholesterol homeostasis" + } + ] + } + ] +} \ No newline at end of file diff --git a/a971e2ea-6dac-4694-ba3b-658d1d82ba23.json b/a971e2ea-6dac-4694-ba3b-658d1d82ba23.json new file mode 100644 index 0000000000000000000000000000000000000000..a9bfa89cde354ef01adae285e6b6a8861da7a1a7 --- /dev/null +++ b/a971e2ea-6dac-4694-ba3b-658d1d82ba23.json @@ -0,0 +1,34 @@ +{ + "id": "a971e2ea-6dac-4694-ba3b-658d1d82ba23", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "23155333", + "text": "Celiac disease (CD) is one of the most common diseases, resulting from both environmental (gluten) and genetic factors [human leukocyte antigen (HLA) and non-HLA genes]. The prevalence of CD has been estimated to approximate 0.5%-1% in different parts of the world. However, the population with diabetes, autoimmune disorder or relatives of CD individuals have even higher risk for the development of CD, at least in part, because of shared HLA typing. Gliadin gains access to the basal surface of the epithelium, and interact directly with the immune system, via both trans- and para-cellular routes. From a diagnostic perspective, symptoms may be viewed as either \"typical\" or \"atypical\". In both positive serological screening results suggestive of CD, should lead to small bowel biopsy followed by a favourable clinical and serological response to the gluten-free diet (GFD) to confirm the diagnosis. Positive anti-tissue transglutaminase antibody or anti-endomysial antibody during the clinical course helps to confirm the diagnosis of CD because of their over 99% specificities when small bowel villous atrophy is present on biopsy. Currently, the only treatment available for CD individuals is a strict life-long GFD. A greater understanding of the pathogenesis of CD allows alternative future CD treatments to hydrolyse toxic gliadin peptide, prevent toxic gliadin peptide absorption, blockage of selective deamidation of specific glutamine residues by tissue, restore immune tolerance towards gluten, modulation of immune response to dietary gliadin, and restoration of intestinal architecture." + }, + "questions": [ + { + "id": "d9b432a8-2100-48e1-9d5f-0c47bb8ea0c9", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 278, + "text": " population with diabetes, autoimmune disorder or relatives of CD individuals" + } + ] + } + ] +} \ No newline at end of file diff --git a/a98b3f60-16fb-45b2-b50a-6b4be2448c10.json b/a98b3f60-16fb-45b2-b50a-6b4be2448c10.json new file mode 100644 index 0000000000000000000000000000000000000000..f7934d515afbd83b21d5b06b53cfe256f34c531d --- /dev/null +++ b/a98b3f60-16fb-45b2-b50a-6b4be2448c10.json @@ -0,0 +1,41 @@ +{ + "id": "a98b3f60-16fb-45b2-b50a-6b4be2448c10", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "18242207", + "text": "BACKGROUND \u0026 AIMS:\nThrough the past 2 decades, a consistent association between cigarette smoking and colorectal adenomatous polyps, recognized precursor lesions of colorectal cancer, has been shown. We performed a meta-analysis to provide a quantitative pooled risk estimate of the association, focusing on the different characteristics of the study populations, study designs, and clinical feature of the polyps.\n\nMETHODS:\nWe performed a comprehensive literature search of studies linking cigarette smoking and adenomas. We used random effects models to evaluate pooled relative risks and performed dose-response, heterogeneity, publication bias, and sensitivity analyses.\n\nRESULTS:\nForty-two independent observational studies were included in the analysis. The pooled risk estimates for current, former, and ever smokers in comparison with never smokers were 2.14 (95% confidence interval [CI], 1.86-2.46), 1.47 (95% CI, 1.29-1.67), and 1.82 (95% CI, 1.65-2.00), respectively. The association was stronger for high-risk adenomas than for low-risk adenomas. Studies in which all controls underwent full colonoscopy showed a higher risk compared with studies in which some or all controls underwent partial colon examination.\n\nCONCLUSIONS:\nThis meta-analysis provides strong evidence of the detrimental effect of cigarette smoking on the development of adenomatous polyps. Smoking is important for both formation and aggressiveness of adenomas." + }, + "questions": [ + { + "id": "a99be6ab-3287-45cc-a0f3-a72521390a62", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 790, + "text": "current, former, and ever smokers" + }, + { + "answer_start": 1314, + "text": "cigarette smoking" + } + ] + } + ] +} \ No newline at end of file diff --git a/a9bfc88b-a172-4c4e-b32b-1d9cc08c3a36.json b/a9bfc88b-a172-4c4e-b32b-1d9cc08c3a36.json new file mode 100644 index 0000000000000000000000000000000000000000..34202ad57f59d2ed76411f62edc766714c7d1cc9 --- /dev/null +++ b/a9bfc88b-a172-4c4e-b32b-1d9cc08c3a36.json @@ -0,0 +1,64 @@ +{ + "id": "a9bfc88b-a172-4c4e-b32b-1d9cc08c3a36", + "disease": { + "id": "M2023_04_26_16_49_01", + "names": [ + "Metabolic syndrome" + ], + "dbLinks": { + "mesh": [ + "C18.452.394.968.500.570", + "C18.452.625" + ] + }, + "description": "Metabolic syndrome is a complex constellation of metabolic derangements that increase the risk of atherosclerotic cardiovascular disease, type 2 diabetes, and all-cause mortality. The key features of metabolic syndrome include central obesity, insulin resistance, dyslipidemia, and hypertension. These abnormalities are believed to arise from a combination of genetic predisposition and environmental factors, such as sedentary behavior, poor dietary habits, and chronic stress. Diagnosis of metabolic syndrome requires meeting three or more established criteria, based on standardized guidelines. Management of metabolic syndrome involves a comprehensive approach, including lifestyle modifications such as weight loss, physical activity, and dietary changes, as well as pharmacotherapy to address underlying risk factors such as hypertension, dyslipidemia, and hyperglycemia. Early intervention and aggressive management of metabolic syndrome are critical to preventing or delaying the onset of complications and improving long-term health outcomes." + }, + "article": { + "id": "12588201", + "text": "BACKGROUND:\nThe metabolic syndrome is an important cluster of coronary heart disease risk factors with common insulin resistance. The extent to which the metabolic syndrome is associated with demographic and potentially modifiable lifestyle factors in the US population is unknown.\n\nMETHODS:\nMetabolic syndrome-associated factors and prevalence, as defined by Adult Treatment Panel III criteria, were evaluated in a representative US sample of 3305 black, 3477 Mexican American, and 5581 white men and nonpregnant or lactating women aged 20 years and older who participated in the cross-sectional Third National Health and Nutrition Examination Survey.\n\nRESULTS:\nThe metabolic syndrome was present in 22.8% and 22.6% of US men and women, respectively (P =.86). The age-specific prevalence was highest in Mexican Americans and lowest in blacks of both sexes. Ethnic differences persisted even after adjusting for age, body mass index, and socioeconomic status. The metabolic syndrome was present in 4.6%, 22.4%, and 59.6% of normal-weight, overweight, and obese men, respectively, and a similar distribution was observed in women. Older age, postmenopausal status, Mexican American ethnicity, higher body mass index, current smoking, low household income, high carbohydrate intake, no alcohol consumption, and physical inactivity were associated with increased odds of the metabolic syndrome.\n\nCONCLUSIONS:\nThe metabolic syndrome is present in more than 20% of the US adult population; varies substantially by ethnicity even after adjusting for body mass index, age, socioeconomic status, and other predictor variables; and is associated with several potentially modifiable lifestyle factors. Identification and clinical management of this high-risk group is an important aspect of coronary heart disease prevention." + }, + "questions": [ + { + "id": "0ae0ab79-5547-4be0-846c-b9cfb12c7792", + "text": "What is a risk factor for Metabolic Syndrome?", + "answers": [ + { + "answer_start": 1130, + "text": "Older age" + }, + { + "answer_start": 1141, + "text": "postmenopausal status" + }, + { + "answer_start": 1164, + "text": "Mexican American ethnicity" + }, + { + "answer_start": 1192, + "text": "higher body mass index" + }, + { + "answer_start": 1216, + "text": "current smoking" + }, + { + "answer_start": 1233, + "text": "low household income" + }, + { + "answer_start": 1255, + "text": "high carbohydrate intake" + }, + { + "answer_start": 1281, + "text": "no alcohol consumption" + }, + { + "answer_start": 1309, + "text": "physical inactivity" + } + ] + } + ] +} \ No newline at end of file diff --git a/aa49646b-d89b-4559-b8d8-b5c5533ffa71.json b/aa49646b-d89b-4559-b8d8-b5c5533ffa71.json new file mode 100644 index 0000000000000000000000000000000000000000..9d003db15def70a5d9c6f951c2f88c41f2a9716f --- /dev/null +++ b/aa49646b-d89b-4559-b8d8-b5c5533ffa71.json @@ -0,0 +1,41 @@ +{ + "id": "aa49646b-d89b-4559-b8d8-b5c5533ffa71", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "15096331", + "text": "BACKGROUND:\nEpidemiologic studies have generally reported positive associations between alcohol consumption and risk for colorectal cancer. However, findings related to specific alcoholic beverages or different anatomic sites in the large bowel have been inconsistent.\n\nOBJECTIVE:\nTo examine the relationship of total alcohol intake and intake from specific beverages to the incidence of colorectal cancer and to evaluate whether other potential risk factors modify the association.\n\nDESIGN:\nPooled analysis of primary data from 8 cohort studies in 5 countries.\n\nSETTING:\nNorth America and Europe.\n\nPARTICIPANTS:\n489,979 women and men with no history of cancer other than nonmelanoma skin cancer at baseline.\n\nMEASUREMENTS:\nAlcohol intake was assessed in each study at baseline by using a validated food-frequency questionnaire.\n\nRESULTS:\nDuring a maximum of 6 to 16 years of follow-up across the studies, 4687 cases of colorectal cancer were documented. In categorical analyses, increased risk for colorectal cancer was limited to persons with an alcohol intake of 30 g/d or greater (approximately \u003e or =2 drinks/d), a consumption level reported by 4% of women and 13% of men. Compared with nondrinkers, the pooled multivariate relative risks were 1.16 (95% CI, 0.99 to 1.36) for persons who consumed 30 to less than 45 g/d and 1.41 (CI, 1.16 to 1.72) for those who consumed 45 g/d or greater. No significant heterogeneity by study or sex was observed. The association was evident for cancer of the proximal colon, distal colon, and rectum. No clear difference in relative risks was found among specific alcoholic beverages.\n\nLIMITATIONS:\nThe study included only one measure of alcohol consumption at baseline and could not investigate lifetime alcohol consumption, alcohol consumption at younger ages, or changes in alcohol consumption during follow-up. It also could not examine drinking patterns or duration of alcohol use.\n\nCONCLUSIONS:\nA single determination of alcohol intake correlated with a modest relative elevation in colorectal cancer rate, mainly at the highest levels of alcohol intake." + }, + "questions": [ + { + "id": "8ac62685-74e3-45f6-a91c-808f6746cf38", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1942, + "text": "A single determination of alcohol intake" + }, + { + "answer_start": 1032, + "text": "persons with an alcohol intake of 30 g/d or greater (approximately \u003e or =2 drinks/d)" + } + ] + } + ] +} \ No newline at end of file diff --git a/aaf78829-c842-43be-b72b-5c4cd409bd54.json b/aaf78829-c842-43be-b72b-5c4cd409bd54.json new file mode 100644 index 0000000000000000000000000000000000000000..7b2e40480763baa54028f5b66dc9d9957a65dbd1 --- /dev/null +++ b/aaf78829-c842-43be-b72b-5c4cd409bd54.json @@ -0,0 +1,39 @@ +{ + "id": "aaf78829-c842-43be-b72b-5c4cd409bd54", + "disease": { + "id": "H00056", + "names": [ + "Alzheimer disease", + "Dementia due to Alzheimer disease" + ], + "dbLinks": { + "icd10": [ + "G30" + ], + "mesh": [ + "D000544" + ] + }, + "category": "Neurodegenerative disease" + }, + "article": { + "id": "23204143", + "text": "A growing body of evidence demonstrates an association between vascular risk factors and Alzheimer's disease. This study investigated the frequency and severity of atherosclerotic plaques in the circle of Willis in Alzheimer's disease and multiple other neurodegenerative diseases. Semi-quantitative data from gross and microscopic neuropathological examinations in 1000 cases were analysed, including 410 with a primary diagnosis of Alzheimer's disease, 230 with synucleinopathies, 157 with TDP-43 proteinopathies, 144 with tauopathies and 59 with normal ageing. More than 77% of subjects with Alzheimer's disease had grossly apparent circle of Willis atherosclerosis, a percentage that was significantly higher than normal (47%), or other neurodegenerative diseases (43-67%). Age- and sex-adjusted atherosclerosis ratings were highly correlated with neuritic plaque, paired helical filaments tau neurofibrillary tangle and cerebral amyloid angiopathy ratings in the whole sample and within individual groups. We found no associations between atherosclerosis ratings and α-synuclein or TDP-43 lesion ratings. The association between age-adjusted circle of Willis atherosclerosis and Alzheimer's disease-type pathology was more robust for female subjects than male subjects. These results provide further confirmation and specificity that vascular disease and Alzheimer's disease are interrelated and suggest that common aetiologic or reciprocally synergistic pathophysiological mechanisms promote both vascular pathology and plaque and tangle pathology." + }, + "questions": [ + { + "id": "1c63b401-af9c-4481-90dd-0f7e1dbf7d28", + "text": "What are the risk factors of Alzheimer disease?", + "answers": [ + { + "answer_start": 1134, + "text": "age-adjusted circle of Willis atherosclerosis" + }, + { + "answer_start": 1339, + "text": "vascular disease" + } + ] + } + ] +} \ No newline at end of file diff --git a/ac81c591-1380-4582-bb13-e428987b7046.json b/ac81c591-1380-4582-bb13-e428987b7046.json new file mode 100644 index 0000000000000000000000000000000000000000..2b1dae87e38c5c5ed6947b1f81ab59bdbea1aa25 --- /dev/null +++ b/ac81c591-1380-4582-bb13-e428987b7046.json @@ -0,0 +1,43 @@ +{ + "id": "ac81c591-1380-4582-bb13-e428987b7046", + "disease": { + "id": "H00056", + "names": [ + "Alzheimer disease", + "Dementia due to Alzheimer disease" + ], + "dbLinks": { + "icd10": [ + "G30" + ], + "mesh": [ + "D000544" + ] + }, + "category": "Neurodegenerative disease" + }, + "article": { + "id": "20458069", + "text": "BACKGROUND:\nCommonly used organophosphate and organochlorine pesticides inhibit acetylcholinesterase at synapses in the somatic, autonomic, and central nervous systems and may therefore have lasting effects on the nervous system. Few studies have examined the relationship of pesticide exposure and risk of dementia or Alzheimer disease (AD). We sought to examine the association of occupational pesticide exposure and the risk of incident dementia and AD in later life.\n\nMETHODS:\nResidents of the agricultural community of Cache County, UT, who were aged 65 years and older as of January 1995, were invited to participate in the study. At baseline, participants completed detailed occupational history questionnaires that included information about exposures to various types of pesticides. Cognitive status was assessed at baseline and after 3, 7, and 10 years. Standardized methods were used for detection and diagnosis of dementia and AD. Cox proportional hazards survival analyses were used to evaluate the risk of incident dementia and AD associated with pesticide exposure.\n\nRESULTS:\nAmong 3,084 enrollees without dementia, more men than women reported pesticide exposure (p \u003c 0.0001). Exposed individuals (n = 572) had more years of education (p \u003c 0.01) but did not differ from others in age. Some 500 individuals developed incident dementia, 344 with AD. After adjustment for baseline age, sex, education, APOE epsilon4 status, and baseline Modified Mini-Mental State Examination scores, Cox proportional hazards models showed increased risks among pesticide-exposed individuals for all-cause dementia, with hazard ratio (HR) 1.38 and 95% confidence interval (CI) 1.09-1.76, and for AD (HR 1.42, 95% CI 1.06-1.91). The risk of AD associated with organophosphate exposure (HR 1.53, 95% CI 1.05-2.23) was slightly higher than the risk associated with organochlorines (HR 1.49, 95% CI 0.99-2.24), which was nearly significant.\n\nCONCLUSIONS:\nPesticide exposure may increase the risk of dementia and Alzheimer disease in late life." + }, + "questions": [ + { + "id": "dcc55f13-609c-4943-8331-9263635a75fc", + "text": "What are the risk factors of Alzheimer disease?", + "answers": [ + { + "answer_start": 1947, + "text": "Pesticide exposure" + }, + { + "answer_start": 1755, + "text": "organophosphate exposure" + }, + { + "answer_start": 1558, + "text": "pesticide-exposed individuals" + } + ] + } + ] +} \ No newline at end of file diff --git a/acbfa848-850c-4a06-b586-9c62844ee43e.json b/acbfa848-850c-4a06-b586-9c62844ee43e.json new file mode 100644 index 0000000000000000000000000000000000000000..d60771add7b723dfb2954f358dbff486ee11291d --- /dev/null +++ b/acbfa848-850c-4a06-b586-9c62844ee43e.json @@ -0,0 +1,46 @@ +{ + "id": "acbfa848-850c-4a06-b586-9c62844ee43e", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "20571017", + "text": "CONTEXT:\nAdiposity is a well-recognized risk factor for type 2 diabetes among young and middle-aged adults, but the relationship between body composition and type 2 diabetes is not well described among older adults.\n\nOBJECTIVE:\nTo examine the relationship between adiposity, changes in adiposity, and risk of incident type 2 diabetes in adults 65 years of age and older.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nProspective cohort study (1989-2007) of 4193 men and women 65 years of age and older in the Cardiovascular Health Study. Measures of adiposity were derived from anthropometry and bioelectrical impedance data at baseline and anthropometry repeated 3 years later.\n\nMAIN OUTCOME MEASURE:\nIncident diabetes was ascertained based on use of antidiabetic medication or a fasting glucose level of 126 mg/dL or greater.\n\nRESULTS:\nOver median follow-up of 12.4 years (range, 0.9-17.8 years), 339 cases of incident diabetes were ascertained (7.1/1000 person-years). The adjusted hazard ratio (HR) (95% confidence interval [CI]) of type 2 diabetes for participants in the highest quintile of baseline measures compared with those in the lowest was 4.3 (95% CI, 2.9-6.5) for body mass index (BMI [calculated as weight in kilograms divided by height in meters squared]), 3.0 (95% CI, 2.0-4.3) for BMI at 50 years of age, 4.2 (95% CI, 2.8-6.4) for weight, 4.0 (95% CI, 2.6-6.0) for fat mass, 4.2 (95% CI, 2.8-6.2) for waist circumference, 2.4 (95% CI, 1.6-3.5) for waist-hip ratio, and 3.8 (95% CI, 2.6-5.5) for waist-height ratio. However, when stratified by age, participants 75 years of age and older had HRs approximately half as large as those 65 to 74 years of age. Compared with weight-stable participants (+/-2 kg), those who gained the most weight from 50 years of age to baseline (\u003e or = 9 kg), and from baseline to the third follow-up visit (\u003e or = 6 kg), had HRs for type 2 diabetes of 2.8 (95% CI, 1.9-4.3) and 2.0 (95% CI, 1.1-3.7), respectively. Participants with a greater than 10-cm increase in waist size from baseline to the third follow-up visit had an HR of type 2 diabetes of 1.7 (95% CI, 1.1-2.8) compared with those who gained or lost 2 cm or less.\n\nCONCLUSION:\nAmong older adults, overall and central adiposity, and weight gain during middle age and after the age of 65 years are associated with risk of diabetes." + }, + "questions": [ + { + "id": "6c46cf1e-1a4f-4946-ac18-93d565891d1a", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 2198, + "text": "overall and central adiposity" + }, + { + "answer_start": 2233, + "text": "weight gain during middle age and after the age of 65 years" + }, + { + "answer_start": 1726, + "text": "gained the most weight from 50 years of age to baseline (\u003e or = 9 kg), and from baseline to the third follow-up visit (\u003e or = 6 kg)" + }, + { + "answer_start": 1953, + "text": "Participants with a greater than 10-cm increase in waist size from baseline to the third follow-up visit" + } + ] + } + ] +} \ No newline at end of file diff --git a/ad154f7d-3b02-4131-ad86-1e4b03a56461.json b/ad154f7d-3b02-4131-ad86-1e4b03a56461.json new file mode 100644 index 0000000000000000000000000000000000000000..1f968c73c4dae3b2debba785214ee70b156c2712 --- /dev/null +++ b/ad154f7d-3b02-4131-ad86-1e4b03a56461.json @@ -0,0 +1,47 @@ +{ + "id": "ad154f7d-3b02-4131-ad86-1e4b03a56461", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "15150307", + "text": "BACKGROUND:\nFew family studies have investigated the effects of genetic, environmental, and host factors on melanoma risk, and most have been restricted to high-risk families. We assessed the role of these factors on melanoma risk in two types of families: families ascertained through melanoma probands but unselected by family history and melanoma-prone families.\n\nMETHODS:\nData on pigmentary traits, nevus phenotypes, exposure to sun, and reactions to sunlight were collected from 295 families unselected by family history and 53 melanoma-prone families. We modeled melanoma risk using a logistic regressive model incorporating the effect of a melanoma-predisposing gene, familial dependence, and potential risk factors (e.g., pigmentary traits, nevus phenotypes, history of sun exposure, skin reactions to sunlight). Maximum-likelihood estimates of the parameters of the regressive model were used to compute odds ratios associated with each risk factor and age-specific melanoma risk depending on the genotype at the melanoma-predisposing gene and the effects of risk factors. All statistical tests were two-sided.\n\nRESULTS:\nIn the families unselected by family history, there was statistically significant evidence (P\u003c.001) for a dominant gene, with melanoma risk reaching 0.49 and 0.67 by age 80 years in male and female gene carriers, respectively. Melanoma risk was statistically significantly influenced by total nevi (odds ratio of hazard function [OR] = 5.81, 95% confidence interval [CI] = 3.47 to 8.99), sun exposure (OR = 5.37, 95% CI = 4.44 to 6.36), and sunburn interacting with the gene (OR = 26.31, 95% CI = 7.56 to 99.22 in gene carriers and OR = 1.67, 95% CI = 1.36 to 2.03 in noncarriers). Twenty of the 53 melanoma-prone families had cosegregating mutations in CDKN2A, a gene known to be associated with melanoma. In these 53 families, three risk factors in addition to CDKN2A mutations increased melanoma risk: dysplastic nevi (OR = 2.32, 95% CI = 2.08 to 2.58), total nevi (OR = 1.99, 95% CI = 1.61 to 2.20) and sunburn (OR = 5.16, 95% CI = 4.82 to 5.52).\n\nCONCLUSIONS:\nTogether, a melanoma-predisposing gene (identified as being CDKN2A in melanoma-prone families), number of nevi and/or dysplastic nevi, and sun-related covariates influence melanoma risk in both families unselected by family history and melanoma-prone families." + }, + "questions": [ + { + "id": "9d272022-8722-414c-ac78-d1cb6f29a45d", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 2107, + "text": "melanoma-predisposing gene (identified as being CDKN2A in melanoma-prone families)" + }, + { + "answer_start": 2191, + "text": "number of nevi" + }, + { + "answer_start": 2213, + "text": "dysplastic nevi" + }, + { + "answer_start": 2234, + "text": "sun-related covariates" + } + ] + } + ] +} \ No newline at end of file diff --git a/ad425071-f76f-4d3b-983f-f554905d831d.json b/ad425071-f76f-4d3b-983f-f554905d831d.json new file mode 100644 index 0000000000000000000000000000000000000000..ddfbde6326e20dfdea2ffb595e2874f341fed401 --- /dev/null +++ b/ad425071-f76f-4d3b-983f-f554905d831d.json @@ -0,0 +1,35 @@ +{ + "id": "ad425071-f76f-4d3b-983f-f554905d831d", + "disease": { + "id": "H01633", + "names": [ + "High blood pressure", + "Hypertension" + ], + "dbLinks": { + "icd10": [ + "I10" + ], + "mesh": [ + "D006973" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "32609894", + "text": "BACKGROUND:\nAlcohol is consumed by over 2 billion people worldwide. It is a common substance of abuse and its use can lead to more than 200 disorders including hypertension. Alcohol has both acute and chronic effects on blood pressure. This review aimed to quantify the acute effects of different doses of alcohol over time on blood pressure and heart rate in an adult population.\n\nOBJECTIVES:\nPrimary objective To determine short-term dose-related effects of alcohol versus placebo on systolic blood pressure and diastolic blood pressure in healthy and hypertensive adults over 18 years of age. Secondary objective To determine short-term dose-related effects of alcohol versus placebo on heart rate in healthy and hypertensive adults over 18 years of age.\n\nSEARCH METHODS:\nThe Cochrane Hypertension Information Specialist searched the following databases for randomised controlled trials up to March 2019: the Cochrane Hypertension Specialised Register; the Cochrane Central Register of Controlled Trials (CENTRAL; 2019, Issue 2), in the Cochrane Library; MEDLINE (from 1946); Embase (from 1974); the World Health Organization International Clinical Trials Registry Platform; and ClinicalTrials.gov. We also contacted authors of relevant articles regarding further published and unpublished work. These searches had no language restrictions.\n\nSELECTION CRITERIA:\nRandomised controlled trials (RCTs) comparing effects of a single dose of alcohol versus placebo on blood pressure (BP) or heart rate (HR) in adults (≥ 18 years of age).\n\nDATA COLLECTION AND ANALYSIS:\nTwo review authors (ST and CT) independently extracted data and assessed the quality of included studies. We also contacted trial authors for missing or unclear information. Mean difference (MD) from placebo with 95% confidence interval (CI) was the outcome measure, and a fixed-effect model was used to combine effect sizes across studies. MAIN RESULTS: We included 32 RCTs involving 767 participants. Most of the study participants were male (N = 642) and were healthy. The mean age of participants was 33 years, and mean body weight was 78 kilograms. Low-dose alcohol (\u003c 14 g) within six hours (2 RCTs, N = 28) did not affect BP but did increase HR by 5.1 bpm (95% CI 1.9 to 8.2) (moderate-certainty evidence). Medium-dose alcohol (14 to 28 g) within six hours (10 RCTs, N = 149) decreased systolic blood pressure (SBP) by 5.6 mmHg (95% CI -8.3 to -3.0) and diastolic blood pressure (DBP) by 4.0 mmHg (95% CI -6.0 to -2.0) and increased HR by 4.6 bpm (95% CI 3.1 to 6.1) (moderate-certainty evidence for all). Medium-dose alcohol within 7 to 12 hours (4 RCTs, N = 54) did not affect BP or HR. Medium-dose alcohol \u003e 13 hours after consumption (4 RCTs, N = 66) did not affect BP or HR. High-dose alcohol (\u003e 30 g) within six hours (16 RCTs, N = 418) decreased SBP by 3.5 mmHg (95% CI -6.0 to -1.0), decreased DBP by 1.9 mmHg (95% CI-3.9 to 0.04), and increased HR by 5.8 bpm (95% CI 4.0 to 7.5). The certainty of evidence was moderate for SBP and HR, and was low for DBP. High-dose alcohol within 7 to 12 hours of consumption (3 RCTs, N = 54) decreased SBP by 3.7 mmHg (95% CI -7.0 to -0.5) and DBP by 1.7 mmHg (95% CI -4.6 to 1.8) and increased HR by 6.2 bpm (95% CI 3.0 to 9.3). The certainty of evidence was moderate for SBP and HR, and low for DBP. High-dose alcohol ≥ 13 hours after consumption (4 RCTs, N = 154) increased SBP by 3.7 mmHg (95% CI 2.3 to 5.1), DBP by 2.4 mmHg (95% CI 0.2 to 4.5), and HR by 2.7 bpm (95% CI 0.8 to 4.6) (moderate-certainty evidence for all). AUTHORS' CONCLUSIONS: High-dose alcohol has a biphasic effect on BP; it decreases BP up to 12 hours after consumption and increases BP \u003e 13 hours after consumption. High-dose alcohol increases HR at all times up to 24 hours. Findings of this review are relevant mainly to healthy males, as only small numbers of women were included in the included trials." + }, + "questions": [ + { + "id": "f87af02a-aebe-4e67-8df9-a17607bf526b", + "text": "What are the risk factors for Hypertension?", + "answers": [ + { + "answer_start": 3319, + "text": "High-dose alcohol ≥ 13 hours after consumption " + } + ] + } + ] +} \ No newline at end of file diff --git a/ade0bc2e-e4d4-4cba-99ad-a7cc9783839d.json b/ade0bc2e-e4d4-4cba-99ad-a7cc9783839d.json new file mode 100644 index 0000000000000000000000000000000000000000..6ecb4c7dd3c077aba7d12d7daeef7d4b4980eec3 --- /dev/null +++ b/ade0bc2e-e4d4-4cba-99ad-a7cc9783839d.json @@ -0,0 +1,38 @@ +{ + "id": "ade0bc2e-e4d4-4cba-99ad-a7cc9783839d", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "18206936", + "text": "PURPOSE:\nAugmentation gastrocystoplasty has been proposed as an alternative to enterocystoplasty because of potential benefits, including decreased risk of mucus production, stone formation and urinary tract infections. Although cancer has rarely been reported in this patient population, it is a well recognized potential risk of all augmentation cystoplasties. To define better the risk of malignancy associated with gastric augmentation and the appropriate surveillance protocol for these patients, we describe our experience in 2 patients with metastatic adenocarcinoma following gastrocystoplasty.\n\nMATERIALS AND METHODS:\nWe retrospectively reviewed the charts of all patients who had undergone augmentation gastrocystoplasty between 1990 and 1994. Of the 72 patients identified 2 were diagnosed with a primary malignancy arising from the augmented bladder. Charts were reviewed for medical history, clinical outcomes and pathology.\n\nRESULTS:\nTwo patients were identified with a primary bladder malignancy after gastrocystoplasty. Both patients had metastatic disease at initial presentation. Neither patient had a history of gross hematuria, recurrent urinary tract infections or pain before initial presentation. Mean patient age at augmentation was 5.5 years. Mean age at diagnosis of malignancy was 19.5 years, with a mean time from augmentation of 14 years.\n\nCONCLUSIONS:\nAlthough the risk of bladder cancer is low after gastric augmentation, the effects may be life threatening. Therefore, we advocate routine annual surveillance with cystoscopy, bladder biopsy and upper tract imaging in all patients who have undergone augmentation gastrocystoplasty." + }, + "questions": [ + { + "id": "a8081028-5bfa-4b1d-b508-b5061e7c994f", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 673, + "text": "patients who had undergone augmentation gastrocystoplasty between 1990 and 1994" + }, + { + "answer_start": 1431, + "text": "gastric augmentation" + } + ] + } + ] +} \ No newline at end of file diff --git a/adf21221-9bd7-476a-a502-d9bf017c30d5.json b/adf21221-9bd7-476a-a502-d9bf017c30d5.json new file mode 100644 index 0000000000000000000000000000000000000000..0b65b8a760eff74bba61e5ebfe6242b1fcf3613d --- /dev/null +++ b/adf21221-9bd7-476a-a502-d9bf017c30d5.json @@ -0,0 +1,34 @@ +{ + "id": "adf21221-9bd7-476a-a502-d9bf017c30d5", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "30183083", + "text": "Prior studies on red and processed meat consumption with breast cancer risk have generated inconsistent results. We performed a systematic review and meta-analysis of prospective studies to summarize the evidence regarding the relation of red meat and processed meat consumption with breast cancer incidence. We searched in MEDLINE and EMBASE databases through January 2018 for prospective studies that reported the association between red meat and processed meat consumption with incident breast cancer. The multivariable-adjusted relative risk (RR) was combined comparing the highest with the lowest category of red meat (unprocessed) and processed meat consumption using a random-effect meta-analysis. We identified 13 cohort, 3 nested case-control and two clinical trial studies. Comparing the highest to the lowest category, red meat (unprocessed) consumption was associated with a 6% higher breast cancer risk (pooled RR,1.06; 95% confidence intervals (95%CI):0.99-1.14; I = 56.3%), and processed meat consumption was associated with a 9% higher breast cancer risk (pooled RR, 1.09; 95%CI, 1.03-1.16; I = 44.4%). In addition, we identified two nested case-control studies evaluating the association between red meat and breast cancer stratified by N-acetyltransferase 2 acetylator genotype. We did not observe any association among those with either fast (per 25 g/day pooled odds ratio (OR), 1.18; 95%CI, 0.93-1.50) or slow N-acetyltransferase 2 acetylators (per 25 g/day pooled OR, 0.99; 95%CI, 0.91-1.08). In the prospective observational studies, high processed meat consumption was associated with increased breast cancer risk." + }, + "questions": [ + { + "id": "fa14ea95-7429-41f7-845f-ccbb374bc9c3", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1556, + "text": " high processed meat consumption" + } + ] + } + ] +} \ No newline at end of file diff --git a/ae268587-10e8-4378-aaac-7779979b59fa.json b/ae268587-10e8-4378-aaac-7779979b59fa.json new file mode 100644 index 0000000000000000000000000000000000000000..204a429153e24ca52a81955187522e45a275f2e3 --- /dev/null +++ b/ae268587-10e8-4378-aaac-7779979b59fa.json @@ -0,0 +1,34 @@ +{ + "id": "ae268587-10e8-4378-aaac-7779979b59fa", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "22325189", + "text": "BACKGROUND:\nA sexual dimorphism exists in the incidence and prevalence of coronary artery disease--men are more commonly affected than are age-matched women. We explored the role of the Y chromosome in coronary artery disease in the context of this sexual inequity.\n\nMETHODS:\nWe genotyped 11 markers of the male-specific region of the Y chromosome in 3233 biologically unrelated British men from three cohorts: the British Heart Foundation Family Heart Study (BHF-FHS), West of Scotland Coronary Prevention Study (WOSCOPS), and Cardiogenics Study. On the basis of this information, each Y chromosome was tracked back into one of 13 ancient lineages defined as haplogroups. We then examined associations between common Y chromosome haplogroups and the risk of coronary artery disease in cross-sectional BHF-FHS and prospective WOSCOPS. Finally, we undertook functional analysis of Y chromosome effects on monocyte and macrophage transcriptome in British men from the Cardiogenics Study.\n\nFINDINGS:\nOf nine haplogroups identified, two (R1b1b2 and I) accounted for roughly 90% of the Y chromosome variants among British men. Carriers of haplogroup I had about a 50% higher age-adjusted risk of coronary artery disease than did men with other Y chromosome lineages in BHF-FHS (odds ratio 1·75, 95% CI 1·20-2·54, p=0·004), WOSCOPS (1·45, 1·08-1·95, p=0·012), and joint analysis of both populations (1·56, 1·24-1·97, p=0·0002). The association between haplogroup I and increased risk of coronary artery disease was independent of traditional cardiovascular and socioeconomic risk factors. Analysis of macrophage transcriptome in the Cardiogenics Study revealed that 19 molecular pathways showing strong differential expression between men with haplogroup I and other lineages of the Y chromosome were interconnected by common genes related to inflammation and immunity, and that some of them have a strong relevance to atherosclerosis.\n\nINTERPRETATION:\nThe human Y chromosome is associated with risk of coronary artery disease in men of European ancestry, possibly through interactions of immunity and inflammation.\n\nFUNDING:\nBritish Heart Foundation; UK National Institute for Health Research; LEW Carty Charitable Fund; National Health and Medical Research Council of Australia; European Union 6th Framework Programme; Wellcome Trust." + }, + "questions": [ + { + "id": "96434424-8f48-4034-950d-39db226ed470", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1947, + "text": "The human Y chromosome" + } + ] + } + ] +} \ No newline at end of file diff --git a/ae37147d-5b53-4af8-a96f-bb26c70d83fc.json b/ae37147d-5b53-4af8-a96f-bb26c70d83fc.json new file mode 100644 index 0000000000000000000000000000000000000000..b9af9cfa92d150a6c3790999d1019c07ab30ff57 --- /dev/null +++ b/ae37147d-5b53-4af8-a96f-bb26c70d83fc.json @@ -0,0 +1,36 @@ +{ + "id": "ae37147d-5b53-4af8-a96f-bb26c70d83fc", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "11254539", + "text": "Pulmonary emphysema is believed to result from an imbalance between proteolytic enzymes and their inhibitors. Multiple studies have examined the presence of various proteases within the bronchoalveolar lavage fluid from patients with chronic obstructive pulmonary disease (COPD). However, to date extensive examination of the lung parenchyma for the expression of destructive enzymes has not yet been determined. The following study examines the lung parenchyma of 23 patients with emphysema and 8 normal control samples for the expression of matrix matalloproteinase-1 (MMP-1), MMP-12, and MMP-9. We report here that interstitial collagenase (MMP-1) RNA, protein, and activity are present in the lung parenchyma of patients with emphysema and not in the lung of normal control subjects. In contrast, metalloelastase (MMP-12) expression is absent in these samples. Immunohistochemistry studies localized MMP-1 to the Type II pneumocyte in patients with emphysema and not normal control subjects or smokers without emphysema. This observation demonstrates that the lung is altered in emphysema such that the Type II pneumocyte secretes MMP-1 and suggests that MMP-1 may be an important enzyme involved in the destruction of the lung in the human disease. In addition, the induction of a proteolytic enzyme within the Type II pneumocyte suggests that the cells within the lung itself are capable of producing degradative enzymes in this disease process." + }, + "questions": [ + { + "id": "e88f0f46-2a84-4189-aa39-8885a10a2127", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 904, + "text": "MMP-1 to the Type II pneumocyte" + } + ] + } + ] +} \ No newline at end of file diff --git a/af2040e8-8c70-4f83-b17d-bc1c3d16d4af.json b/af2040e8-8c70-4f83-b17d-bc1c3d16d4af.json new file mode 100644 index 0000000000000000000000000000000000000000..ef3b7372f533c577ca47e6755b75499fe0183a0c --- /dev/null +++ b/af2040e8-8c70-4f83-b17d-bc1c3d16d4af.json @@ -0,0 +1,39 @@ +{ + "id": "af2040e8-8c70-4f83-b17d-bc1c3d16d4af", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "21051083", + "text": "BACKGROUND:\nPrenatal and infant acetaminophen exposure has been associated with an increased risk of childhood asthma phenotypes. Demonstration of biologically plausible interactions between these exposures and maternal and child antioxidant gene polymorphisms would strengthen causal inference.\n\nOBJECTIVE:\nTo explore potential interactions between prenatal and infant acetaminophen exposure and antioxidant genotypes on childhood asthma.\n\nMETHODS:\nIn the Avon Longitudinal Study of Parents and Children, we typed a functional nuclear erythroid 2 p45-related factor 2 (Nrf2) polymorphism and glutathione S-transferase (GST) M1, T1, and P1 polymorphisms. Effects of prenatal and infant acetaminophen exposure on asthma phenotypes at 7 years were stratified by genotype in \u003e4000 mothers and \u003e5000 children.\n\nRESULTS:\nRisk of asthma and wheezing associated with early gestation acetaminophen exposure was increased when maternal copies of the minor T allele of Nrf2 were present (P interactions, .02 and .04, respectively). Risk of asthma associated with late gestation exposure was higher when maternal GSTT1 genotype was present rather than absent (P interaction, .006), and risk of wheezing was increased when maternal GSTM1 was present (P interaction, .04). Although acetaminophen use in infancy was associated with an increased risk of atopy, child antioxidant genotype did not modify associations between infant acetaminophen use and asthma phenotypes. However, the increased risk of asthma and wheezing associated with late gestation acetaminophen exposure in the presence of maternal GSTM1 was further enhanced when GSTM1 was also present in the child.\n\nCONCLUSION:\nMaternal antioxidant gene polymorphisms may modify the relation between prenatal acetaminophen exposure and childhood asthma, strengthening evidence for a causal association. In contrast, relations between infant acetaminophen use and asthma and atopy were not modified by child genotype and may be confounded by pre-existing wheeze or allergy." + }, + "questions": [ + { + "id": "a0ec4384-16fe-4745-883e-ef01655fc4f3", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 860, + "text": "early gestation acetaminophen exposure was increased when maternal copies of the minor T allele of Nrf2 were present (P interactions, .02 and .04, respectively)" + }, + { + "answer_start": 1053, + "text": "late gestation exposure was higher when maternal GSTT1 genotype was present rather than absent (P interaction, .006)" + } + ] + } + ] +} \ No newline at end of file diff --git a/af3eee3f-5281-407d-ba56-ef0b59ec1136.json b/af3eee3f-5281-407d-ba56-ef0b59ec1136.json new file mode 100644 index 0000000000000000000000000000000000000000..4bc6320ff5ad547062c573004ae3050d02bab5b5 --- /dev/null +++ b/af3eee3f-5281-407d-ba56-ef0b59ec1136.json @@ -0,0 +1,35 @@ +{ + "id": "af3eee3f-5281-407d-ba56-ef0b59ec1136", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "18571547", + "text": "OBJECTIVE:\nTo explore the possible association between delivery by cesarean section (CS) and later development of asthma.\n\nSTUDY DESIGN:\nA population-based cohort study of 1,756,700 singletons reported to the Medical Birth Registry of Norway between 1967 and 1998, followed up to age 18 years or the year 2002. Exposure was the mode of delivery (spontaneous vaginal, instrumental vaginal, or CS, with planned and emergency CS separately from 1988 onward). Outcome was asthma registered in the National Insurance Scheme, which provides cash benefits to families of children with severe chronic illnesses. We used multivariate Cox proportional hazard models to examine associations between exposure and outcome.\n\nRESULTS:\nThe cumulative incidence of asthma was 4.0/1000. Children delivered by CS had a 52% increased risk of asthma compared with spontaneously vaginally delivered children (adjusted hazard ratio [HR] = 1.52; 95% confidence interval [CI] = 1.42 to 1.62). Between 1988 and 1998, planned and emergency CS was associated with a 42% (HR = 1.42; 95% CI = 1.25 to 1.61) and 59% (HR = 1.59; 95% CI = 1.44 to 1.75) increased risk of asthma, respectively.\n\nCONCLUSION:\nWe found a moderately increased risk of asthma in the children delivered by CS. The possibly stronger association with emergency CS compared with planned CS could be worth pursuing to investigate possible causal mechanisms." + }, + "questions": [ + { + "id": "533fbb2a-6ed4-4a23-9b3b-d579edfd7012", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1227, + "text": "children delivered by CS" + } + ] + } + ] +} \ No newline at end of file diff --git a/afe6ac9b-294f-413d-a79d-2f1aad73ab36.json b/afe6ac9b-294f-413d-a79d-2f1aad73ab36.json new file mode 100644 index 0000000000000000000000000000000000000000..e3bec9bc18b70ce0f1d17064776c4c7e504501f1 --- /dev/null +++ b/afe6ac9b-294f-413d-a79d-2f1aad73ab36.json @@ -0,0 +1,39 @@ +{ + "id": "afe6ac9b-294f-413d-a79d-2f1aad73ab36", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "15735054", + "text": "RATIONALE:\nOxidative stress may increase the risk of asthma, contribute to asthma progression, and decrease lung function. Previous research suggests that use of acetaminophen, which is hypothesized to reduce antioxidant capacity in the lung, is associated with an increased risk of asthma. We hypothesized that acetaminophen use may also be associated with chronic obstructive pulmonary disease (COPD) and decreased lung function.\n\nOBJECTIVES:\nTo investigate the associations between use of pain medication, particularly acetaminophen, and asthma, COPD, and FEV1 in adults.\n\nMETHODS:\nA cross-sectional analysis using the Third National Health and Nutrition Examination Survey.\n\nMEASUREMENT AND MAIN RESULTS:\nIncreased use of acetaminophen had a positive, dose-dependent association with COPD (adjusted odds ratio for increasing category of intake, 1.16; 95% confidence interval [CI], 1.09-1.24; p value for trend \u003c 0.001) and an inverse association with lung function (daily user compared with never users, -54.0 ml; 95% CI, -90.3 to -17.7, adjusted). Neither of these associations was explained by overlap between COPD and asthma occurrence. We confirmed a dose-response association of acetaminophen use and asthma (adjusted odds ratio, 1.20; 95% CI, 1.12-1.28; p value for trend \u003c 0.001).\n\nCONCLUSIONS:\nThis study provides further evidence that use of acetaminophen is associated with an increased risk of asthma and COPD, and with decreased lung function." + }, + "questions": [ + { + "id": "4fde4ca6-2850-494b-9e69-f8b1b8d90c5d", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1348, + "text": "use of acetaminophen" + }, + { + "answer_start": 1188, + "text": "acetaminophen use" + } + ] + } + ] +} \ No newline at end of file diff --git a/b00d34dc-5f4c-4bcf-be33-a2e891ae0fc3.json b/b00d34dc-5f4c-4bcf-be33-a2e891ae0fc3.json new file mode 100644 index 0000000000000000000000000000000000000000..ac748f79bb8c9023e735efe9a0d6caf69505890c --- /dev/null +++ b/b00d34dc-5f4c-4bcf-be33-a2e891ae0fc3.json @@ -0,0 +1,39 @@ +{ + "id": "b00d34dc-5f4c-4bcf-be33-a2e891ae0fc3", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "19654914", + "text": "BACKGROUND:\nRheumatoid arthritis (RA) is a chronic systemic inflammatory disease that affects approximately 1% of the adult population, and to date, genetic factors explain \u003c 50% of the risk. Particulate air pollution, especially of traffic origin, has been linked to systemic inflammation in many studies.\n\nOBJECTIVES:\nWe examined the association of distance to road, a marker of traffic pollution exposure, and incidence of RA in a prospective cohort study.\n\nMETHODS:\nWe studied 90,297 U.S. women in the Nurses' Health Study. We used a geographic information system to determine distance to road at the residence in 2000 as a measure of traffic exposure. Using Cox proportional hazard models, we examined the association of distance to road and incident RA (1976-2004) with adjustment for a large number of potential confounders.\n\nRESULTS:\nIn models adjusted for age, calendar year, race, cigarette smoking, parity, lactation, menopausal status and hormone use, oral contraceptive use, body mass index, physical activity, and census-tract-level median income and house value, we observed an elevated risk of RA [hazard ratio (HR) = 1.31; 95% confidence interval (CI), 0.98-1.74] in women living within 50 m of a road, compared with those women living 200 m or farther away. We also observed this association in analyses among nonsmokers (HR = 1.62; 95% CI, 1.04-2.52), nonsmokers with rheumatoid factor (RF)-negative RA (HR = 1.77; 95% CI, 0.93-3.38), and nonsmokers with RF-positive RA (HR = 1.51; 95% CI, 0.82-2.77). We saw no elevations in risk in women living 50-200 m from the road.\n\nCONCLUSIONS:\nThe observed association between exposure to traffic pollution and RA suggests that pollution from traffic in adulthood may be a newly identified environmental risk factor for RA." + }, + "questions": [ + { + "id": "615a61c9-1cab-4d59-85e9-65482bd8365f", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 1184, + "text": "women living within 50 m of a road, compared with those women living 200 m or farther away" + }, + { + "answer_start": 1649, + "text": "traffic pollution" + } + ] + } + ] +} \ No newline at end of file diff --git a/b0326ff5-86fe-40cc-bc83-9898e8f6506c.json b/b0326ff5-86fe-40cc-bc83-9898e8f6506c.json new file mode 100644 index 0000000000000000000000000000000000000000..ca3abf9f45e84c5848c8f60ecd7c715ce0961f94 --- /dev/null +++ b/b0326ff5-86fe-40cc-bc83-9898e8f6506c.json @@ -0,0 +1,34 @@ +{ + "id": "b0326ff5-86fe-40cc-bc83-9898e8f6506c", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "2769783", + "text": "Although exposure to ionizing radiation is a recognized risk factor for breast cancer, the potential hazard from low-dose, fractionated exposures during early breast development has not been thoroughly evaluated. Women with scoliosis represent a valuable population for studying this issue because they are exposed to multiple diagnostic x rays during childhood and adolescence, times when the breast may be highly sensitive to the carcinogenic effects of radiation. A study was conducted of 1,030 women with scoliosis who were seen at four Minneapolis area medical facilities between 1935 and 1965. The average age at diagnosis was 12.3 years; 60% of the women had idiopathic scoliosis. Individual x-ray films were counted and the number per patient ranged from 0 to 618 films (mean, 41.5). On average, the x-ray exposures were given over an 8.7-year period. Ninety percent of the women were located, of whom over 92% responded to a mail questionnaire or telephone interview. The average period of observation was 26 years. Overall, 11 cases of breast cancer were reported, compared with six expected (standardized incidence ratio = 1.82, 90% confidence interval = 1.0-3.0). Excess risk increased with time since exposure and was highest among those followed for more than 30 years (standardized incidence ratio = 2.4). Risk also increased with the number of x rays and with the estimated radiation dose to the breast (mean, 13 rad). These data suggest that frequent exposure to low-level diagnostic radiation during childhood or adolescence may increase the risk of breast cancer." + }, + "questions": [ + { + "id": "a3d6fa28-b4c2-4e1e-ba29-9dd08c7747d9", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1459, + "text": "frequent exposure to low-level diagnostic radiation during childhood or adolescence" + } + ] + } + ] +} \ No newline at end of file diff --git a/b0505975-a8c4-4672-9ac9-7d2b53c19f17.json b/b0505975-a8c4-4672-9ac9-7d2b53c19f17.json new file mode 100644 index 0000000000000000000000000000000000000000..55289e90ec3df3e3c8c01795316f285b702b792d --- /dev/null +++ b/b0505975-a8c4-4672-9ac9-7d2b53c19f17.json @@ -0,0 +1,39 @@ +{ + "id": "b0505975-a8c4-4672-9ac9-7d2b53c19f17", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "10913061", + "text": "BACKGROUND:\nRecent epidemiological studies have suggested that smoking is a risk factor for rheumatoid factor (RF) positive rheumatoid arthritis (RA). Being overweight, high serum cholesterol, and dietary factors have in some studies been found to be associated with the risk of RA. No attention, however, has been paid to coffee consumption as a risk determinant, though it is a shared covariate of the alleged risk factors.\n\nOBJECTIVES:\nThis study aimed at examining coffee consumption for its associations with RF positivity and with the risk of RA.\n\nMETHODS:\nCoffee consumption was studied, firstly, for its association with RF (sensitised sheep cell agglutination titre \u003e/=128) in a cross sectional survey of 6809 subjects with no clinical arthritis, and secondly, for its prediction of RA in a cohort of 18 981 men and women who had neither arthritis nor a history of it at the baseline examination in 1973-76. Up to late 1989, 126 subjects of the cohort study had developed RA, of whom, 89 were positive for RF by the time of diagnosis.\n\nRESULTS:\nIn the cross sectional survey the number of cups of coffee drunk daily was directly proportional to the prevalence of RF positivity. Adjusted for age and sex this association was significant (p value for linear trend, 0.008), but after further adjustment for smoking the linear trend declined below significance (p=0.06). In the cohort study there was an association between coffee consumption and the risk of RF positive RA that was not due to age, sex, level of education, smoking, alcohol intake, body mass index, or serum cholesterol. After adjustment for these potential confounders the users of four or more cups a day still had a relative risk of 2.20 (95% confidence interval 1.13 to 4.27) for developing RF positive RA compared with those drinking less. Coffee consumption did not predict the development of RF negative RA.\n\nCONCLUSION:\nCoffee consumption may be a risk factor for RA, possibly through mechanisms contributing to the production of RF. This hypothesis remains to be tested in further studies." + }, + "questions": [ + { + "id": "e9a4d8c6-c127-49d5-bddd-389c6a8a6c47", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 1646, + "text": "users of four or more cups a day" + }, + { + "answer_start": 1900, + "text": "Coffee consumption" + } + ] + } + ] +} \ No newline at end of file diff --git a/b1022c2b-acb0-40d8-af3f-6e939a548261.json b/b1022c2b-acb0-40d8-af3f-6e939a548261.json new file mode 100644 index 0000000000000000000000000000000000000000..46bc302fdc768009db5df97d760b52104469e070 --- /dev/null +++ b/b1022c2b-acb0-40d8-af3f-6e939a548261.json @@ -0,0 +1,45 @@ +{ + "id": "b1022c2b-acb0-40d8-af3f-6e939a548261", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "30401889", + "text": "BACKGROUND:\nPrevious studies have shown a positive association between type 2 diabetes (T2D) and colorectal cancer (CRC) risk. However, it is uncertain whether this association differs by duration of T2D or sex. We thus investigated the associations of T2D and its duration with the risk of incident CRC.\n\nMETHODS:\nWe followed 87,523 women from the Nurses' Health Study (1980-2012) and 47,240 men from the Health Professionals Follow-up Study (1986-2012). Data on physician-diagnosed T2D was collected at baseline with a questionnaire and updated biennially. Cox regression models were used to estimate multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs).\n\nRESULTS:\nWe documented 3000 CRC cases during up to 32 years of follow-up. Among men, T2D was associated with increased risk of CRC compared to those without T2D (HR: 1.42; 95% CI: 1.12-1.81). This positive association persisted in sensitivity analyses by excluding CRC identified within 1 year of diabetes diagnosis and patients with T2D who used hypoglycaemic medications. Among women, T2D was positively, but not statistically significantly, associated with CRC risk (HR: 1.17; 95% CI: 0.98-1.39).\n\nCONCLUSIONS:\nOur findings support that T2D was associated with a moderately higher risk of developing CRC in men; a weaker, nonsignificant positive association was observed in women." + }, + "questions": [ + { + "id": "b6d9a0a4-7f66-46b2-b2fb-9ccaa6b8df5a", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 768, + "text": "T2D" + }, + { + "answer_start": 71, + "text": "type 2 diabetes (T2D)" + }, + { + "answer_start": 1223, + "text": "T2D" + } + ] + } + ] +} \ No newline at end of file diff --git a/b108d04b-e5ef-4970-a30f-3b8a37d6e8b3.json b/b108d04b-e5ef-4970-a30f-3b8a37d6e8b3.json new file mode 100644 index 0000000000000000000000000000000000000000..43cd83e256f10e607ef6a23abae3e8be574ca630 --- /dev/null +++ b/b108d04b-e5ef-4970-a30f-3b8a37d6e8b3.json @@ -0,0 +1,46 @@ +{ + "id": "b108d04b-e5ef-4970-a30f-3b8a37d6e8b3", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "21700918", + "text": "OBJECTIVE:\nPersistent organic pollutants (POPs), lipophilic chemicals that accumulate mainly in adipose tissue, have recently been linked to type 2 diabetes. However, evidence from prospective studies is sparse. This study was performed to evaluate prospective associations of type 2 diabetes with selected POPs among the elderly.\n\nRESEARCH DESIGN AND METHODS:\nNineteen POPs (14 polychlorinated biphenyl [PCB] congeners, 3 organochlorine pesticides, 1 brominated diphenyl ether, and 1 dioxin) were measured in plasma collected at baseline in 725 participants, aged 70 years, of the Prospective Investigation of the Vasculature in Uppsala Seniors (PIVUS).\n\nRESULTS:\nAfter adjusting for known type 2 diabetes risk factors, including obesity, odds ratios (ORs) (95% CIs) for type 2 diabetes at age 75 years (n = 36) according to the quintiles of a summary measure of concentrations of PCBs (vs. the lowest quintile) were 4.5, 5.1, 8.8 (1.8-42.7), and 7.5 (1.4-38.8) (P(trend) \u003c0.01). Among organochlorine pesticides, adjusted ORs across concentrations of trans-nonachlor showed that P(trend) = 0.03. Adjusted ORs (95% CIs) across quintiles of the sum of three organochlorine pesticides were 1.1, 1.6, 1.5, and 3.4 (1.0-11.7) (P(trend) = 0.03). Neither brominated diphenyl ether 47 nor dioxin was significantly associated with incident diabetes. The sum of PCBs improved reclassification significantly when added to traditional risk factors for diabetes.\n\nCONCLUSIONS:\nDespite the small number of incident cases, this study found that environmental exposure to some POPs substantially increased risk of future type 2 diabetes in an elderly population." + }, + "questions": [ + { + "id": "fb5ddbfa-272e-41fb-826c-15e7bc9316b3", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 864, + "text": "concentrations of PCBs" + }, + { + "answer_start": 379, + "text": "polychlorinated biphenyl [PCB]" + }, + { + "answer_start": 1531, + "text": "environmental exposure to some POPs" + }, + { + "answer_start": 11, + "text": "Persistent organic pollutants (POPs)" + } + ] + } + ] +} \ No newline at end of file diff --git a/b1174641-ae0b-4b81-be45-bdf65e06cce5.json b/b1174641-ae0b-4b81-be45-bdf65e06cce5.json new file mode 100644 index 0000000000000000000000000000000000000000..21c7b818f010b07156b05b17a9140a73f386e5fc --- /dev/null +++ b/b1174641-ae0b-4b81-be45-bdf65e06cce5.json @@ -0,0 +1,67 @@ +{ + "id": "b1174641-ae0b-4b81-be45-bdf65e06cce5", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "11434792", + "text": "BACKGROUND:\nPatients with asthma commonly have other medical problems such as obesity, but it is unclear if obesity independently relates to asthma occurrence.\n\nOBJECTIVE:\nTo examine the association between asthma and obesity.\n\nMETHODS:\nWe studied enrollees aged 17 to 96 years in region 11 of TRICARE, a military managed health care program encompassing Washington, Oregon, and northern Idaho, using an enrollment questionnaire from January 1997 to December 1998. We performed case-control analyses on 2788 asthma cases and 39 637 controls. From these cases and controls, we selected a random sample of 1000 asthma cases and 1000 controls, linking them to a computerized military health record system to verify if medications indicated for asthma therapy were prescribed. After excluding cases not prescribed bronchodilator medications and excluding controls prescribed bronchodilator medications or steroids, we used logistic regression to estimate associations among asthma, body mass index, and demographic, lifestyle, and comorbid risk factors in 386 verified cases and 744 verified controls.\n\nRESULTS:\nIncreasing body mass index, younger age, female sex, non-active duty beneficiary status, and arthritis were significant independent predictors of asthma prevalence in both our larger analysis and our verified substudy, whereas stomach ulcer, depression, hypertension, and white race are also independent predictors of asthma prevalence in our larger analysis.\n\nCONCLUSIONS:\nIncreasing body mass index is a key factor predicting prevalence of asthma and, if determined to be etiologically related to asthma incidence, is a potentially modifiable risk factor for asthma." + }, + "questions": [ + { + "id": "0c9e4038-b2f7-4966-a249-ee73a8d9cc21", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1108, + "text": "Increasing body mass index" + }, + { + "answer_start": 1136, + "text": "younger age" + }, + { + "answer_start": 1149, + "text": "female sex" + }, + { + "answer_start": 1161, + "text": "non-active duty beneficiary status" + }, + { + "answer_start": 1201, + "text": "arthritis" + }, + { + "answer_start": 1335, + "text": "stomach ulcer" + }, + { + "answer_start": 1350, + "text": "depression" + }, + { + "answer_start": 1362, + "text": "hypertension" + }, + { + "answer_start": 1380, + "text": "white race" + } + ] + } + ] +} \ No newline at end of file diff --git a/b1471f65-01e3-4a2e-aced-8e44d5b1e2e5.json b/b1471f65-01e3-4a2e-aced-8e44d5b1e2e5.json new file mode 100644 index 0000000000000000000000000000000000000000..a81ffeee79b7f9e65d46d6c474bfbad9b820d6cb --- /dev/null +++ b/b1471f65-01e3-4a2e-aced-8e44d5b1e2e5.json @@ -0,0 +1,35 @@ +{ + "id": "b1471f65-01e3-4a2e-aced-8e44d5b1e2e5", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "15184262", + "text": "BACKGROUND:\nMalignant melanoma has been one of the most rapidly increasing cancers within the United States with few modifiable risk factors. This study investigates risk related to dietary factors, which are potentially modifiable.\n\nMETHODS:\nNewly diagnosed patients with melanoma (n = 502) were recruited from pigment lesion clinics and controls (n = 565) were recruited from outpatient clinics. To investigate the relationship between melanoma and dietary factors in this case-control study, study subjects were requested to complete a food frequency questionnaire, which assessed diet over the previous year. Using logistic regression, odds ratios (ORs) for melanoma were computed for nutrient and alcohol intake.\n\nRESULTS:\nPersons in high versus low quintiles of energy-adjusted vitamin D, alpha-carotene, beta-carotene, cryptoxanthin, lutein, and lycopene had significantly reduced risk for melanoma (ORs \u003c or = 0.67), which remained after adjustment for presence of dysplastic nevi, education, and skin response to repeated sun exposure. Addition of micronutrients from supplements did not add an additional reduction in risk. High alcohol consumption was associated with an increased risk for melanoma, which remained after adjustment for confounders [OR (95% confidence interval) in highest versus lowest quintiles, 1.65 (1.09-2.49)].\n\nCONCLUSIONS:\nDiets consisting of foods rich in vitamin D and carotenoids and low in alcohol may be associated with a reduction in risk for melanoma. These analyses should be repeated in large, prospective studies." + }, + "questions": [ + { + "id": "f286091d-6dc9-4931-9769-de3ac0f18047", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 1134, + "text": "High alcohol consumption" + } + ] + } + ] +} \ No newline at end of file diff --git a/b19da8de-da43-42f0-9153-dc818292a72e.json b/b19da8de-da43-42f0-9153-dc818292a72e.json new file mode 100644 index 0000000000000000000000000000000000000000..6b22ea9e94ee5c0b44bf94533232ffcf7691d153 --- /dev/null +++ b/b19da8de-da43-42f0-9153-dc818292a72e.json @@ -0,0 +1,34 @@ +{ + "id": "b19da8de-da43-42f0-9153-dc818292a72e", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "15070788", + "text": "BACKGROUND:\nC-reactive protein is an inflammatory marker believed to be of value in the prediction of coronary events. We report data from a large study of C-reactive protein and other circulating inflammatory markers, as well as updated meta-analyses, to evaluate their relevance to the prediction of coronary heart disease.\n\nMETHODS:\nMeasurements were made in samples obtained at base line from up to 2459 patients who had a nonfatal myocardial infarction or died of coronary heart disease during the study and from up to 3969 controls without a coronary heart disease event in the Reykjavik prospective study of 18,569 participants. Measurements were made in paired samples obtained an average of 12 years apart from 379 of these participants in order to quantify within-person fluctuations in inflammatory marker levels.\n\nRESULTS:\nThe long-term stability of C-reactive protein values (within-person correlation coefficient, 0.59; 95 percent confidence interval, 0.52 to 0.66) was similar to that of both blood pressure and total serum cholesterol. After adjustment for base-line values for established risk factors, the odds ratio for coronary heart disease was 1.45 (95 percent confidence interval, 1.25 to 1.68) in a comparison of participants in the top third of the group with respect to base-line C-reactive protein values with those in the bottom third, and similar overall findings were observed in an updated meta-analysis involving a total of 7068 patients with coronary heart disease. By comparison, the odds ratios in the Reykjavik Study for coronary heart disease were somewhat weaker for the erythrocyte sedimentation rate (1.30; 95 percent confidence interval, 1.13 to 1.51) and the von Willebrand factor concentration (1.11; 95 percent confidence interval, 0.97 to 1.27) but generally stronger for established risk factors, such as an increased total cholesterol concentration (2.35; 95 percent confidence interval, 2.03 to 2.74) and cigarette smoking (1.87; 95 percent confidence interval, 1.62 to 2.16).\n\nCONCLUSIONS:\nC-reactive protein is a relatively moderate predictor of coronary heart disease. Recommendations regarding its use in predicting the likelihood of coronary heart disease may need to be reviewed." + }, + "questions": [ + { + "id": "323958fb-4bbf-494e-9ae1-5b2b7d4436ef", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 2039, + "text": "C-reactive protein" + } + ] + } + ] +} \ No newline at end of file diff --git a/b1fbc4ca-ba06-454c-8c22-b3fc17bf0492.json b/b1fbc4ca-ba06-454c-8c22-b3fc17bf0492.json new file mode 100644 index 0000000000000000000000000000000000000000..138c7dacff2ed95db4b68d8e4347537aaee622f0 --- /dev/null +++ b/b1fbc4ca-ba06-454c-8c22-b3fc17bf0492.json @@ -0,0 +1,34 @@ +{ + "id": "b1fbc4ca-ba06-454c-8c22-b3fc17bf0492", + "disease": { + "id": "H00408", + "names": [ + "Type 1 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E10" + ], + "mesh": [ + "D003922" + ] + }, + "category": "Metabolic disease; Immune system disease; Endocrine disease" + }, + "article": { + "id": "10074012", + "text": "OBJECTIVE:\nTo test the hypothesis that non-diabetic dizygotic and monozygotic twin siblings of patients with type 1 diabetes have a similar high prevalence of islet cell autoantibodies, thus suggesting that islet cell autoimmunity is mainly environmentally determined.\n\nDESIGN:\nProspective twin study.\n\nSETTING:\nTwo specialist centres for diabetes in the United States.\n\nPARTICIPANTS:\nNon-diabetic monozygotic twin (n=53), dizygotic twin (n=30), and non-twin (n=149) siblings of patients with type 1 diabetes; 101 controls.\n\nMAIN OUTCOME MEASURES:\nAnalysis of progression to diabetes and expression of anti-islet autoantibodies.\n\nRESULTS:\nMonozygotic twin siblings had a higher risk of progression to diabetes (12/53) than dizygotic twin siblings (0/30; P\u003c0.005). At the last follow up 22 (41.5%) monozygotic twin siblings expressed autoantibodies compared with 6 (20%) dizygotic twin siblings (P\u003c0.05), 16 (10.7%) non-twin siblings (P\u003c0.0001), and 6 (5.9%) controls (P\u003c0.0001). Monozygotic twin siblings expressed multiple (\u003e/=2) antibodies more often than dizygotic twin siblings (10/38 v 1/23; P\u003c0.05). By life table analysis the probability of developing positive autoantibodies was higher among the monozygotic twin siblings bearing the diabetes associated HLA DQ8/DQ2 genotype than in those without this genotype (64.2% (95% confidence interval 32.5% to 96%) v 23.5% (7% to 40%) at 10 years of discordance; P\u003c0.05).\n\nCONCLUSION:\nMonozygotic and dizygotic twins differ in progression to diabetes and expression of islet cell autoantibodies. Dizygotic twin siblings are similar to non-twin siblings. These two observations suggest that genetic factors play an important part in determination of islet cell autoimmunity, thus rejecting the hypothesis. In addition, there is a high penetrance of islet cell autoimmunity in DQ8/DQ2 monozygotic twin siblings." + }, + "questions": [ + { + "id": "796cceb4-13ff-4c74-b664-23b81443a37c", + "text": "What are the risk factors of Type 1 diabetes mellitus?", + "answers": [ + { + "answer_start": 1825, + "text": "DQ8/DQ2 monozygotic twin siblings" + } + ] + } + ] +} \ No newline at end of file diff --git a/b23c819f-e016-4d89-b2cd-62214cdd6913.json b/b23c819f-e016-4d89-b2cd-62214cdd6913.json new file mode 100644 index 0000000000000000000000000000000000000000..09cf481bfcb6f293245860b4fc1366241fd0d3c7 --- /dev/null +++ b/b23c819f-e016-4d89-b2cd-62214cdd6913.json @@ -0,0 +1,34 @@ +{ + "id": "b23c819f-e016-4d89-b2cd-62214cdd6913", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "23584433", + "text": "AIMS/HYPOTHESIS:\nPrecise estimates of progression rates from 'prediabetes' to type 2 diabetes are needed to optimise prevention strategies for high-risk individuals. There is acceptance of prediabetes defined by impaired fasting glucose (IFG) and impaired glucose tolerance (IGT), but there is some controversy surrounding HbA1c-defined prediabetes ranges, with some favouring 6.0-6.4% (42-46 mmol/mol). Comparing progression rates between groups might aid this issue, thus we aimed to accurately estimate progression rates to diabetes from different prediabetes categories.\n\nMETHODS:\nMeta-analysis of prospective observational studies in which participants had prediabetes at baseline (ADA-defined IFG [5.6-6.9 mmol/l], WHO-defined IFG [6.1-6.9 mmol/l], IGT (7.8-11.0 mmol/l) or raised HbA1c [6.0-6.4%/42-46 mmol/mol]) and were followed up for incident diabetes. Incidence rates were combined using Bayesian random effects models.\n\nRESULTS:\nOverall, 70 studies met the inclusion criteria. In the six studies that used raised HbA1c, the pooled incidence rate (95% credible interval) of diabetes was 35.6 (15.1, 83.0) per 1,000 person-years. This rate was most similar to that for ADA-defined IFG (11 studies; 35.5 [26.6, 48.0]) and was non-significantly lower than WHO-defined IFG (34 studies; 47.4 [37.4, 59.8]), IGT (46 studies, 45.5 [37.8, 54.5]) and IFG plus IGT (15 studies, 70.4 [53.8, 89.7]). Similar results were seen when the data were analysed by the criteria used to diagnose diabetes.\n\nCONCLUSIONS/INTERPRETATION:\nThis study provides evidence that progression rates differ by prediabetes definition, which has implications for the planning and implementation of diabetes prevention programmes. HbA1c 6.0-6.4% might identify people at a lower diabetes risk than other prediabetes definitions, but further research is needed." + }, + "questions": [ + { + "id": "933ea450-3be7-45ab-9d72-72cca0be893f", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1706, + "text": "HbA1c 6.0-6.4%" + } + ] + } + ] +} \ No newline at end of file diff --git a/b2dd580e-359c-4a95-919d-8728e403c650.json b/b2dd580e-359c-4a95-919d-8728e403c650.json new file mode 100644 index 0000000000000000000000000000000000000000..63d65f562c773bf7147b9df479d26373bf0894fa --- /dev/null +++ b/b2dd580e-359c-4a95-919d-8728e403c650.json @@ -0,0 +1,34 @@ +{ + "id": "b2dd580e-359c-4a95-919d-8728e403c650", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "32774890", + "text": "BACKGROUND:\nRadiation-induced coronary artery disease (R-CAD) has become an increasingly recognized phenomenon. Although the clinical relationship between radiation therapy and CAD risk is well known, there is minimal investigation of the gender relationship to radiation-induced CAD events and the resulting cardiovascular (CV) events/mortality. We study the gender variation in the incidence of CV events/mortality related to R-CAD in Hodgkin's Lymphoma (HL) patients.\n\nMETHODS:\nThe Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines were used in this systematic review and network meta-analysis. OVID, Cochrane Central Register of Controlled Trials via the Wiley Interface, Web of Science Core Collection, MEDLINE, EMBASE, and Google Scholar were investigated to identify prospective and retrospective observational studies comparing women and men following radiation treatment for Hodgkin's lymphoma. Ten studies were included (4 prospective, 6 retrospective). The primary outcome was incidence of cardiovascular events/mortality. The secondary outcome was all-cause mortality. Meta-regression for age was also performed.\n\nRESULTS:\nOf 13,975 patients, including 41% females and 59% males, CV events/mortality were noted to be significantly higher in women compared to men (OR 3.74, 95% CI 2.44-5.72, \u003c 0.001). All-cause mortality was also higher in women compared to men (OR 1.94, 95% CI 1.10-3.44, \u003c 0.023). On meta-regression analysis, elderly populations have a higher rate of mortality, which was even higher for women than men (coefficient = 0.0458, = 0.0374).\n\nCONCLUSIONS:\nWomen have a higher rate of R-CAD related CV events/mortality and all-cause mortality compared to men amongst radiation-treated patients. These data highlight the need for increased surveillance to better monitor for R-CAD in female patients treated with mantle or mediastinal radiation." + }, + "questions": [ + { + "id": "c2cc3c63-f0a0-4c18-bd54-9bcccc2f362c", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 12, + "text": "Radiation-induced coronary artery disease (R-CAD)" + } + ] + } + ] +} \ No newline at end of file diff --git a/b3db0bf6-fa9b-446f-87f8-10397903c514.json b/b3db0bf6-fa9b-446f-87f8-10397903c514.json new file mode 100644 index 0000000000000000000000000000000000000000..2e8c03c5e2517b9dea91676551b3754dfb6dcc27 --- /dev/null +++ b/b3db0bf6-fa9b-446f-87f8-10397903c514.json @@ -0,0 +1,50 @@ +{ + "id": "b3db0bf6-fa9b-446f-87f8-10397903c514", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "16835425", + "text": "CONTEXT:\nEndogenous hormones are a primary cause of breast cancer. Adiposity affects circulating hormones, particularly in postmenopausal women, and may be a modifiable risk factor for breast cancer.\n\nOBJECTIVE:\nTo assess the associations of adult weight change since age 18 years and since menopause with the risk of breast cancer among postmenopausal women.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nProspective cohort study within the Nurses' Health Study. A total of 87,143 postmenopausal women, aged 30 to 55 years and free of cancer, were followed up for up to 26 years (1976-2002) to assess weight change since age 18 years. Weight change since menopause was assessed among 49,514 women who were followed up for up to 24 years.\n\nMAIN OUTCOME MEASURE:\nIncidence of invasive breast cancer.\n\nRESULTS:\nOverall, 4393 cases of invasive breast cancer were documented. Compared with those who maintained weight, women who gained 25.0 kg or more since age 18 years were at an increased risk of breast cancer (relative risk [RR], 1.45; 95% confidence interval [CI], 1.27-1.66; P\u003c.001 for trend), with a stronger association among women who have never taken postmenopausal hormones (RR,1.98; 95% CI, 1.55-2.53). Compared with weight maintenance, women who gained 10.0 kg or more since menopause were at an increased risk of breast cancer (RR, 1.18; 95% CI, 1.03-1.35; P = .002 for trend). Women who had never used postmenopausal hormones, lost 10.0 kg or more since menopause, and kept the weight off were at a lower risk than those who maintained weight (RR, 0.43; 95% CI, 0.21-0.86; P = .01 for weight loss trend). Overall, 15.0% (95% CI, 12.8%-17.4%) of breast cancer cases in this population may be attributable to weight gain of 2.0 kg or more since age 18 years and 4.4% (95% CI, 3.6%-5.5%) attributable to weight gain of 2.0 kg or more since menopause. Among those who did not use postmenopausal hormones, the population attributable risks are 24.2% (95% CI, 19.8%-29.1%) for a weight gain since age 18 years and 7.6% (95% CI, 5.9%-9.7%) for weight gain since menopause.\n\nCONCLUSIONS:\nThese data suggest that weight gain during adult life, specifically since menopause, increases the risk of breast cancer among postmenopausal women, whereas weight loss after menopause is associated with a decreased risk of breast cancer. Thus, in addition to other known benefits of healthy weight, our results provide another reason for women approaching menopause to maintain or lose weight, as appropriate." + }, + "questions": [ + { + "id": "aa5b7202-af38-4ca8-bed5-a1e7e3ad2561", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 905, + "text": "women who gained 25.0 kg or more since age 18 years" + }, + { + "answer_start": 1121, + "text": "women who have never taken postmenopausal hormones" + }, + { + "answer_start": 1236, + "text": "women who gained 10.0 kg or more since menopause" + }, + { + "answer_start": 1709, + "text": "weight gain of 2.0 kg or more since age 18 years" + }, + { + "answer_start": 2106, + "text": "weight gain during adult life" + } + ] + } + ] +} \ No newline at end of file diff --git a/b40e3d37-7188-4805-b253-2c6dc32a4c87.json b/b40e3d37-7188-4805-b253-2c6dc32a4c87.json new file mode 100644 index 0000000000000000000000000000000000000000..2817fe8794a67bd0f6ab9e85da26a289393945ea --- /dev/null +++ b/b40e3d37-7188-4805-b253-2c6dc32a4c87.json @@ -0,0 +1,37 @@ +{ + "id": "b40e3d37-7188-4805-b253-2c6dc32a4c87", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "26584600", + "text": "BACKGROUND \u0026 AIMS:\nThe risk of colorectal neoplasms among siblings of patients with advanced adenomas is not clear. We determined the prevalence of advanced adenomas in the siblings of patients with advanced adenomas and compared it with that of siblings of individuals without these lesions.\n\nMETHODS:\nIn a blinded, cross-sectional study, colonoscopies were performed (from 2010 through 2014), at 2 hospitals in Hong Kong on 200 asymptomatic siblings of patients with advanced adenomas (exposed; mean age, 58.2 ± 6.3 years; adenomas ≥10 mm, high-grade dysplasia, villous, or tubulovillous) and 400 age- and sex-matched siblings of subjects with normal findings from colonoscopies and no family history of colorectal cancer (unexposed; mean age, 58.1 ± 6 years). We recruited 1 sibling per family. The primary outcome was prevalence of advanced adenomas.\n\nRESULTS:\nBaseline demographics (ie, aspirin use, smoking, body mass index, and metabolic diseases) did not differ significantly between exposed and unexposed individuals. The prevalence of advanced adenoma was 11.5% among the exposed subjects and 2.5% among the unexposed subjects (matched odds ratio [mOR] = 6.05; 95% confidence interval [CI]: 2.74-13.36; P \u003c .001). The prevalence of adenomas ≥10 mm was higher among exposed than unexposed siblings (10.5% vs 1.8%; mOR = 8.59; 95% CI: 3.44-21.45; P \u003c .001), as was the prevalence of villous adenomas (5.5% vs 1.3% in unexposed; mOR = 6.28; 95% CI: 2.02-19.53; P = .001) and all colorectal adenomas (39.0% vs 19.0% in unexposed; mOR = 3.29; 95% CI: 2.16-5.03; P \u003c .001). Two cancers were detected in exposed siblings and none in unexposed siblings.\n\nCONCLUSIONS:\nIn a cross-sectional study of subjects undergoing colonoscopy in Hong Kong, siblings of individuals with at least 1 advanced adenoma had a 6-fold increased odds of advanced adenoma compared with subjects who had a sibling with a screening colonoscopy with no identified neoplasia. ClinicalTrials.gov, Number: NCT01593098." + }, + "questions": [ + { + "id": "7876ad55-06bb-4405-8827-80a2257dbcbb", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1746, + "text": "siblings of individuals with at least 1 advanced adenoma" + } + ] + } + ] +} \ No newline at end of file diff --git a/b43e15c2-17c4-43e2-8328-90a59b266fed.json b/b43e15c2-17c4-43e2-8328-90a59b266fed.json new file mode 100644 index 0000000000000000000000000000000000000000..c2c9b4830d4e0853c752c0bb79648e1121c97b07 --- /dev/null +++ b/b43e15c2-17c4-43e2-8328-90a59b266fed.json @@ -0,0 +1,43 @@ +{ + "id": "b43e15c2-17c4-43e2-8328-90a59b266fed", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "19696122", + "text": "BACKGROUND:\nEpidemiologic studies have identified an increased risk of asthma with acetaminophen use, but the results have been conflicting. We sought to quantify the association between acetaminophen use and the risk of asthma in children and adults.\n\nMETHODS:\nWe searched all the major medical databases, including MEDLINE (from 1966 to 2008) and EMBASE (from 1980 to 2008) to identify pertinent articles. All clinical trials and observational studies were considered. For observational studies, we selected those that clearly defined acetaminophen use and asthma diagnosis. Study quality was assessed by two reviewers, and data were extracted into a spreadsheet. A random-effects model was used to combine studies with asthma and wheezing among both children and adults.\n\nRESULTS:\nThirteen cross-sectional studies, four cohort studies, and two case-control studies comprising 425,140 subjects were included in the review. The pooled odds ratio (OR) for asthma among subjects using acetaminophen was 1.63 (95% CI, 1.46 to 1.77). The risk of asthma in children among users of acetaminophen in the year prior to asthma diagnosis and within the first year of life was elevated (OR: 1.60 [95% CI, 1.48 to 1.74] and 1.47 [95% CI, 1.36 to 1.56], respectively). Only one study reported the association between high acetaminophen dose and asthma in children (OR, 3.23; 95% CI, 2.9 to 3.6). There was an increase in the risk of asthma and wheezing with prenatal use of acetaminophen (OR: 1.28 [95% CI, 1.16 to 41] and 1.50 [95% CI, 1.10 to 2.05], respectively).\n\nCONCLUSIONS:\nThe results of our review are consistent with an increase in the risk of asthma and wheezing in both children and adults exposed to acetaminophen. Future studies are needed to confirm these results." + }, + "questions": [ + { + "id": "1d7411cf-59bb-469c-931c-f4f186f529b1", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1670, + "text": "children and adults exposed to acetaminophen" + }, + { + "answer_start": 969, + "text": "subjects using acetaminophen" + }, + { + "answer_start": 1446, + "text": "prenatal use of acetaminophen" + } + ] + } + ] +} \ No newline at end of file diff --git a/b519be53-0042-4b09-8a8e-8001fcf8c95a.json b/b519be53-0042-4b09-8a8e-8001fcf8c95a.json new file mode 100644 index 0000000000000000000000000000000000000000..5f3910bf51249f1284187832126777ece6284044 --- /dev/null +++ b/b519be53-0042-4b09-8a8e-8001fcf8c95a.json @@ -0,0 +1,34 @@ +{ + "id": "b519be53-0042-4b09-8a8e-8001fcf8c95a", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "8427325", + "text": "OBJECTIVES:\nNoninsulin-dependent diabetes mellitus, a major risk factor for cardiovascular disease, is prevalent in more than 12 million Americans. A voluminous amount of data demonstrates that cigarette smoking is an important cause of cancer and coronary heart disease. However, the association between cigarette smoking and the risk of diabetes is virtually unexplored, especially in women.\n\nMETHODS:\nWe examined the association between smoking and the incidence of noninsulin-dependent diabetes mellitus among 114,247 female nurses who were free of diabetes, cardiovascular disease, and cancer in 1976. We collected exposure information and disease status prospectively for 12 years from biennially self-administered questionnaires.\n\nRESULTS:\nCurrent smokers had an increased risk of diabetes, and we observed a significant dose-response trend for higher risk among heavier smokers. During 1,277,589 person-years of follow-up, 2333 women were clinically diagnosed with diabetes. The relative risk of diabetes, adjusted for obesity and other risk factors, was 1.42 among women who smoked 25 or more cigarettes per day compared with nonsmokers.\n\nCONCLUSIONS:\nThese data suggest that cigarette smoking may be an independent, modifiable risk factor for noninsulin-dependent diabetes mellitus." + }, + "questions": [ + { + "id": "c057e460-4374-4b21-bd09-cf28a7ec477d", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 747, + "text": "Current smokers" + } + ] + } + ] +} \ No newline at end of file diff --git a/b53ed75a-e17c-4a31-a4b1-ac58c603039f.json b/b53ed75a-e17c-4a31-a4b1-ac58c603039f.json new file mode 100644 index 0000000000000000000000000000000000000000..4571cd64fd4194b986fe9cb065f9fbf94cf60946 --- /dev/null +++ b/b53ed75a-e17c-4a31-a4b1-ac58c603039f.json @@ -0,0 +1,38 @@ +{ + "id": "b53ed75a-e17c-4a31-a4b1-ac58c603039f", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "16207847", + "text": "BACKGROUND:\nThe normal fasting plasma glucose level was recently defined as less than 100 mg per deciliter (5.55 mmol per liter). Whether higher fasting plasma glucose levels within this range independently predict type 2 diabetes in young adults is unclear.\n\nMETHODS:\nWe obtained blood measurements, data from physical examinations, and medical and lifestyle information from men in the Israel Defense Forces who were 26 to 45 years of age.\n\nRESULTS:\nA total of 208 incident cases of type 2 diabetes occurred during 74,309 person-years of follow-up (from 1992 through 2004) among 13,163 subjects who had baseline fasting plasma glucose levels of less than 100 mg per deciliter. A multivariate model, adjusted for age, family history of diabetes, body-mass index, physical-activity level, smoking status, and serum triglyceride levels, revealed a progressively increased risk of type 2 diabetes in men with fasting plasma glucose levels of 87 mg per deciliter (4.83 mmol per liter) or more, as compared with those whose levels were in the bottom quintile (less than 81 mg per deciliter [4.5 mmol per liter], P for trend \u003c0.001). In multivariate models, men with serum triglyceride levels of 150 mg per deciliter (1.69 mmol per liter) or more, combined with fasting plasma glucose levels of 91 to 99 mg per deciliter (5.05 to 5.50 mmol per liter), had a hazard ratio of 8.23 (95 percent confidence interval, 3.6 to 19.0) for diabetes, as compared with men with a combined triglyceride level of less than 150 mg per deciliter and fasting glucose levels of less than 86 mg per deciliter (4.77 mmol per liter). The joint effect of a body-mass index (the weight in kilograms divided by the square of the height in meters) of 30 or more and a fasting plasma glucose level of 91 to 99 mg per deciliter resulted in a hazard ratio of 8.29 (95 percent confidence interval, 3.8 to 17.8), as compared with a body-mass index of less than 25 and a fasting plasma glucose level of less than 86 mg per deciliter.\n\nCONCLUSIONS:\nHigher fasting plasma glucose levels within the normoglycemic range constitute an independent risk factor for type 2 diabetes among young men, and such levels may help, along with body-mass index and triglyceride levels, to identify apparently healthy men at increased risk for diabetes." + }, + "questions": [ + { + "id": "6dab95cc-45c5-4cbf-80ef-85d58bb74cfa", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 2011, + "text": "Higher fasting plasma glucose levels within the normoglycemic range" + }, + { + "answer_start": 898, + "text": "men with fasting plasma glucose levels of 87 mg per deciliter (4.83 mmol per liter) or more" + } + ] + } + ] +} \ No newline at end of file diff --git a/b5dcaccc-e114-4538-b596-68ec7958b97b.json b/b5dcaccc-e114-4538-b596-68ec7958b97b.json new file mode 100644 index 0000000000000000000000000000000000000000..ecc88af1c99b8fe3215e8d476fe6b73d79b991a0 --- /dev/null +++ b/b5dcaccc-e114-4538-b596-68ec7958b97b.json @@ -0,0 +1,47 @@ +{ + "id": "b5dcaccc-e114-4538-b596-68ec7958b97b", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "12922955", + "text": "OBJECTIVE:\nTo quantify the influence of cigarette smoking on the risk of developing rheumatoid arthritis (RA).\n\nMETHODS:\n679 cases and 847 controls included during May 1996-June 2000 in a case-control study, using incident cases, comprising the population aged 18-70 years of a defined area of Sweden, were investigated. A case was defined as a person from the study base who received for the first time a diagnosis of RA using the 1987 American College of Rheumatology criteria, and controls were randomly selected from the study base. Self reported smoking habits among cases and controls, and rheumatoid factor status among cases were registered. The incidence of RA in current smokers, ex-smokers, and ever-smokers, respectively, was compared with that of never-smokers.\n\nRESULTS:\nCurrent smokers, ex-smokers, and ever-smokers of both sexes had an increased risk for seropositive RA (for ever-smokers the odds ratio was 1.7 (95% confidence interval (95% CI) 1.2 to 2.3) for women, and 1.9 (95% CI 1.0 to 3.5) for men), but not for seronegative RA. The increased risk was only apparent among subjects who had smoked \u003e or =20 years, was evident at an intensity of smoking of 6-9 cigarettes/day, and remained for up to 10-19 years after smoking cessation. The risk increased with increasing cumulative dose of smoking.\n\nCONCLUSION:\nSmokers of both sexes have an increased risk of developing seropositive, but not seronegative, RA. The increased risk occurs after a long duration, but merely a moderate intensity, of smoking and may remain for several years after smoking cessation." + }, + "questions": [ + { + "id": "daf1c2b6-0575-41f6-b5d5-cb9f6d8b3eba", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 1333, + "text": "Smokers of both sexes" + }, + { + "answer_start": 785, + "text": "Current smokers" + }, + { + "answer_start": 802, + "text": "ex-smokers" + }, + { + "answer_start": 818, + "text": "ever-smokers" + } + ] + } + ] +} \ No newline at end of file diff --git a/b5fcd3b5-fe6b-4d0c-9dc5-6b163ce1d8f4.json b/b5fcd3b5-fe6b-4d0c-9dc5-6b163ce1d8f4.json new file mode 100644 index 0000000000000000000000000000000000000000..e08a6de4d90a27077973c17c830f419c9de507d6 --- /dev/null +++ b/b5fcd3b5-fe6b-4d0c-9dc5-6b163ce1d8f4.json @@ -0,0 +1,41 @@ +{ + "id": "b5fcd3b5-fe6b-4d0c-9dc5-6b163ce1d8f4", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "11161410", + "text": "A sedentary lifestyle, obesity, and a Westernized diet have been implicated in the aetiology of both colorectal cancer and non-insulin dependent diabetes mellitus, leading to the hypothesis that hyperinsulinaemia may promote colorectal cancer. We prospectively examined the association between colorectal cancer risk and factors related to insulin resistance and hyperinsulinaemia, including BMI, physical activity, diabetes mellitus, and blood glucose, in a cohort of 75 219 Norwegian men and women. Information on incident cases of colorectal cancer was made available from the Norwegian Cancer Registry. Reported P values are two-sided. During 12 years of follow up, 730 cases of colorectal cancer were registered. In men, but not in women, we found a negative association with leisure-time physical activity (P for trend = 0.002), with an age-adjusted RR for the highest versus the lowest category of activity of 0.54 (95% CI = 0.37-0.79). Women, but not men, with a history of diabetes were at increased risk of colorectal cancer (age-adjusted RR = 1.55; 95% CI = 1.04-2.31), as were women with non-fasting blood glucose \u003e or = 8.0 mmol l(-1)(age-adjusted RR = 1.98; 95% CI = 1.31-2.98) compared with glucose \u003c8.0 mmol l(-1). Overall, we found no association between BMI and risk of colorectal cancer. Additional adjustment including each of the main variables, marital status, and educational attainment did not materially change the results. We conclude that the inverse association between leisure-time physical activity and colorectal cancer in men, and the positive association between diabetes, blood glucose, and colorectal cancer in women, at least in part, support the hypothesis that insulin may act as a tumour promoter in colorectal carcinogenesis." + }, + "questions": [ + { + "id": "22bc4998-927d-4f93-b319-fc167759de6a", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 944, + "text": "Women, but not men, with a history of diabetes" + }, + { + "answer_start": 1089, + "text": "women with non-fasting blood glucose \u003e or = 8.0 mmol l(-1)" + } + ] + } + ] +} \ No newline at end of file diff --git a/b6057078-4b39-4392-845e-dce6d52aed17.json b/b6057078-4b39-4392-845e-dce6d52aed17.json new file mode 100644 index 0000000000000000000000000000000000000000..2cf3e7b88e63a892781d3d638dff4f0ab21bae78 --- /dev/null +++ b/b6057078-4b39-4392-845e-dce6d52aed17.json @@ -0,0 +1,38 @@ +{ + "id": "b6057078-4b39-4392-845e-dce6d52aed17", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "30316996", + "text": "Celiac disease is a small intestinal inflammatory disease with autoimmune features that is triggered and maintained by the ingestion of the storage proteins (gluten) of wheat, barley and rye. The prevalence of celiac disease is increased in patients with monoglandular and/or polyglandular autoimmunity and their relatives. Between 10 and 30% of patients with celiac disease are thyroid and/or type 1 diabetes antibody positive, while around 5 to 7% of patients with autoimmune thyroid disease and/or type 1 diabetes are IgA anti-tissue transglutaminase antibody positive. The close relationship between celiac disease and endocrine autoimmunity is largely explained by sharing a common genetic background. The HLA antigens DQ2 (DQA1*0501-DQB1*0201) and/or DQ8 (DQA1*0301-DQB1*0302), that are tightly linked to DR3 and DR4, respectively, are the major common genetic predisposition. Moreover, functional single nucleotide polymorphisms of various genes that are involved in immune regulation have been identified as \"overlap\" susceptibility genes for both celiac disease and monoglandular or polyglandular autoimmunity. While plausible, it remains to be established how far a gluten free diet may prevent or ameliorate glandular autoimmunity. In conclusion, all patients with celiac disease should be screened for type 1 diabetes and/or autoimmune thyroid disease. Conversely, patients with the above autoimmune endocrine disorders should be also screened for celiac disease." + }, + "questions": [ + { + "id": "7199c1bf-80c1-4f10-9bdb-a78cb42ead54", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 241, + "text": "patients with monoglandular and/or polyglandular autoimmunity and their relatives" + }, + { + "answer_start": 707, + "text": "The HLA antigens DQ2 (DQA1*0501-DQB1*0201) and/or DQ8 (DQA1*0301-DQB1*0302), that are tightly linked to DR3 and DR4" + } + ] + } + ] +} \ No newline at end of file diff --git a/b653d3a2-594d-4f6a-92bd-a3c7892c7d29.json b/b653d3a2-594d-4f6a-92bd-a3c7892c7d29.json new file mode 100644 index 0000000000000000000000000000000000000000..519c6c405f67c66b2b168ffeea413131db03537f --- /dev/null +++ b/b653d3a2-594d-4f6a-92bd-a3c7892c7d29.json @@ -0,0 +1,38 @@ +{ + "id": "b653d3a2-594d-4f6a-92bd-a3c7892c7d29", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "17565158", + "text": "BACKGROUND:\nRegion II of Chile (the second most northerly administrative region) experienced dramatic increases in average arsenic water concentrations beginning in 1958, followed by marked declines in the 1970s when water treatment plants were installed. This history provides a unique opportunity to study time trends in the development of arsenic-related cancers, including lung and bladder cancers.\n\nMETHODS:\nWe investigated lung and bladder cancer mortality from 1950 to 2000 for region II compared with region V, where drinking water was not contaminated with arsenic. Mortality data were obtained from 218,174 death certificates for the two regions for 1950-1970 and from mortality data tapes that identified 307,541 deaths in the two regions for 1971-2000. Poisson regression models were used to identify time trends in rate ratios (RRs) of mortality from lung and bladder cancers comparing region II with region V.\n\nRESULTS:\nLung and bladder cancer mortality rate ratios for region II compared with region V started to increase about 10 years after high arsenic exposures commenced and continued to rise until peaking in 1986-1997. The peak lung cancer mortality RRs were 3.61 (95% confidence interval [CI] = 3.13 to 4.16) for men and 3.26 (95% CI = 2.50 to 4.23) for women. The peak bladder cancer RRs were 6.10 (95% CI = 3.97 to 9.39) for men and 13.8 (95% CI = 7.74 to 24.5) for women. Combined lung and bladder cancer mortality rates in region II were highest in the period 1992-1994, with mortality rates of 153 and 50 per 100,000 men and women, respectively, in region II compared with 54 and 19 per 100,000 in region V.\n\nCONCLUSIONS:\nSuch large increases in total population cancer mortality rates have, to our knowledge, not been documented for any other environmental exposure. The long latency pattern is noteworthy, with mortality from lung and bladder cancers continuing to be high until the late 1990s, even though major decreases in arsenic exposure occurred more than 25 years earlier." + }, + "questions": [ + { + "id": "3eb2208d-1571-4803-ba7f-98d8e6fc36ab", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 123, + "text": "arsenic water concentrations" + }, + { + "answer_start": 1058, + "text": "high arsenic exposures" + } + ] + } + ] +} \ No newline at end of file diff --git a/b6a1294b-3c86-4f26-82c7-cb4481fb7b40.json b/b6a1294b-3c86-4f26-82c7-cb4481fb7b40.json new file mode 100644 index 0000000000000000000000000000000000000000..5c33451e2641e1128619de9fbc3e08ca1261c62b --- /dev/null +++ b/b6a1294b-3c86-4f26-82c7-cb4481fb7b40.json @@ -0,0 +1,55 @@ +{ + "id": "b6a1294b-3c86-4f26-82c7-cb4481fb7b40", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "27286779", + "text": "To summarize the principal findings on risk and protective factors for childhood asthma, we retrieved systematic reviews on these topics in children (aged 1 to 18 years), up to January 2016, through MEDLINE, EMBASE, CINAHL, SCOPUS, and CDSR. A total of 227 studies were searched from databases. Among those, 41 systematic reviews (SRs) were included: 9 focused on prenatal factors, 5 on perinatal factors, and 27 on postnatal factors. Of these 41 SRs, 83% had good methodological quality, as determined by the Assess Systematic Reviews tool. After reviewing all evidence, parental asthma, prenatal environmental tobacco smoke, and prematurity (particularly very preterm birth) are well-established risk factors for childhood asthma. Current findings do suggest mild-to-moderate causal effects of certain modifiable behaviors or exposures during pregnancy (maternal weight gain or obesity, maternal use of antibiotics or paracetamol, and maternal stress), the perinatal period (birth by Caesarean delivery), or postnatal life (severe respiratory syncytial virus infection, overweight or obesity, indoor exposure to mold or fungi, and outdoor air pollution) on childhood asthma, but this suggestive evidence must be confirmed in interventional studies or (if interventions are not feasible) well-designed prospective studies." + }, + "questions": [ + { + "id": "22054a76-d69c-45e4-8293-bd1b4bbd1273", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 572, + "text": "parental asthma" + }, + { + "answer_start": 589, + "text": "prenatal environmental tobacco smoke" + }, + { + "answer_start": 631, + "text": "prematurity (particularly very preterm birth)" + }, + { + "answer_start": 804, + "text": "modifiable behaviors or exposures during pregnancy (maternal weight gain or obesity, maternal use of antibiotics or paracetamol, and maternal stress)" + }, + { + "answer_start": 959, + "text": "perinatal period (birth by Caesarean delivery)" + }, + { + "answer_start": 1010, + "text": "postnatal life (severe respiratory syncytial virus infection, overweight or obesity, indoor exposure to mold or fungi, and outdoor air pollution)" + } + ] + } + ] +} \ No newline at end of file diff --git a/b6e9cc96-8121-4674-8bf4-7e048deaca84.json b/b6e9cc96-8121-4674-8bf4-7e048deaca84.json new file mode 100644 index 0000000000000000000000000000000000000000..043db942abfe7f35c019c40c3e0225f9634cee4c --- /dev/null +++ b/b6e9cc96-8121-4674-8bf4-7e048deaca84.json @@ -0,0 +1,39 @@ +{ + "id": "b6e9cc96-8121-4674-8bf4-7e048deaca84", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "20732985", + "text": "RATIONALE:\nhormonal and metabolic status appears to influence lung health in women, and there are findings suggesting that early menarche may be related to asthma, cardiovascular disease, diabetes, and breast cancer.\n\nOBJECTIVES:\nthis study investigates whether age at menarche is related to adult lung function and asthma.\n\nMETHODS:\namong participants in the European Community Respiratory Health Survey II, 3,354 women aged 27-57 years from random population samples in 21 centers responded to a questionnaire concerning women's health (1998-2002). Of these women, 2,873 had lung function measurements, 2,136 had measurements of bronchial hyperreactivity, and 2,743 had IgE measurements. Logistic, linear, and negative binomial regression analyses included adjustment for age, height, body mass index, education, smoking, family size, and center.\n\nMEASUREMENTS AND MAIN RESULTS:\nFEV(1) and FVC were lower and asthma was more common in women with early menarche. Women reporting menarche at age 10 years or less, as compared with women with menarche at age 13 years (reference category), had lower FEV(1) (adjusted difference, -113 ml; 95% confidence interval [CI], -196 to -33 ml) and FVC (-126 ml; 95% CI, -223 to -28 ml); also lower FEV(1) expressed as a percentage of the predicted value (-3.28%; 95% CI, -6.25 to -0.30%) and FVC expressed as a percentage of the predicted value (-3.63%; 95% CI, -6.64 to -0.62%). Women with early menarche more often had asthma symptoms (odds ratio, 1.80; 95% CI, 1.09-2.97), asthma with bronchial hyperreactivity (odds ratio, 2.79; 95% CI, 1.06-7.34), and higher asthma symptom score (mean ratio, 1.58; 95% CI, 1.12-2.21).\n\nCONCLUSIONS:\nwomen with early menarche had lower lung function and more asthma in adulthood. This supports a role for metabolic and hormonal factors in women's respiratory health." + }, + "questions": [ + { + "id": "4c58788f-7a64-423a-b8f9-fe084bcb9611", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1677, + "text": "women with early menarche" + }, + { + "answer_start": 1419, + "text": "Women with early menarche" + } + ] + } + ] +} \ No newline at end of file diff --git a/b757ec85-c6e2-458d-85f6-d0eba0c699c6.json b/b757ec85-c6e2-458d-85f6-d0eba0c699c6.json new file mode 100644 index 0000000000000000000000000000000000000000..15e6fb26fbe342980e2cdc3b4161d13b2c1db5ee --- /dev/null +++ b/b757ec85-c6e2-458d-85f6-d0eba0c699c6.json @@ -0,0 +1,34 @@ +{ + "id": "b757ec85-c6e2-458d-85f6-d0eba0c699c6", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "23727170", + "text": "Since the first description of the association between chronic kidney disease and heart disease, many epidemiological studies have confirmed and extended this finding. As chronic kidney disease progresses, kidney-specific risk factors for cardiovascular events and disease come into play. As a result, the risk for cardiovascular disease is notably increased in individuals with chronic kidney disease. When adjusted for traditional cardiovascular risk factors, impaired kidney function and raised concentrations of albumin in urine increase the risk of cardiovascular disease by two to four times. Yet, cardiovascular disease is frequently underdiagnosed and undertreated in patients with chronic kidney disease. This group of patients should, therefore, be acknowledged as having high cardiovascular risk that needs particular medical attention at an individual level. This view should be incorporated in the development of guidelines and when defining research priorities. Here, we discuss the epidemiology and pathophysiological mechanisms of cardiovascular risk in patients with chronic kidney disease, and discuss methods of prevention." + }, + "questions": [ + { + "id": "79713a0b-e88a-4da3-96c4-de71c5d5a34c", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 362, + "text": "individuals with chronic kidney disease" + } + ] + } + ] +} \ No newline at end of file diff --git a/b80db73e-4461-4e78-bd57-477879c9edb5.json b/b80db73e-4461-4e78-bd57-477879c9edb5.json new file mode 100644 index 0000000000000000000000000000000000000000..a00b52d635d001f7bc7c671febdd9e20a90b98c5 --- /dev/null +++ b/b80db73e-4461-4e78-bd57-477879c9edb5.json @@ -0,0 +1,54 @@ +{ + "id": "b80db73e-4461-4e78-bd57-477879c9edb5", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "26149669", + "text": "CONTEXT:\nTobacco smoke includes a mix of carcinogens implicated in the etiology of bladder cancer (BC) and renal cell cancer (RCC).\n\nOBJECTIVE:\nWe reviewed the impact of tobacco exposure on BCC and RCC incidence and mortality, and whether smoking cessation decreases the risk.\n\nEVIDENCE ACQUISITION:\nA systematic review of original articles in English was performed in August 2013. Meta-analysis of risks was performed using adjusted risk ratios where available. Publication bias was assessed using Begg and Egger tests.\n\nEVIDENCE SYNTHESIS:\nWe identified 2683 papers, of which 107 fulfilled our inclusion criteria, of which 83 studies investigated BC and 24 investigated RCC. The pooled relative risk (RR) of BC incidence was 2.58 (95% confidence interval [CI] 2.37-2.80) for all smokers, 3.47 (3.07-3.91) for current smokers, and 2.04 (1.85-2.25) for former smokers. The corresponding pooled RR of BC disease-specific mortality (DSM) was 1.47 (1.24-1.75), 1.53 (1.12-2.09) and 1.44 (0.99-2.11). The pooled RR of RCC incidence was 1.31 (1.22-1.40) for all smokers, 1.36 (1.19-1.56) for current smokers, and 1.16 (1.08-1.25) for former smokers. The corresponding RCC DSM risk was 1.23 (1.08-1.40), 1.37 (1.19-1.59), and 1.02 (0.90-1.15).\n\nCONCLUSIONS:\nWe present an up-to-date review of tobacco smoking and BC and RCC incidence and mortality. Tobacco smoking significantly increases the risk of BC and RCC incidence. BC incidence and DSM risk are greatest in current smokers and lowest in former smokers, indicating that smoking cessation confers benefit. We found that secondhand smoke exposure is associated with a significant increase in BC risk.\n\nPATIENT SUMMARY:\nTobacco smoking affects the development and progression of bladder cancer and renal cell cancer. Smoking cessation reduces the risks of developing and dying from these common cancers. We quantify these risks using the most up-to-date results published in the literature." + }, + "questions": [ + { + "id": "ea09db0a-f06e-4544-9a01-b9c6b2aa1f2a", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 777, + "text": "all smokers" + }, + { + "answer_start": 811, + "text": "current smokers" + }, + { + "answer_start": 853, + "text": "former smokers" + }, + { + "answer_start": 1343, + "text": "Tobacco smoking" + }, + { + "answer_start": 1459, + "text": "current smokers" + }, + { + "answer_start": 1668, + "text": "Tobacco smoking" + } + ] + } + ] +} \ No newline at end of file diff --git a/b8af41b2-ac21-479c-a3d8-b487e1c690fb.json b/b8af41b2-ac21-479c-a3d8-b487e1c690fb.json new file mode 100644 index 0000000000000000000000000000000000000000..c23370db3a6a1633a4aa1d54fe9afb22022ef39d --- /dev/null +++ b/b8af41b2-ac21-479c-a3d8-b487e1c690fb.json @@ -0,0 +1,51 @@ +{ + "id": "b8af41b2-ac21-479c-a3d8-b487e1c690fb", + "disease": { + "id": "H00056", + "names": [ + "Alzheimer disease", + "Dementia due to Alzheimer disease" + ], + "dbLinks": { + "icd10": [ + "G30" + ], + "mesh": [ + "D000544" + ] + }, + "category": "Neurodegenerative disease" + }, + "article": { + "id": "24358824", + "text": "BACKGROUND:\nOver 20 genetic risk factors have been confirmed to associate with elevated risk for Alzheimer's disease (AD), but the identification of environmental and/or acquired risk factors has been more elusive. At present, recognized acquired risks for AD include traumatic brain injury, hypercholesterolemia, obesity, hypertension, and type 2 diabetes.\n\nMETHODS:\nBased on reports associating various inhalants with AD pathology, we investigated the possibility that air pollution might contribute to AD risk by exposing wild-type mice to a standard air pollution modeling system employing nickel nanoparticle-enriched atmosphere for 3 hr.\n\nRESULTS:\nMice exposed to air pollution showed 72-129% increases in brain levels of both amyloid-β peptides Aβ40 and Aβ42, as well as Aβ42/40 (p \u003c0.01).\n\nCONCLUSIONS:\nThese effects on elevation of brain Aβ exceed those associated with trisomy 21, a known risk for early onset AD pathology, raising the possibility that clinical importance might be attached. Further work is required to establish the molecular and physiological basis for these phenomena. The rapid, dramatic effect, if verified, would suggest that inhalant exposures should be evaluated for their possible roles in contributing to the environmental risk for common forms of AD." + }, + "questions": [ + { + "id": "87db1b66-8c8e-438a-8454-1d9892e1bdc1", + "text": "What are the risk factors of Alzheimer disease?", + "answers": [ + { + "answer_start": 268, + "text": "traumatic brain injury" + }, + { + "answer_start": 292, + "text": "hypercholesterolemia" + }, + { + "answer_start": 314, + "text": "obesity" + }, + { + "answer_start": 323, + "text": "hypertension" + }, + { + "answer_start": 341, + "text": "type 2 diabetes" + } + ] + } + ] +} \ No newline at end of file diff --git a/b8e20bd3-aa14-48e6-969d-4f0eee9cd483.json b/b8e20bd3-aa14-48e6-969d-4f0eee9cd483.json new file mode 100644 index 0000000000000000000000000000000000000000..d6681c19a80f796729c830c31f17679302b0c924 --- /dev/null +++ b/b8e20bd3-aa14-48e6-969d-4f0eee9cd483.json @@ -0,0 +1,34 @@ +{ + "id": "b8e20bd3-aa14-48e6-969d-4f0eee9cd483", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "15699277", + "text": "BACKGROUND:\nLipoprotein-associated phospholipase A2 (Lp-PLA2) has been proposed as an inflammatory marker of cardiovascular disease. In the present study, we investigated whether Lp-PLA2 is an independent predictor of coronary heart disease and ischemic stroke.\n\nMETHODS AND RESULTS:\nThe Rotterdam Study is a population-based follow-up study in 7983 subjects \u003e or =55 years of age. We performed a case-cohort study, including 308 coronary heart disease cases, 110 ischemic stroke cases, and a random sample of 1820 subjects. We used Cox proportional-hazard models with modification of the standard errors based on robust variance estimates to compute hazard ratios adjusted for age, sex, body mass index, systolic blood pressure, non-HDL cholesterol, HDL cholesterol, diabetes, smoking, alcohol consumption, cholesterol-lowering medication, white blood cell count, and C-reactive protein. Compared with the first quartile of Lp-PLA2 activity, multivariate-adjusted hazard ratios for coronary heart disease for the second, third, and fourth quartiles were 1.39 (95% CI, 0.92 to 2.10), 1.99 (95% CI, 1.32 to 3.00), and 1.97 (95% CI, 1.28 to 3.02), respectively (P for trend=0.01). Corresponding multivariate-adjusted hazard ratios for ischemic stroke were 1.08 (95% CI, 0.55 to 2.11), 1.58 (95% CI, 0.82 to 3.04), and 1.97 (95% CI, 1.03 to 3.79) (P for trend=0.03). The relation between Lp-PLA2 and coronary heart disease was present in both subjects with non-HDL cholesterol levels below the median and those with non-HDL cholesterol levels above the median.\n\nCONCLUSIONS:\nThis study shows that Lp-PLA2 activity is an independent predictor of coronary heart disease and ischemic stroke in the general population." + }, + "questions": [ + { + "id": "7d0950da-8e75-4744-84f1-db0ab2a48c42", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1594, + "text": "Lp-PLA2 activity" + } + ] + } + ] +} \ No newline at end of file diff --git a/bb135c5e-501a-4333-a517-9ccc9c468c59.json b/bb135c5e-501a-4333-a517-9ccc9c468c59.json new file mode 100644 index 0000000000000000000000000000000000000000..41f0b2c3f7a292bbecd9eb213b09a7918d646c86 --- /dev/null +++ b/bb135c5e-501a-4333-a517-9ccc9c468c59.json @@ -0,0 +1,54 @@ +{ + "id": "bb135c5e-501a-4333-a517-9ccc9c468c59", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "28031315", + "text": "BACKGROUND:\nThe 2014 US Surgeon General's report noted research gaps necessary to determine a causal relationship between active cigarette smoking and invasive breast cancer risk, including the role of alcohol consumption, timing of exposure, modification by menopausal status and heterogeneity by oestrogen receptor (ER) status.\n\nMETHODS:\nTo address these issues, we pooled data from 14 cohort studies contributing 934 681 participants (36 060 invasive breast cancer cases). Cox proportional hazard regression models were used to calculate multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs).\n\nRESULTS:\nSmoking duration before first birth was positively associated with risk ( P -value for trend = 2 × 10 -7 ) with the highest HR for initiation \u003e10 years before first birth (HR = 1.18, CI 1.12-1.24). Effect modification by current alcohol consumption was evident for the association with smoking duration before first birth ( P -value=2×10 -4 ); compared with never-smoking non-drinkers, initiation \u003e10 years before first birth was associated with risk in every category of alcohol intake, including non-drinkers (HR = 1.15, CI 1.04-1.28) and those who consumed at least three drinks per day (1.85, 1.55-2.21). Associations with smoking before first birth were limited to risk of ER+ breast cancer ( P -value for homogeneity=3×10 -3 ). Other smoking timing and duration characteristics were associated with risk even after controlling for alcohol, but were not associated with risk in non-drinkers. Effect modification by menopause was not evident.\n\nCONCLUSIONS:\nSmoking, particularly if initiated before first birth, was modestly associated with ER+ breast cancer risk that was not confounded by amount of adult alcohol intake. Possible links with breast cancer provide additional motivation for young women to not initiate smoking." + }, + "questions": [ + { + "id": "8b72814e-a7d1-4213-82e8-4557970ae92e", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 630, + "text": "Smoking duration before first birth" + }, + { + "answer_start": 761, + "text": "initiation \u003e10 years before first birth" + }, + { + "answer_start": 916, + "text": "smoking duration before first birth " + }, + { + "answer_start": 1016, + "text": "initiation \u003e10 years before first birth was associated with risk in every category of alcohol intake" + }, + { + "answer_start": 1364, + "text": "Other smoking timing and duration characteristics" + }, + { + "answer_start": 1591, + "text": "Smoking, particularly if initiated before first birth" + } + ] + } + ] +} \ No newline at end of file diff --git a/bb1d88bc-879f-4612-a196-8bd928ae9a87.json b/bb1d88bc-879f-4612-a196-8bd928ae9a87.json new file mode 100644 index 0000000000000000000000000000000000000000..d5ae63ac4587e151b351499b8da7ecd8da4fb965 --- /dev/null +++ b/bb1d88bc-879f-4612-a196-8bd928ae9a87.json @@ -0,0 +1,53 @@ +{ + "id": "bb1d88bc-879f-4612-a196-8bd928ae9a87", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "24150925", + "text": "BACKGROUND:\nGuidelines recommend that individuals with a first-degree relative (FDR) diagnosed with colorectal cancer (CRC) or advanced adenoma before age 60 years should undergo colonoscopy starting at age 40 years. The authors quantified the risk of adenomas and CRC in FDRs, second-degree relatives (SDRs), and third-degree relatives (TDRs) of patients diagnosed with adenomas and advanced adenomas.\n\nMETHODS:\nA population-based, retrospective, case-control study was performed of residents of the state of Utah aged 50 years to 80 years who underwent colonoscopy between 1995 and 2009 at Intermountain Healthcare or the University of Utah. Controls were selected from the population of colonoscopy patients who were free of adenomas or CRC and matched to each case based on sex and birth year. Colonoscopy results were linked with cancer and pedigree information from the Utah Population Database to investigate the familial aggregation of adenomas and CRC using Cox regression analysis. The unit of analysis was the relatives of cases and controls.\n\nRESULTS:\nOf 126,936 patients who underwent colonoscopy, 43,189 had adenomas and 5563 had advanced adenomas and defined the case population. An elevated risk of CRC was found in FDRs (relative risk [RR], 1.35; 95% confidence interval [95% CI], 1.25-1.46), SDRs (RR, 1.15; 95% CI, 1.07-1.23) of adenoma cases, and in FDRs of advanced adenoma cases (RR, 1.68; 95% CI, 1.29-2.18) compared with controls. Approximately 10% of CRCs diagnosed in relatives would have been missed if the current screening guidelines were strictly adhered to.\n\nCONCLUSIONS:\nRelatives of colonoscopy patients with adenomas and advanced adenomas appear to have a significantly elevated risk of developing colorectal neoplasia. These data should be considered when establishing CRC screening guidelines for individuals and their families." + }, + "questions": [ + { + "id": "f55ccc20-6680-47f5-8f4f-774455b71da0", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1232, + "text": "FDRs" + }, + { + "answer_start": 57, + "text": "first-degree relative (FDR)" + }, + { + "answer_start": 1310, + "text": "SDRs" + }, + { + "answer_start": 278, + "text": "second-degree relatives (SDRs)" + }, + { + "answer_start": 1603, + "text": "Relatives of colonoscopy patients with adenomas and advanced adenomas" + } + ] + } + ] +} \ No newline at end of file diff --git a/bb27a7be-e470-4b63-92ee-68dad3abf754.json b/bb27a7be-e470-4b63-92ee-68dad3abf754.json new file mode 100644 index 0000000000000000000000000000000000000000..a61f61094fbd69c0180a1e251323877c21d81c34 --- /dev/null +++ b/bb27a7be-e470-4b63-92ee-68dad3abf754.json @@ -0,0 +1,61 @@ +{ + "id": "bb27a7be-e470-4b63-92ee-68dad3abf754", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "20798970", + "text": "Patients with longstanding extensive colitis, both ulcerative colitis and Crohn's colitis, have an increased risk of developing colorectal cancer. Because of this risk, colonoscopic surveillance for neoplasia is recommended by most authorities. Although there has been no randomised controlled trial to demonstrate surveillance effectiveness, there are several retrospective comparative studies, which suggest that surveillance reduces colorectal cancer mortality. Over the past decade there have been a number of developments in our understanding of colitis cancer. We have discovered that the severity of colorectal inflammation is an important risk factor, in addition to other known risk factors such as the extent and duration of colitis, primary sclerosing cholangitis and a family history of colorectal cancer. Endoscopic techniques have also improved and evidence now demonstrates that pancolonic chromoendoscopy yields significantly more intraepithelial neoplasia than random biopsies. Endoscopic resection of well-circumscribed lesions is now also recognised as being an appropriate strategy, potentially reducing the number of patients requiring colectomy. It is hoped that such developments will further improve the effectiveness of colitis surveillance." + }, + "questions": [ + { + "id": "10b19e10-bd0a-487e-ac7f-6d2713e33977", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 0, + "text": "Patients with longstanding extensive colitis" + }, + { + "answer_start": 51, + "text": "ulcerative colitis" + }, + { + "answer_start": 74, + "text": "Crohn's colitis" + }, + { + "answer_start": 591, + "text": "the severity of colorectal inflammation" + }, + { + "answer_start": 708, + "text": "the extent and duration of colitis" + }, + { + "answer_start": 781, + "text": "family history of colorectal cancer" + }, + { + "answer_start": 744, + "text": "primary sclerosing cholangitis" + } + ] + } + ] +} \ No newline at end of file diff --git a/bb31015f-bdee-4162-b8d8-dfcde5066f73.json b/bb31015f-bdee-4162-b8d8-dfcde5066f73.json new file mode 100644 index 0000000000000000000000000000000000000000..98ff696e61980ede039f2fa80f5dc53af03e7859 --- /dev/null +++ b/bb31015f-bdee-4162-b8d8-dfcde5066f73.json @@ -0,0 +1,37 @@ +{ + "id": "bb31015f-bdee-4162-b8d8-dfcde5066f73", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "21307158", + "text": "BACKGROUND:\nThe International Agency for Research on Cancer (IARC) concluded that alcohol consumption is related to colorectal cancer (CRC). However, several issues remain unresolved, including quantification of the association for light (≤1 drink/day) and moderate (2-3 drinks/day) alcohol drinking, investigation of the dose-response relationship, and potential heterogeneity of effects by sex, colorectal site, and geographical region.\n\nMETHODS:\nTwenty-seven cohort and 34 case-control studies presenting results for at least three categories of alcohol intake were identified from a PubMed search of articles published before May 2010. The summary relative risks (RRs) were estimated by the random effects model. Second-order fractional polynomials and random effects meta-regression models were used for modeling the dose-risk relation.\n\nRESULTS:\nThe RRs were 1.21 [95% confidence interval (CI) 1.13-1.28] for moderate and 1.52 (95% CI 1.27-1.81) for heavy (≥4 drinks/day) alcohol drinking. The RR for moderate drinkers, compared with non-/occasional drinkers, was stronger for men (RR = 1.24, 95% CI 1.13-1.37) than for women (RR = 1.08, 95% CI 1.03-1.13; P(heterogeneity) = 0.02). For heavy drinkers, the association was stronger in Asian studies (RR = 1.81, 95% CI 1.33-2.46; P(heterogeneity) = 0.04). The dose-risk analysis estimated RRs of 1.07 (95% CI 1.04-1.10), 1.38 (95% CI 1.28-1.50), and 1.82 (95% CI 1.41-2.35) for 10, 50, and 100 g/day of alcohol, respectively.\n\nCONCLUSIONS:\nThis meta-analysis provides strong evidence for an association between alcohol drinking of \u003e1 drink/day and colorectal cancer risk." + }, + "questions": [ + { + "id": "e91113b8-1c4a-4c0e-b8f1-fc6f8746ab60", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1565, + "text": "alcohol drinking of \u003e1 drink/day" + } + ] + } + ] +} \ No newline at end of file diff --git a/bb763107-36a0-4945-89ee-e9f386407141.json b/bb763107-36a0-4945-89ee-e9f386407141.json new file mode 100644 index 0000000000000000000000000000000000000000..e2314a55784a5949f14bf94ce171b53f29bbc6ed --- /dev/null +++ b/bb763107-36a0-4945-89ee-e9f386407141.json @@ -0,0 +1,50 @@ +{ + "id": "bb763107-36a0-4945-89ee-e9f386407141", + "disease": { + "id": "H00408", + "names": [ + "Type 1 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E10" + ], + "mesh": [ + "D003922" + ] + }, + "category": "Metabolic disease; Immune system disease; Endocrine disease" + }, + "article": { + "id": "29128935", + "text": "AIMS/HYPOTHESIS:\nWith genetics thought to explain only 40-50% of the total risk of type 1 diabetes, environmental risk factors in early life have been proposed. Previous findings from studies of type 1 diabetes incidence by birthweight and gestational age at birth have been inconsistent. This study aimed to investigate the relationships between birthweight, gestational age at birth and subsequent type 1 diabetes in England.\n\nMETHODS:\nData were obtained from a population-based database comprising linked mother-infant pairs using English national Hospital Episode Statistics from 1998 to 2012. In total, 3,834,405 children, categorised by birthweight and gestational age at birth, were followed up through record linkage to compare their incidence of type 1 diabetes through calculation of multivariable-adjusted HRs.\n\nRESULTS:\nOut of 3,834,405 children, 2969 had a subsequent hospital diagnosis of type 1 diabetes in childhood. Children born preterm (\u003c37 weeks) or early term (37-38 weeks) experienced significantly higher incidence of type 1 diabetes than full term children (39-40 weeks) (HR 1.19 [95% CI 1.03, 1.38] and 1.27 [95% CI 1.16, 1.39], respectively). Children born at higher than average birthweight (3500-3999 g or 4000-5499 g) after controlling for gestational age experienced higher incidence of type 1 diabetes than children born at medium birthweight (3000-3499 g) (HR 1.13 [95% CI 1.03, 1.23] and 1.16 [95% CI 1.02, 1.31], respectively), while children at low birthweight (\u003c2500 g) experienced lower incidence (0.81 [95% CI 0.67, 0.98]), signifying a statistically significant trend (p trend 0.001).\n\nCONCLUSIONS/INTERPRETATION:\nHigh birthweight for gestational age and low gestational age at birth are both independently associated with subsequent type 1 diabetes. These findings help contextualise the debate about the potential role of gestational and early life environmental risk factors in the pathogenesis of type 1 diabetes, including the potential roles of insulin sensitivity and gut microbiota." + }, + "questions": [ + { + "id": "07265a88-1d97-4a93-bffa-28c9475e7ad1", + "text": "What are the risk factors of Type 1 diabetes mellitus?", + "answers": [ + { + "answer_start": 933, + "text": "Children born preterm (\u003c37 weeks)" + }, + { + "answer_start": 970, + "text": "early term (37-38 weeks)" + }, + { + "answer_start": 1169, + "text": "Children born at higher than average birthweight (3500-3999 g or 4000-5499 g)" + }, + { + "answer_start": 1653, + "text": "High birthweight for gestational age" + }, + { + "answer_start": 1694, + "text": "low gestational age at birth" + } + ] + } + ] +} \ No newline at end of file diff --git a/bbb049ee-d7e8-447c-9116-e3e65639db46.json b/bbb049ee-d7e8-447c-9116-e3e65639db46.json new file mode 100644 index 0000000000000000000000000000000000000000..65c4409e02988a7a16cd35060410b72e652bad43 --- /dev/null +++ b/bbb049ee-d7e8-447c-9116-e3e65639db46.json @@ -0,0 +1,55 @@ +{ + "id": "bbb049ee-d7e8-447c-9116-e3e65639db46", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "2400347", + "text": "Uveal melanoma threatens life, as well as sight. To evaluate the effect of constitutional factors and UV radiation on the risk of uveal melanoma, 197 cases in New England were compared with 385 matched population controls, identified by random-digit dialing, and 337 cases residing within the United States were compared with 800 sibling controls. In the population-based comparison, estimated relative risks (RRs) of uveal melanoma, after adjustment for other factors, were elevated for the following: ancestry from more northern latitudes with a substantially elevated risk for Northern European ancestry (RR, 6.5; 95% confidence interval [CI], 1.9 to 22.4) and more than a twofold risk for British ancestry (RR, 2.4; 95% CI, 1.1 to 5.1), as compared with Southern European or other Mediterranean heritage; light skin color as compared with dark (RR, 3.8; 95% CI, 1.1 to 12.6); and 10 or more cutaneous nevi as compared with none (RR, 2.7; 95% CI, 1.5 to 4.9). There was a statistically significant trend for increasing risk with more northern heritage and more moles. Southern residence (below latitude 40 degrees N) for more than 5 years also increased risk (RR, 2.8; 95% CI, 1.1 to 6.9), as compared with none. In both comparisons, use of sunlamps was a risk determinant (RR, 3.4; 95% CI, 1.1 to 10.3 with random-digit dialed controls and RR, 2.3; 95% CI, 1.2 to 4.3 with sibling controls, comparing occasional or frequent use to never use), as was intense sun exposure (RR, 1.7; 95% CI, 0.9 to 3.0 and RR, 2.1; 95% CI, 1.4 to 3.2, respectively). However, birthplace below latitude 40 degrees N and outdoor work were associated with a lower risk.(ABSTRACT TRUNCATED AT 250 WORDS)" + }, + "questions": [ + { + "id": "5b9ac463-a811-4a17-b71e-83ff79ac0519", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 503, + "text": "ancestry from more northern latitudes" + }, + { + "answer_start": 580, + "text": "Northern European ancestry" + }, + { + "answer_start": 693, + "text": "British ancestry" + }, + { + "answer_start": 809, + "text": "light skin color as compared with dark" + }, + { + "answer_start": 884, + "text": "10 or more cutaneous nevi as compared with none" + }, + { + "answer_start": 1032, + "text": "more northern heritage and more moles" + } + ] + } + ] +} \ No newline at end of file diff --git a/bc144440-556a-40ff-9af0-d95aa297973b.json b/bc144440-556a-40ff-9af0-d95aa297973b.json new file mode 100644 index 0000000000000000000000000000000000000000..4fe9ab534a8ba524436c05a5a12e0afe092c5777 --- /dev/null +++ b/bc144440-556a-40ff-9af0-d95aa297973b.json @@ -0,0 +1,34 @@ +{ + "id": "bc144440-556a-40ff-9af0-d95aa297973b", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "23090881", + "text": "Associations of breast cancer overall with indicators of exposures during puberty are reasonably well characterized; however, uncertainty remains regarding the associations of height, leg length, sitting height and menarcheal age with hormone receptor-defined malignancies. Within the European Prospective Investigation into Cancer and Nutrition cohort, Cox proportional hazards models were used to describe the relationships of adult height, leg length and sitting height and age at menarche with risk of estrogen and progesterone receptor negative (ER-PR-) (n = 990) and ER+PR+ (n = 3,524) breast tumors. Height as a single risk factor was compared to a model combining leg length and sitting height. The possible interactions of height, leg length and sitting height with menarche were also analyzed. Risk of both ER-PR- and ER+PR+ malignancies was positively associated with standing height, leg length and sitting height and inversely associated with increasing age at menarche. For ER+PR+ disease, sitting height (hazard ratios: 1.14[95% confidence interval: 1.08-1.20]) had a stronger risk association than leg length (1.05[1.00-1.11]). In comparison, for ER-PR- disease, no distinct differences were observed between leg length and sitting height. Women who were tall and had an early menarche (≤13 years) showed an almost twofold increase in risk of ER+PR+ tumors but no such increase in risk was observed for ER-PR- disease. Indicators of exposures during rapid growth periods were associated with risks of both HR-defined breast cancers. Exposures during childhood promoting faster development may establish risk associations for both HR-positive and -negative malignancies. The stronger associations of the components of height with ER+PR+ tumors among older women suggest possible hormonal links that could be specific for postmenopausal women." + }, + "questions": [ + { + "id": "8b9d2908-9a85-4837-b36f-48de87c5e99f", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1256, + "text": "Women who were tall and had an early menarche (≤13 years)" + } + ] + } + ] +} \ No newline at end of file diff --git a/bdd20b80-09c7-4956-9856-ae031d018c3c.json b/bdd20b80-09c7-4956-9856-ae031d018c3c.json new file mode 100644 index 0000000000000000000000000000000000000000..d268bae89d1a7e834258debfeb403d8ea7afbe45 --- /dev/null +++ b/bdd20b80-09c7-4956-9856-ae031d018c3c.json @@ -0,0 +1,42 @@ +{ + "id": "bdd20b80-09c7-4956-9856-ae031d018c3c", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "14712349", + "text": "AIMS/HYPOTHESIS:\nRecently, a clear biological link between iron metabolism and diabetes has emerged from epidemiological and experimental studies. We carried out a prospective study of dietary iron intake and incidence of Type 2 diabetes.\n\nMETHODS:\n35,698 postmenopausal women initially aged 55 to 69 years were followed for 11 years. Diet was assessed with a food frequency questionnaire at baseline.\n\nRESULTS:\nIntake of heme iron showed a positive association with incident Type 2 diabetes; the relative risks were 1.0, 1.07, 1.12, 1.14, and 1.28 across quintiles of heme iron (p trend =0.02) after adjustment for non-dietary and dietary risk factors. Heme iron showed a weak positive association among non-drinkers, but the association appeared to be stronger among subjects who consumed more alcohol. For example, in a model restricted to those who drank alcohol at least 15 g/day, adjusted relative risks across quintiles of heme iron were 1.0, 2.26, 3.22, 1.92, and 4.42 (p trend =0.05); and consumers of 30 g/day of more of supplemental iron had an adjusted relative risk equal to 3.03 (95% CI, 1.29-7.12)], compared to those who took no iron supplement. Non-heme iron was inversely associated with incidence of Type 2 diabetes. Amongst non-drinkers adjusted relative risks were 1.0, 0.83, 0.87, 0.72, and 0.67 across quintiles (p trend \u003c0.01). This inverse association was lost among drinkers, in whom there was no association of diabetes incidence with non-heme iron.\n\nCONCLUSIONS/INTERPRETATION:\nGreater dietary heme-iron intake and/or supplemental iron were associated with an increased risk of Type 2 diabetes, especially amongst those who drink alcohol." + }, + "questions": [ + { + "id": "dfde8e61-1890-4d63-a234-ceee72f7c2ad", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 412, + "text": "Intake of heme iron" + }, + { + "answer_start": 1506, + "text": "Greater dietary heme-iron intake and/or supplemental iron" + }, + { + "answer_start": 998, + "text": "consumers of 30 g/day of more of supplemental iron" + } + ] + } + ] +} \ No newline at end of file diff --git a/bdd22e5b-7f72-44a9-975c-7ae3a9c5a229.json b/bdd22e5b-7f72-44a9-975c-7ae3a9c5a229.json new file mode 100644 index 0000000000000000000000000000000000000000..ca4d22d095d7fdf286f9373e3477bc45d793e94f --- /dev/null +++ b/bdd22e5b-7f72-44a9-975c-7ae3a9c5a229.json @@ -0,0 +1,42 @@ +{ + "id": "bdd22e5b-7f72-44a9-975c-7ae3a9c5a229", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "32404325", + "text": "OBJECTIVE:\nTo estimate and compare progression rates to type 2 diabetes mellitus (T2DM) in women with gestational diabetes mellitus (GDM) and healthy controls.\n\nDESIGN:\nSystematic review and meta-analysis.\n\nDATA SOURCES:\nMedline and Embase between January 2000 and December 2019, studies published in English and conducted on humans.\n\nELIGIBILITY CRITERIA FOR SELECTING STUDIES:\nObservational studies investigating progression to T2DM. Inclusion criteria were postpartum follow-up for at least 12 months, incident physician based diagnosis of diabetes, T2DM reported as a separate outcome rather than combined with impaired fasting glucose or impaired glucose tolerance, and studies with both a group of patients with GDM and a control group.\n\nRESULTS:\nThis meta-analysis of 20 studies assessed a total of 1 332 373 individuals (67 956 women with GDM and 1 264 417 controls). Data were pooled by random effects meta-analysis models, and heterogeneity was assessed by use of the I statistic. The pooled relative risk for the incidence of T2DM between participants with GDM and controls was estimated. Reasons for heterogeneity between studies were investigated by prespecified subgroup and meta-regression analyses. Publication bias was assessed by funnel plots and, overall, studies were deemed to have a low risk of bias (P=0.58 and P=0.90). The overall relative risk for T2DM was almost 10 times higher in women with previous GDM than in healthy controls (9.51, 95% confidence interval 7.14 to 12.67, P\u003c0.001). In populations of women with previous GDM, the cumulative incidence of T2DM was 16.46% (95% confidence interval 16.16% to 16.77%) in women of mixed ethnicity, 15.58% (13.30% to 17.86%) in a predominantly non-white population, and 9.91% (9.39% to 10.42%) in a white population. These differences were not statistically significant between subgroups (white mixed populations, P=0.26; white non-white populations, P=0.54). Meta-regression analyses showed that the study effect size was not significantly associated with mean study age, body mass index, publication year, and length of follow-up.\n\nCONCLUSIONS:\nWomen with a history of GDM appear to have a nearly 10-fold higher risk of developing T2DM than those with a normoglycaemic pregnancy. The magnitude of this risk highlights the importance of intervening to prevent the onset of T2DM, particularly in the early years after pregnancy.\n\nSYSTEMATIC REVIEW REGISTRATION:\nPROSPERO CRD42019123079." + }, + "questions": [ + { + "id": "d3664a81-71d3-495b-b0ea-aa7456ec3878", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1407, + "text": " women with previous GDM" + }, + { + "answer_start": 1531, + "text": "women with previous GDM" + }, + { + "answer_start": 2120, + "text": "Women with a history of GDM" + } + ] + } + ] +} \ No newline at end of file diff --git a/bdfa5111-57a0-4b02-a465-b833d0f93188.json b/bdfa5111-57a0-4b02-a465-b833d0f93188.json new file mode 100644 index 0000000000000000000000000000000000000000..69229dc10466a3a280c7492a5b6211ed3d16b546 --- /dev/null +++ b/bdfa5111-57a0-4b02-a465-b833d0f93188.json @@ -0,0 +1,38 @@ +{ + "id": "bdfa5111-57a0-4b02-a465-b833d0f93188", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "23620537", + "text": "BACKGROUND:\nHyperuricemia is known to be a risk factor for incident type 2 diabetes mellitus, but the absolute magnitude of the association is not known. We aimed to evaluate the strength of association between hyperuricemia and the risk of developing diabetes among the US veterans with gout.\n\nMETHODS:\nPatients (age ≥ 18 years) with ≥2 clinical encounters with gout diagnoses, no history of inflammatory diseases or diabetes and two serum urate (sUA) measurements between 1 January 2002 and 1 January 2011 were selected. Diabetes was identified using International Classification of Disease-9-Clinical Modification codes, use of anti-diabetic medications or HbA1c ≥6.5%. sUA levels were assessed at 6-month cycles (hyperuricemia: sUA \u003e7 mg/dl). Accumulated hazard curves for time to first diabetes diagnosis were derived from Kaplan-Meier (KM) analysis. Risk of diabetes associated with hyperuricemia was estimated using a Cox proportional hazards model. Population attributable fraction (AF) of new-onset diabetes within 1 year was estimated using logistic regression.\n\nRESULTS:\nAmong 1923 patients, average age was 62.9 years, body mass index was 30.6 kg/m(2), and follow-up time was 80 months. Diabetes rates from KM were 19% for sUA ≤ 7 mg/dl, 23% for 7 mg/dl \u003c sUA ≤ 9 mg/dl and 27% for sUA \u003e 9 mg/dl at the end of follow-up period (P \u003c 0.001). Hyperuricemia was associated with a significantly higher risk of developing diabetes, after adjusting for confounding factors (hazard ratio: 1.19, 95% confidence interval: [1.01-1.41]). Approximately, 8.7% of all new cases of diabetes were statistically attributed to hyperuricemia.\n\nCONCLUSIONS:\nAmong veterans, hyperuricemia was associated with excess risk for developing diabetes. Approximately, 1 in 11 new cases of diabetes were statistically attributed to hyperuricemia." + }, + "questions": [ + { + "id": "76315cf7-64da-4e6c-afd0-59f3b6bd039a", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1352, + "text": "Hyperuricemia" + }, + { + "answer_start": 1665, + "text": "hyperuricemia" + } + ] + } + ] +} \ No newline at end of file diff --git a/be7189bd-69d6-4913-965c-7212ee50f13d.json b/be7189bd-69d6-4913-965c-7212ee50f13d.json new file mode 100644 index 0000000000000000000000000000000000000000..05583e75ab3978ee00ccffeec4d9829eb98a83df --- /dev/null +++ b/be7189bd-69d6-4913-965c-7212ee50f13d.json @@ -0,0 +1,43 @@ +{ + "id": "be7189bd-69d6-4913-965c-7212ee50f13d", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "17548411", + "text": "BACKGROUND:\nRheumatoid factor (RF) and autoantibodies against cyclic citrullinated peptide (CCP) are markers that might help physicians diagnose rheumatoid arthritis.\n\nPURPOSE:\nTo determine whether anti-CCP antibody more accurately identifies patients with rheumatoid arthritis and better predicts radiographic progression than does RF.\n\nDATA SOURCES:\nMEDLINE through September 2006 and reference lists of retrieved studies and review articles.\n\nSTUDY SELECTION:\nStudies in any language that enrolled at least 10 participants and that examined the role of anti-CCP antibody and RF in the diagnosis or prognosis of known or suspected rheumatoid arthritis.\n\nDATA EXTRACTION:\nTwo authors independently evaluated studies for inclusion, rated methodological quality, and abstracted relevant data.\n\nDATA SYNTHESIS:\nThe DerSimonian-Laird random-effects method was used to summarize sensitivities, specificities, and positive and negative likelihood ratios from 37 studies of anti-CCP antibody and 50 studies of RF. The pooled sensitivity, specificity, and positive and negative likelihood ratios for anti-CCP antibody were 67% (95% CI, 62% to 72%), 95% (CI, 94% to 97%), 12.46 (CI, 9.72 to 15.98), and 0.36 (CI, 0.31 to 0.42), respectively. For IgM RF, the values were 69% (CI, 65% to 73%), 85% (CI, 82% to 88%), 4.86 (CI, 3.95 to 5.97), and 0.38 (CI, 0.33 to 0.44). Likelihood ratios among IgM RF, IgG RF, and IgA RF seemed to be similar. Results from studies of patients with early rheumatoid arthritis were similar to those from all studies. Three of 4 studies found that risk for radiographic progression was greater with anti-CCP antibody positivity than with IgM RF positivity.\n\nLIMITATIONS:\nMany studies had methodological limitations. Studies of RF were heterogeneous and had wide ranges of sensitivity and specificity.\n\nCONCLUSIONS:\nAnti-CCP antibodies are more specific than RF for diagnosing rheumatoid arthritis and may better predict erosivedisease." + }, + "questions": [ + { + "id": "05eec9f3-6a9c-4006-af54-5121b91f8f30", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 1835, + "text": "Anti-CCP" + }, + { + "answer_start": 1619, + "text": "anti-CCP antibody positivity" + }, + { + "answer_start": 1093, + "text": "anti-CCP antibody" + } + ] + } + ] +} \ No newline at end of file diff --git a/bed5d786-2138-4964-be5d-1e0740d91213.json b/bed5d786-2138-4964-be5d-1e0740d91213.json new file mode 100644 index 0000000000000000000000000000000000000000..506cd0e80e23803b4a8191e37cce85b842e2e4db --- /dev/null +++ b/bed5d786-2138-4964-be5d-1e0740d91213.json @@ -0,0 +1,34 @@ +{ + "id": "bed5d786-2138-4964-be5d-1e0740d91213", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "18458146", + "text": "OBJECTIVE:\nWe assessed the lifetime risk of cardiovascular disease (CVD) among individuals with and without obesity and diabetes.\n\nRESEARCH DESIGN AND METHODS:\nParticipants were drawn from the original and offspring cohorts of the Framingham Heart Study. Lifetime (30-year) risk of CVD was assessed using a modified Kaplan-Meier approach adjusting for the competing risk of death, beginning from age 50 years.\n\nRESULTS:\nOver 30 years, the lifetime risk of CVD among women with diabetes was 54.8% among normal-weight women and 78.8% among obese women. Among normal-weight men with diabetes, the lifetime risk of CVD was 78.6%, whereas it was 86.9% among obese men.\n\nCONCLUSIONS:\nThe lifetime risk of CVD among individuals with diabetes is high, and this relationship is further accentuated with increasing adiposity." + }, + "questions": [ + { + "id": "993da506-a44b-4506-a598-b340949dc17c", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 709, + "text": "individuals with diabetes" + } + ] + } + ] +} \ No newline at end of file diff --git a/bedf5d70-ac5e-4d4e-8958-ef857ef4cd70.json b/bedf5d70-ac5e-4d4e-8958-ef857ef4cd70.json new file mode 100644 index 0000000000000000000000000000000000000000..a53b220ef84e2769ccf475fab375a333903eef27 --- /dev/null +++ b/bedf5d70-ac5e-4d4e-8958-ef857ef4cd70.json @@ -0,0 +1,34 @@ +{ + "id": "bedf5d70-ac5e-4d4e-8958-ef857ef4cd70", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "17513405", + "text": "The role of intakes of different sugars in the development of type 2 diabetes was studied in a cohort of 4,304 men and women aged 40-60 y and initially free of diabetes at baseline in 1967-1972. Food consumption data were collected using a dietary history interview covering the habitual diet during the previous year. The intakes of different sugars were calculated and divided in quartiles. During a 12-y follow-up, 177 incidents of type 2 diabetes cases were identified from a nationwide register. Combined intake of fructose and glucose was associated with the risk of type 2 diabetes but no significant association was observed for intakes of sucrose, lactose, or maltose. The relative risk between the highest and lowest quartiles of combined fructose and glucose intake was 1.87 (95% [CI] = 1.19, 2.93; P = 0.003). The corresponding relative risks between the extreme quartiles of consumption of food items contributing to sugar intakes were 1.69 (95% [CI] = 1.17, 2.43; P \u003c 0.001) for sweetened berry juice and 1.67 (95% [CI] = 0.98, 2.87; P = 0.01) for soft drinks. Our findings support the view that higher intake of fructose and glucose and sweetened beverages may increase type 2 diabetes risk." + }, + "questions": [ + { + "id": "f527e79d-50c3-4cbb-a0bb-4032b89ca64b", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1110, + "text": "higher intake of fructose and glucose and sweetened beverages" + } + ] + } + ] +} \ No newline at end of file diff --git a/bf2300af-7ccf-49cb-a505-a1b727001aa7.json b/bf2300af-7ccf-49cb-a505-a1b727001aa7.json new file mode 100644 index 0000000000000000000000000000000000000000..94664b6ff8a118c663b0e7ab0723f26b36894729 --- /dev/null +++ b/bf2300af-7ccf-49cb-a505-a1b727001aa7.json @@ -0,0 +1,44 @@ +{ + "id": "bf2300af-7ccf-49cb-a505-a1b727001aa7", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "16670173", + "text": "BACKGROUND:\nBronchial hyperresponsiveness (BHR) is a common feature of asthma. However, BHR is also present in asymptomatic individuals and its clinical and prognostic significance is unclear. We hypothesised that BHR might play a role in the development of chronic obstructive pulmonary disease (COPD) as well as asthma.\n\nMETHODS:\nIn 1991 respiratory symptoms and BHR to methacholine were evaluated in 7126 of the 9651 participants in the SAPALDIA cohort study. Eleven years later 5825 of these participants were re-evaluated, of whom 4852 performed spirometric tests. COPD was defined as an FEV1/FVC ratio of \u003c0.70.\n\nRESULTS:\nIn 1991 17% of participants had BHR, of whom 51% were asymptomatic. Eleven years later the prevalence of asthma, wheeze, and shortness of breath in formerly asymptomatic subjects with or without BHR was, respectively, 5.7% v 2.0%, 8.3% v 3.4%, and 19.1% v 11.9% (all p\u003c0.001). Similar differences were observed for chronic cough (5.9% v 2.3%; p = 0.002) and COPD (37.9% v 14.3%; p\u003c0.001). BHR conferred an adjusted odds ratio (OR) of 2.9 (95% CI 1.8 to 4.5) for wheezing at follow up among asymptomatic participants. The adjusted OR for COPD was 4.5 (95% CI 3.3 to 6.0). Silent BHR was associated with a significantly accelerated decline in FEV1 by 12 (5-18), 11 (5-16), and 4 (2-8) ml/year in current smokers, former smokers and never smokers, respectively, at SAPALDIA 2.\n\nCONCLUSIONS:\nBHR is a risk factor for an accelerated decline in FEV1 and the development of asthma and COPD, irrespective of atopic status. Current smokers with BHR have a particularly high loss of FEV1." + }, + "questions": [ + { + "id": "54aae63e-7853-45ad-8d2a-0a973dcd7ebb", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 1416, + "text": "BHR" + }, + { + "answer_start": 12, + "text": "Bronchial hyperresponsiveness (BHR)" + }, + { + "answer_start": 1543, + "text": "Current smokers with BHR" + } + ] + } + ] +} \ No newline at end of file diff --git a/c00cabf7-244a-44ef-a038-b89a293e8dd2.json b/c00cabf7-244a-44ef-a038-b89a293e8dd2.json new file mode 100644 index 0000000000000000000000000000000000000000..320caf2bcd1638bd90c8d9be3614669caf659b14 --- /dev/null +++ b/c00cabf7-244a-44ef-a038-b89a293e8dd2.json @@ -0,0 +1,39 @@ +{ + "id": "c00cabf7-244a-44ef-a038-b89a293e8dd2", + "disease": { + "id": "H00056", + "names": [ + "Alzheimer disease", + "Dementia due to Alzheimer disease" + ], + "dbLinks": { + "icd10": [ + "G30" + ], + "mesh": [ + "D000544" + ] + }, + "category": "Neurodegenerative disease" + }, + "article": { + "id": "21115952", + "text": "OBJECTIVE:\nDiabetes mellitus has been associated with an increased risk of Alzheimer disease (AD), but how it exerts its effect remains controversial. Possible pathophysiologic mechanisms are glucose toxicity and a direct effect of insulin on amyloid metabolism. Most studies had short follow-up, and longer-term effects of diabetes on AD risk are unknown. We investigated whether fasting glucose and insulin levels and insulin resistance are associated with the risk of AD and whether this risk is constant over time.\n\nMETHODS:\nThe study was based on 3,139 participants of the Rotterdam Study, a population-based cohort study. All subjects were free from dementia, did not have a history of diabetes, and had fasting levels of glucose and insulin measured at baseline. Insulin resistance was estimated with the homeostasis model assessment. We investigated how fasting glucose, insulin, and insulin resistance are related to the risk of AD in 3 different strata according to time-to-event, using Cox proportional hazards models.\n\nRESULTS:\nDuring follow-up, 211 participants developed AD, 71 of them within 3 years of baseline. Levels of insulin and insulin resistance were associated with a higher risk of AD within 3 years of baseline. After 3 years, the risk was no longer increased. Glucose was not associated with a higher risk of AD. There was no interaction of APOE ε4 carriership and insulin metabolism on the risk of AD.\n\nCONCLUSIONS:\nOur findings suggest that insulin metabolism influences the clinical manifestation of AD only within 3 years." + }, + "questions": [ + { + "id": "be3d4a5c-3b36-4a6f-84b3-41f52212ae1c", + "text": "What are the risk factors of Alzheimer disease?", + "answers": [ + { + "answer_start": 1128, + "text": "Levels of insulin" + }, + { + "answer_start": 1150, + "text": "insulin resistance" + } + ] + } + ] +} \ No newline at end of file diff --git a/c02e18c5-d382-40f3-92c9-3e1fb1478916.json b/c02e18c5-d382-40f3-92c9-3e1fb1478916.json new file mode 100644 index 0000000000000000000000000000000000000000..2b4eecb47d3a029049b7df6fff2388b3ec23f683 --- /dev/null +++ b/c02e18c5-d382-40f3-92c9-3e1fb1478916.json @@ -0,0 +1,45 @@ +{ + "id": "c02e18c5-d382-40f3-92c9-3e1fb1478916", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "17895457", + "text": "CONTEXT:\nColorectal neoplasm and coronary artery disease (CAD) share similar risk factors, and their co-occurrence may be associated.\n\nOBJECTIVES:\nTo investigate the prevalence of colorectal neoplasm in patients with CAD in a cross-sectional study and to identify the predisposing factors for the association of the 2 diseases.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nPatients in Hong Kong, China, were recruited for screening colonoscopy after undergoing coronary angiography for suspected CAD during November 2004 to June 2006. Presence of CAD (n = 206) was defined as at least 50% diameter stenosis in any 1 of the major coronary arteries; otherwise, patients were considered CAD-negative (n = 208). An age- and sex-matched control group was recruited from the general population (n = 207). Patients were excluded for use of aspirin or statins, personal history of colonic disease, or colonoscopy in the past 10 years.\n\nMAIN OUTCOME MEASURES:\nThe prevalence of colorectal neoplasm in CAD-positive, CAD-negative, and general population participants was determined. Bivariate logistic regression was performed to study the association between colorectal neoplasm and CAD and to identify risk factors for the association of the 2 diseases after adjusting for age and sex.\n\nRESULTS:\nThe prevalence of colorectal neoplasm in the CAD-positive, CAD-negative, and general population groups was 34.0%, 18.8%, and 20.8% (P \u003c .001 by chi2 test), prevalence of advanced lesions was 18.4%, 8.7%, and 5.8% (P \u003c .001), and prevalence of cancer was 4.4%, 0.5%, and 1.4% (P = .02), respectively. Fifty percent of the cancers in CAD-positive participants were early stage. After adjusting for age and sex, an association still existed between colorectal neoplasm and presence of CAD (odds ratio [OR], 1.88; 95% confidence interval [CI], 1.25-2.70; P = .002) and between advanced lesions and presence of CAD (OR, 2.51; 95% CI, 1.43-4.35; P = .001). The metabolic syndrome (OR, 5.99; 95% CI, 1.43-27.94; P = .02) and history of smoking (OR, 4.74; 95% CI, 1.38-18.92; P = .02) were independent factors for the association of advanced colonic lesions and CAD.\n\nCONCLUSIONS:\nIn this study population undergoing coronary angiography, the prevalence of colorectal neoplasm was greater in patients with CAD. The association between the presence of advanced colonic lesions and CAD was stronger in persons with the metabolic syndrome and a history of smoking." + }, + "questions": [ + { + "id": "0cc0e2d3-1d3b-4eb3-bb13-986d51eff066", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 2262, + "text": "patients with CAD" + }, + { + "answer_start": 33, + "text": "coronary artery disease (CAD)" + }, + { + "answer_start": 1323, + "text": "CAD-positive" + } + ] + } + ] +} \ No newline at end of file diff --git a/c02e7646-8cb1-4d6e-8f32-670ec79d0652.json b/c02e7646-8cb1-4d6e-8f32-670ec79d0652.json new file mode 100644 index 0000000000000000000000000000000000000000..f304666d6b469b1d4c6ecf190d56a7ec0ddc50d6 --- /dev/null +++ b/c02e7646-8cb1-4d6e-8f32-670ec79d0652.json @@ -0,0 +1,35 @@ +{ + "id": "c02e7646-8cb1-4d6e-8f32-670ec79d0652", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "19196817", + "text": "Obesity is a risk factor for asthma. Adipose tissue expresses pro-inflammatory molecules including tumour necrosis factor (TNF), and levels of TNF are also related to polymorphisms in the TNF-alpha (TNFA) gene. The current authors examined the joint effect of obesity and TNFA variability on asthma in adults by combining two population-based studies. The European Community Respiratory Health Survey and the Swiss Cohort Study on Air Pollution and Lung and Heart Disease in Adults used comparable protocols, questionnaires and measures of lung function and atopy. DNA samples from 9,167 participants were genotyped for TNFA -308 and lymphotoxin-alpha (LTA) +252 gene variants. Obesity and TNFA were associated with asthma when mutually adjusting for their independent effects (odds ratio (OR) for obesity 2.4, 95% confidence interval (CI) 1.7-3.2; OR for TNFA -308 polymorphism 1.3, 95% CI 1.1-1.6). The association of obesity with asthma was stronger for subjects carrying the G/A and A/A TNFA -308 genotypes compared with the more common G/G genotype, particularly among nonatopics (OR for G/A and A/A genotypes 6.1, 95% CI 2.5-14.4; OR for G/G genotype 1.7, 95% CI 0.8-3.3). The present findings provide, for the first time, evidence for a complex pattern of interaction between obesity, a pro-inflammatory genetic factor and asthma." + }, + "questions": [ + { + "id": "ead8dbb8-7055-45eb-8efd-95db91dceb20", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 905, + "text": "association of obesity with asthma was stronger for subjects carrying the G/A and A/A TNFA -308 genotypes" + } + ] + } + ] +} \ No newline at end of file diff --git a/c0922f9e-fb9f-4091-ab64-a65366c641a2.json b/c0922f9e-fb9f-4091-ab64-a65366c641a2.json new file mode 100644 index 0000000000000000000000000000000000000000..67638358d0200138560a309b8c5fd1b1c803f5b0 --- /dev/null +++ b/c0922f9e-fb9f-4091-ab64-a65366c641a2.json @@ -0,0 +1,38 @@ +{ + "id": "c0922f9e-fb9f-4091-ab64-a65366c641a2", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "26416192", + "text": "OBJECTIVES:\nFirst-degree relatives (FDRs) of patients with celiac disease (CD) are at high risk for CD and prevalence among them varies from 1.6 to 38%. The risk of having CD among FDRs if the FDR is sister, brother, mother, father, son, or daughter of index patient with CD is not known. We conducted a meta-analysis and calculated pooled prevalence of CD among FDRs, second-degree relatives (SDRs), and specific relations with index patient.\n\nMETHODS:\nOn search of literature, 2,259 articles appeared of which 54 articles were included in this meta-analysis. Diagnosis of CD was based on standard criteria.\n\nRESULTS:\nPooled prevalence of CD was 7.5% (95% confidence interval (CI) 6.3%, 8.8%) in 10,252 FDRs and 2.3% (95% CI 1.3%, 3.8%) in 642 SDRs. Pooled prevalence of CD was highest in siblings (8.9%), followed by offsprings (7.9%) and parents (3.0%). Female FDRs had higher prevalence than male FDRs (8.4% vs. 5.2%, P=0.047). While sisters and daughters of index patient had the highest risk of having CD (1 in 7 and 1 in 8, respectively), the risk was 1 in 13 in sons, 1 in 16 in brothers, 1 in 32 in mothers, and 1 in 33 in fathers. There were also differences in the pooled prevalence of CD in FDRs according to their geographic location.\n\nCONCLUSIONS:\nPooled prevalence of CD among FDRs is 7.5% and varies considerably with their relationship with the index patient. The risk of CD in FDRs also varies according to gender and geographical location." + }, + "questions": [ + { + "id": "85f386f2-7803-416a-9334-3ec502c691b4", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 12, + "text": "First-degree relatives (FDRs) of patients with celiac disease (CD)" + }, + { + "answer_start": 857, + "text": "Female FDRs" + } + ] + } + ] +} \ No newline at end of file diff --git a/c0f91fc0-1f01-478b-a55e-0ebd86792c3c.json b/c0f91fc0-1f01-478b-a55e-0ebd86792c3c.json new file mode 100644 index 0000000000000000000000000000000000000000..b8f41db432ec59254a072ed486342c5304a224d7 --- /dev/null +++ b/c0f91fc0-1f01-478b-a55e-0ebd86792c3c.json @@ -0,0 +1,43 @@ +{ + "id": "c0f91fc0-1f01-478b-a55e-0ebd86792c3c", + "disease": { + "id": "H01633", + "names": [ + "High blood pressure", + "Hypertension" + ], + "dbLinks": { + "icd10": [ + "I10" + ], + "mesh": [ + "D006973" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "9441586", + "text": "BACKGROUND:\nObesity increases the risk for hypertension, but the effects of modest long-term weight changes have not been precisely quantified.\n\nOBJECTIVE:\nTo investigate body mass index (BMI) and weight change in relation to risk for hypertension.\n\nDESIGN:\nCohort study.\n\nSETTING:\nGeneral community.\n\nPARTICIPANTS:\nCohort of 82,473 U.S. female nurses 30 to 55 years of age followed every 2 years since 1976. The follow-up rate was 95%.\n\nMEASUREMENTS:\nPrimary risk factors examined were 1) BMI at age 18 years and midlife and 2) long-term and medium-term weight changes. The outcome was incident cases of hypertension.\n\nRESULTS:\nBy 1992, 16,395 incident cases of hypertension had been diagnosed. After adjustment for multiple covariates, BMI at 18 years of age and midlife were positively associated with occurrence of hypertension (P for trend \u003c 0.001). Long-term weight loss after 18 years of age was related to a significantly lower risk for hypertension, and weight gain dramatically increased the risk for hypertension (compared with weight change \u003c or = 2 kg, multivariate relative risks were 0.85 for a loss of 5.0 to 9.9 kg, 0.74 for a loss \u003e or = 10 kg, 1.74 for a gain of 5.0 to 9.9 kg, and 5.21 for a gain \u003e or = 25.0 kg). Among women in the top tertile of baseline BMI at age 18 years, weight loss had a greater apparent benefit. The association between weight change and risk for hypertension was stronger in younger (\u003c 45 years of age) than older women (\u003e or = 55 years of age). Medium-term weight changes after 1976 showed similar relations to risk for hypertension.\n\nCONCLUSIONS:\nExcess weight and even modest adult weight gain substantially increase risk for hypertension. Weight loss reduces the risk for hypertension." + }, + "questions": [ + { + "id": "e429105a-dc3b-4811-a937-be1c4d0640d7", + "text": "What are the risk factors for Hypertension?", + "answers": [ + { + "answer_start": 963, + "text": "weight gain" + }, + { + "answer_start": 1596, + "text": "Excess weight" + }, + { + "answer_start": 1614, + "text": "even modest adult weight gain" + } + ] + } + ] +} \ No newline at end of file diff --git a/c2ece214-c4d8-4caa-bf97-6acf6443b7cd.json b/c2ece214-c4d8-4caa-bf97-6acf6443b7cd.json new file mode 100644 index 0000000000000000000000000000000000000000..88859053d313ea1d43c3fc438eb291bc7679cafe --- /dev/null +++ b/c2ece214-c4d8-4caa-bf97-6acf6443b7cd.json @@ -0,0 +1,42 @@ +{ + "id": "c2ece214-c4d8-4caa-bf97-6acf6443b7cd", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "34341517", + "text": "BACKGROUND:\nDespite a modest association between tobacco smoking and breast cancer risk reported by recent epidemiological studies, it is still equivocal whether smoking is causally related to breast cancer risk.\n\nMETHODS:\nWe applied Mendelian randomisation (MR) to evaluate a potential causal effect of cigarette smoking on breast cancer risk. Both individual-level data as well as summary statistics for 164 single-nucleotide polymorphisms (SNPs) reported in genome-wide association studies of lifetime smoking index (LSI) or cigarette per day (CPD) were used to obtain MR effect estimates. Data from 108,420 invasive breast cancer cases and 87,681 controls were used for the LSI analysis and for the CPD analysis conducted among ever-smokers from 26,147 cancer cases and 26,072 controls. Sensitivity analyses were conducted to address pleiotropy.\n\nRESULTS:\nGenetically predicted LSI was associated with increased breast cancer risk (OR 1.18 per SD, 95% CI: 1.07-1.30, P = 0.11 × 10), but there was no evidence of association for genetically predicted CPD (OR 1.02, 95% CI: 0.78-1.19, P = 0.85). The sensitivity analyses yielded similar results and showed no strong evidence of pleiotropic effect.\n\nCONCLUSION:\nOur MR study provides supportive evidence for a potential causal association with breast cancer risk for lifetime smoking exposure but not cigarettes per day among smokers." + }, + "questions": [ + { + "id": "a6af5ed4-7ec3-4246-b401-c5338be45d3b", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 860, + "text": "Genetically predicted LSI" + }, + { + "answer_start": 496, + "text": "lifetime smoking index (LSI)" + }, + { + "answer_start": 1318, + "text": "lifetime smoking exposure" + } + ] + } + ] +} \ No newline at end of file diff --git a/c41022cd-e6ad-40bd-bd51-8b92330c0627.json b/c41022cd-e6ad-40bd-bd51-8b92330c0627.json new file mode 100644 index 0000000000000000000000000000000000000000..bc16817c3c37cec5fd860fd8d70ce6221c8d965e --- /dev/null +++ b/c41022cd-e6ad-40bd-bd51-8b92330c0627.json @@ -0,0 +1,46 @@ +{ + "id": "c41022cd-e6ad-40bd-bd51-8b92330c0627", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "21245860", + "text": "BACKGROUND:\nJoint effects of mammographic density and other risk factors on breast cancer risk remain unclear.\n\nMETHODS:\nFrom The Singapore Breast Screening Project, we selected 491 cases and 982 controls. Mammographic density was measured quantitatively. Data analysis was by conditional logistic regression.\n\nRESULTS:\nDensity was a significant risk factor, adjusting for other factors. Density of 76-100% had an odds ratio of 5.54 (95% CI 2.38-12.90) compared with 0-10%. Density had significant interactions with body mass index and oral contraceptive use (P=0.02).\n\nCONCLUSIONS:\nPercent density increases breast cancer risk in addition to effects of other risk factors, and modifies the effects of BMI and OCs." + }, + "questions": [ + { + "id": "3401084e-4e51-4ca3-aa4c-7714f1f55ce1", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 320, + "text": "Density" + }, + { + "answer_start": 388, + "text": "Density of 76-100%" + }, + { + "answer_start": 583, + "text": "Percent density" + }, + { + "answer_start": 29, + "text": "mammographic density" + } + ] + } + ] +} \ No newline at end of file diff --git a/c410ef94-bad5-40fc-a871-06cf5d2238ab.json b/c410ef94-bad5-40fc-a871-06cf5d2238ab.json new file mode 100644 index 0000000000000000000000000000000000000000..9d1796acda5aad9d2d9949ad14a15b0907a498bc --- /dev/null +++ b/c410ef94-bad5-40fc-a871-06cf5d2238ab.json @@ -0,0 +1,38 @@ +{ + "id": "c410ef94-bad5-40fc-a871-06cf5d2238ab", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "15150393", + "text": "AIMS:\nTo investigate mortality and cancer incidence of cement producing workers.\n\nMETHODS:\nA total of 2498 cement workers who have been employed at Portland cement producing departments for at least one year from 1956 to 2000 were followed up from 1 January 1978 to 31 December 2000. The cohort contributed 43,490 person-years to the study. Standardised incidence ratios (SIR) and standardised mortality ratios (SMR) were calculated as ratios between observed and expected numbers of cancers and deaths. The expected numbers were based on sex specific incidence and mortality rates for the total Lithuanian population.\n\nRESULTS:\nSignificantly increased SMRs were found for all malignant neoplasms (SMR 1.3, 95% CI 1.0 to 1.5) and for lung cancer (SMR 1.4, 95% CI 1.0 to 1.9) among male cement workers. SIR for all cancer sites was 1.2 (95% CI 1.0 to 1.4). Excess risk was found for cancer of the lung (SIR 1.5, 95% CI 1.1 to 2.1). The SIR for urinary bladder cancer was also increased (SIR 1.8, 95% CI 0.9 to 3.5). The overall cancer incidence was not increased among females (SIR 0.8, 95% CI 0.6 to 1.1). With increasing cumulated exposure to cement dust, there were indications of an increasing risk of lung and stomach cancers among males.\n\nCONCLUSIONS:\nThis study supported the hypothesis that exposure to cement dust may increase the lung and bladder cancer risk. A dose related risk was found for stomach cancer, but no support was found for an increased risk of colorectal cancer." + }, + "questions": [ + { + "id": "dc0dfbf8-b36d-473b-bc29-0b0fbccbc997", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 1298, + "text": "exposure to cement dust" + }, + { + "answer_start": 781, + "text": "male cement workers" + } + ] + } + ] +} \ No newline at end of file diff --git a/c42be20f-baa2-4064-9227-ce166f6ff33e.json b/c42be20f-baa2-4064-9227-ce166f6ff33e.json new file mode 100644 index 0000000000000000000000000000000000000000..d3d98c2239e1c001611fd4a8f466aa8203e18820 --- /dev/null +++ b/c42be20f-baa2-4064-9227-ce166f6ff33e.json @@ -0,0 +1,41 @@ +{ + "id": "c42be20f-baa2-4064-9227-ce166f6ff33e", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "20531412", + "text": "BACKGROUND:\nDiabetics have been found to have a greater risk of colorectal cancer than non-diabetics.\n\nMETHODS:\nWe examined whether this relationship differed by ethnic group, cancer site or tumour stage in a population-based prospective cohort, including 3549 incident colorectal cancer cases identified over a 13-year period (1993-2006) among 199 143 European American, African American, Native Hawaiian, Japanese American and Latino men and women in the Multiethnic Cohort.\n\nRESULTS:\nDiabetics overall had a significantly greater risk of colorectal cancer than did non-diabetics (relative risk (RR)=1.19, 95% confidence interval (CI)=1.09-1.29, P-value (P)\u003c0.001). Positive associations were observed for colon cancer, cancers of both the right and left colon, and cancers diagnosed at a localised and regional/distant stage. The association with colorectal cancer risk was significantly modified by smoking status (P(Interaction)=0.0044), with the RR being higher in never smokers (RR=1.32, 95% CI=1.15-1.53, P\u003c0.001) than past (RR=1.19, 95% CI=1.05-1.34, P=0.007) and current smokers (RR=0.90, 95% CI=0.70-1.15, P=0.40).\n\nCONCLUSION:\nThese findings provide strong support for the hypothesis that diabetes is a risk factor for colorectal cancer." + }, + "questions": [ + { + "id": "4c786f0b-7437-4a16-9cfb-27175dc0d1c1", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 487, + "text": "Diabetics" + }, + { + "answer_start": 1201, + "text": "diabetes" + } + ] + } + ] +} \ No newline at end of file diff --git a/c4b09fbb-aed0-4072-9cf4-19fab66206a4.json b/c4b09fbb-aed0-4072-9cf4-19fab66206a4.json new file mode 100644 index 0000000000000000000000000000000000000000..d50c9f7cd386b020457c0bbb139f267349165c98 --- /dev/null +++ b/c4b09fbb-aed0-4072-9cf4-19fab66206a4.json @@ -0,0 +1,47 @@ +{ + "id": "c4b09fbb-aed0-4072-9cf4-19fab66206a4", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "16495934", + "text": "We directly compared risk factors between 214 histologically confirmed melanomas (CMM), 215 basal-cell carcinomas (BCC) and 139 squamous-cell carcinomas (SCC) in a multiple case-case-control study with 349 controls from patients without dermatological disease admitted to the same hospitals. Subjects with fair hair had a significant risk increase for all types of tumours at a comparable level (OR(adj) for blonde hair: CMM 2.3; SCC 2.4; BCC 2.3). The effect of pale eyes was significant and similar for CMM and BCC (OR(adj) 2.6). Intermittent sun exposure measured in hours spent at beach during holidays was significant for both CMM (OR(adj) 2.6 for more than 7000 lifelong hours) and BCC (OR(adj) 2.1 for more than 7000 lifelong hours), while SCC exhibited a significant risk increase for chronic exposure to sunlight measured in hours of outdoor work (OR(adj) 2.2 for more than 6000 lifelong hours). In the case-case comparison using a multinomial logistic regression model, we found a statistically significant risk difference for pale eyes, and number of naevi in the CMM group, compared to other skin cancers. For intermittent sun exposure, there was a significant risk difference of BCC when compared to the risk of SCC. Factors influencing risk of SCC are different, with chronic exposure to sun playing a major role in causing this type of carcinoma." + }, + "questions": [ + { + "id": "08b05da1-beef-4515-958a-a88bb2a61af6", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 463, + "text": "pale eyes" + }, + { + "answer_start": 532, + "text": "Intermittent sun exposure measured in hours spent at beach during holidays" + }, + { + "answer_start": 1037, + "text": "pale eyes" + }, + { + "answer_start": 1052, + "text": "number of naevi" + } + ] + } + ] +} \ No newline at end of file diff --git a/c4d09189-41a7-4a56-98ad-6d4e6a884c96.json b/c4d09189-41a7-4a56-98ad-6d4e6a884c96.json new file mode 100644 index 0000000000000000000000000000000000000000..c1306fff3e06ec753992c67fdd225f6cde4b2be4 --- /dev/null +++ b/c4d09189-41a7-4a56-98ad-6d4e6a884c96.json @@ -0,0 +1,42 @@ +{ + "id": "c4d09189-41a7-4a56-98ad-6d4e6a884c96", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "22045766", + "text": "CONTEXT:\nMultiple studies have linked alcohol consumption to breast cancer risk, but the risk of lower levels of consumption has not been well quantified. In addition, the role of drinking patterns (ie, frequency of drinking and \"binge\" drinking) and consumption at different times of adult life are not well understood.\n\nOBJECTIVE:\nTo evaluate the association of breast cancer with alcohol consumption during adult life, including quantity, frequency, and age at consumption.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nProspective observational study of 105,986 women enrolled in the Nurses' Health Study followed up from 1980 until 2008 with an early adult alcohol assessment and 8 updated alcohol assessments.\n\nMAIN OUTCOME MEASURES:\nRelative risks of developing invasive breast cancer.\n\nRESULTS:\nDuring 2.4 million person-years of follow-up, 7690 cases of invasive breast cancer were diagnosed. Increasing alcohol consumption was associated with increased breast cancer risk that was statistically significant at levels as low as 5.0 to 9.9 g per day, equivalent to 3 to 6 drinks per week (relative risk, 1.15; 95% CI, 1.06-1.24; 333 cases/100,000 person-years). Binge drinking, but not frequency of drinking, was associated with breast cancer risk after controlling for cumulative alcohol intake. Alcohol intake both earlier and later in adult life was independently associated with risk.\n\nCONCLUSIONS:\nLow levels of alcohol consumption were associated with a small increase in breast cancer risk, with the most consistent measure being cumulative alcohol intake throughout adult life. Alcohol intake both earlier and later in adult life was independently associated with risk." + }, + "questions": [ + { + "id": "8d29d93d-5e59-4906-a481-20f107026559", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 892, + "text": "Increasing alcohol consumption" + }, + { + "answer_start": 1160, + "text": "Binge drinking, but not frequency of drinking" + }, + { + "answer_start": 1401, + "text": "Low levels of alcohol consumption" + } + ] + } + ] +} \ No newline at end of file diff --git a/c5039609-9760-47cf-a0b3-c3a8a2c82d3b.json b/c5039609-9760-47cf-a0b3-c3a8a2c82d3b.json new file mode 100644 index 0000000000000000000000000000000000000000..8f8028e42a07dbbead21356897754dd93ae2a632 --- /dev/null +++ b/c5039609-9760-47cf-a0b3-c3a8a2c82d3b.json @@ -0,0 +1,35 @@ +{ + "id": "c5039609-9760-47cf-a0b3-c3a8a2c82d3b", + "disease": { + "id": "H00056", + "names": [ + "Alzheimer disease", + "Dementia due to Alzheimer disease" + ], + "dbLinks": { + "icd10": [ + "G30" + ], + "mesh": [ + "D000544" + ] + }, + "category": "Neurodegenerative disease" + }, + "article": { + "id": "15341544", + "text": "OBJECTIVES:\nTo investigate whether clinical and neuropathological differences exist between Alzheimer's disease (AD) cases with and without vascular lesions neuropathologically diagnosed using Consortium to Establish a Registry for Alzheimer's Disease (CERAD) criteria.\n\nDESIGN:\nDescriptive observational study.\n\nSETTING:\nA community-based registry that identified incident dementia cases.\n\nPARTICIPANTS:\nOf the 124 subjects with available clinical and neuropathological assessments, 30 had AD lesions alone, and 18 had AD with vascular lesions. Patients with other neuropathological findings were excluded.\n\nMEASUREMENTS:\nDependent measures included demographic, clinical, and neuropathological characteristics. Neuropathological diagnoses were made using the CERAD criteria and Braak and Braak staging.\n\nRESULTS:\nOf the 124 autopsied cases, 85 cases were diagnosed with neuropathological AD. Of these, 30 had pathology consistent with \"pure\" AD, whereas 18 had AD pathology with significant vascular lesions (AD/V). There were no differences in age, sex, or education between groups. AD/V cases had higher baseline and final Mini-Mental State Examination (MMSE) scores than pure AD cases, but after adjusting for education, differences in MMSE scores were not statistically significant. The AD/V group had significantly lower Braak staging than the pure AD group, after adjusting for education and final MMSE scores.\n\nCONCLUSION:\nIn this comparison study of AD cases with and without vascular lesions, AD/V cases had less severe AD pathology than those with AD alone, indicating that cerebrovascular disease likely contributes to the severity of cognitive impairment in those with AD. Controlling for vascular risk factors in patients with AD may have a significant effect on severity of dementia." + }, + "questions": [ + { + "id": "e696d36b-f852-460f-9c22-cb09b2ea0d4c", + "text": "What are the risk factors of Alzheimer disease?", + "answers": [ + { + "answer_start": 1586, + "text": "cerebrovascular disease" + } + ] + } + ] +} \ No newline at end of file diff --git a/c5927082-3a08-4033-8aff-5ac6a42f9047.json b/c5927082-3a08-4033-8aff-5ac6a42f9047.json new file mode 100644 index 0000000000000000000000000000000000000000..d1732358b0b944cbf0bedaa640ef1aa61fd655a2 --- /dev/null +++ b/c5927082-3a08-4033-8aff-5ac6a42f9047.json @@ -0,0 +1,39 @@ +{ + "id": "c5927082-3a08-4033-8aff-5ac6a42f9047", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "34425045", + "text": "OBJECTIVE:\nTo conduct an umbrella review collating the existing evidence to determine whether there is an association between exposure of Paracetamol in-utero or in infancy and the development of childhood Asthma.\n\nMETHODS:\nIn this review, systematic reviews with or without meta-analysis that reported the association between paracetamol and asthma in children were included. To identify relevant reviews, a search was performed in the electronic databases PubMed, the Cochrane Library, and Ovid MEDLINE. The protocol was registered in PROSPERO CRD42020156023. A separate search was conducted for primary studies from the last 5 years not yet included in systematic reviews reporting the association from January 2016 to March 2021.\n\nRESULTS:\nThe electronic searches identified 1966 review titles. After the removal of 493 duplicates, 1475 titles and abstracts were screened against the eligibility criteria. Full-text screening yielded six systematic reviews to be included in this review. The search for primary studies in the last 5 years yielded 1214 hits, out of which 5 studies were found suitable for inclusion. Three of them, that were not included in the systematic reviews, and have been summarised in this paper. The odds ratios (ORs) for the outcome of asthma in offspring of mothers with prenatal paracetamol consumption in any trimester were 1.28 (1.13-1.39) and 1.21 (1.02-1.44). For first trimester exposures, they were 1.12 (0.99-1.27), 1.39 (1.01-1.91), and 1.21 (1.14-1.28), for the second or third trimester, they were 1.49 (1.37-1.63) and 1.13 (1.04-1.23). For the third trimester only, the figure was 1.17 (1.04-1.31). Of the six reviews included, 1 had a low risk of bias, 2 had an unclear risk while 3 had a high risk of bias assessed using the ROBIS tool. There was no significant increased risk of asthma with early infancy exposure. The inter-study heterogeneity varied from I = 41% to I = 76% across reviews. In the primary studies, the OR for prenatal exposure ranged from 1.12 (0.25-4.98) to 4.66 (1.92-11.3) and for infancy exposure was 1.56 (1.06-2.30). All three included primary studies were adjudged to be of high quality using the Newcastle Ottawa scale.\n\nCONCLUSIONS:\nThere is a modest association between paracetamol exposure in-utero and the future development of asthma. Exposure in infancy has a less consistant association. All the studies done thus far are observational in nature, with their inherent biases. Further research, preferably randomized controlled trials are recommended to answer this pertinent question." + }, + "questions": [ + { + "id": "72c76b09-35a3-4b3c-81f3-b02fbca1af94", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 2244, + "text": "paracetamol exposure in-utero" + }, + { + "answer_start": 1289, + "text": "mothers with prenatal paracetamol consumption in any trimester" + } + ] + } + ] +} \ No newline at end of file diff --git a/c5af10f2-36f7-40e3-9176-e9893b682577.json b/c5af10f2-36f7-40e3-9176-e9893b682577.json new file mode 100644 index 0000000000000000000000000000000000000000..0f208a75ba31758e8554030912b125eb0461c5dc --- /dev/null +++ b/c5af10f2-36f7-40e3-9176-e9893b682577.json @@ -0,0 +1,38 @@ +{ + "id": "c5af10f2-36f7-40e3-9176-e9893b682577", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "11694549", + "text": "BACKGROUND:\nCoeliac disease (CD) has been reported in several patients affected by chromosomal disorders, including Down syndrome (DS) and Turner syndrome (TS). CD has also been found in sporadic Williams syndrome (WS) patients. In this study, CD was evaluated in a consecutive series of patients with WS, in order to estimate if the prevalence of CD in WS patients is higher than in the general population.\n\nMETHODS AND RESULTS:\nA consecutive series of 63 Italian patients with WS was studied by analysing the dosage of antigliadin antibodies (AGA) IgA and antiendomisium antibodies (AEA). In patients with positive AGA and AEA, small bowel biopsy was performed. The prevalence of CD in our WS population was compared with that estimated in a published series of 17 201 Italian students. Seven WS patients were found to be positive for AGA IgA and AEA. Six of them underwent small bowel biopsy, which invariably disclosed villous atrophy consistent with CD. The prevalence of CD in the present series of WS patients was 9.5% (6/63), compared to 0.54% (1/184) in the Italian students (p\u003c0.001).\n\nCONCLUSION:\nThe present results suggest that the prevalence of CD in WS is higher than in the general population and is comparable to that reported in DS and TS. AGA and AEA screening is recommended in patients with WS." + }, + "questions": [ + { + "id": "1ec5efc5-249f-47d5-aa17-88bb6ef8df75", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 1165, + "text": "WS" + }, + { + "answer_start": 187, + "text": "sporadic Williams syndrome (WS) patients" + } + ] + } + ] +} \ No newline at end of file diff --git a/c6091e7d-d6f9-4237-b76e-3a64fefaddc9.json b/c6091e7d-d6f9-4237-b76e-3a64fefaddc9.json new file mode 100644 index 0000000000000000000000000000000000000000..3755e1cb16d3880e050413267d7d70bd86049a0a --- /dev/null +++ b/c6091e7d-d6f9-4237-b76e-3a64fefaddc9.json @@ -0,0 +1,46 @@ +{ + "id": "c6091e7d-d6f9-4237-b76e-3a64fefaddc9", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "18501419", + "text": "BACKGROUND:\nClinical use of criteria for metabolic syndrome to simultaneously predict risk of cardiovascular disease and diabetes remains uncertain. We investigated to what extent metabolic syndrome and its individual components were related to risk for these two diseases in elderly populations.\n\nMETHODS:\nWe related metabolic syndrome (defined on the basis of criteria from the Third Report of the National Cholesterol Education Program) and its five individual components to the risk of events of incident cardiovascular disease and type 2 diabetes in 4812 non-diabetic individuals aged 70-82 years from the Prospective Study of Pravastatin in the Elderly at Risk (PROSPER). We corroborated these data in a second prospective study (the British Regional Heart Study [BRHS]) of 2737 non-diabetic men aged 60-79 years.\n\nFINDINGS:\nIn PROSPER, 772 cases of incident cardiovascular disease and 287 of diabetes occurred over 3.2 years. Metabolic syndrome was not associated with increased risk of cardiovascular disease in those without baseline disease (hazard ratio 1.07 [95% CI 0.86-1.32]) but was associated with increased risk of diabetes (4.41 [3.33-5.84]) as was each of its components, particularly fasting glucose (18.4 [13.9-24.5]). Results were similar in participants with existing cardiovascular disease. In BRHS, 440 cases of incident cardiovascular disease and 105 of diabetes occurred over 7 years. Metabolic syndrome was modestly associated with incident cardiovascular disease (relative risk 1.27 [1.04-1.56]) despite strong association with diabetes (7.47 [4.90-11.46]). In both studies, body-mass index or waist circumference, triglyceride, and glucose cutoff points were not associated with risk of cardiovascular disease, but all five components were associated with risk of new-onset diabetes.\n\nINTERPRETATION:\nMetabolic syndrome and its components are associated with type 2 diabetes but have weak or no association with vascular risk in elderly populations, suggesting that attempts to define criteria that simultaneously predict risk for both cardiovascular disease and diabetes are unhelpful. Clinical focus should remain on establishing optimum risk algorithms for each disease." + }, + "questions": [ + { + "id": "7330c592-49da-4608-97a9-a775ae257ca9", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1831, + "text": "Metabolic syndrome" + }, + { + "answer_start": 1604, + "text": "body-mass index or waist circumference" + }, + { + "answer_start": 1644, + "text": "triglyceride" + }, + { + "answer_start": 1662, + "text": "glucose cutoff points" + } + ] + } + ] +} \ No newline at end of file diff --git a/c6191de5-ea98-48aa-84a4-0853b48a3024.json b/c6191de5-ea98-48aa-84a4-0853b48a3024.json new file mode 100644 index 0000000000000000000000000000000000000000..46197f1417ff072fbdc00728d188f2804c08f062 --- /dev/null +++ b/c6191de5-ea98-48aa-84a4-0853b48a3024.json @@ -0,0 +1,46 @@ +{ + "id": "c6191de5-ea98-48aa-84a4-0853b48a3024", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "11705483", + "text": "BACKGROUND:\nWomen with a family history of breast cancer are at increased risk of the disease, but no study has been large enough to characterise reliably how, over women's lives, this risk is influenced by particular familial patterns of breast cancer. This report, on the relevance of breast cancer in first-degree relatives, is based on combined data from 52 epidemiological studies.\n\nMETHODS:\nIndividual data on breast cancer in first-degree relatives (mothers, sisters, and daughters) of 58209 women with breast cancer and of 101986 controls were collected, checked, and analysed centrally. Risk ratios for breast cancer were calculated by conditional logistic regression, stratified by study, age, menopausal status, number of sisters, parity, and age when the first child was born. Breast-cancer incidence and mortality rates for particular family histories were calculated by applying age-specific risk ratios to breast-cancer rates typical for more-developed countries.\n\nFINDINGS:\nAltogether 7496 (12.9%) women with breast cancer and 7438 (7.3%) controls reported that one or more first-degree relatives had a history of breast cancer: 12% of women with breast cancer had one affected relative and 1% had two or more. Risk ratios for breast cancer increased with increasing numbers of affected first-degree relatives: compared with women who had no affected relative, the ratios were 1.80 (99% CI 1.69-1.91), 2.93 (2.36-3.64), and 3.90 (2.03-7.49), respectively, for one, two, and three or more affected first-degree relatives (p\u003c0.0001 each). The risk ratios were greatest at young ages, and for women of a given age, were greater the younger the relative was when diagnosed. The results did not differ substantially between women reporting an affected mother (9104) or sister (6386). Other factors, such as childbearing history, did not significantly alter the risk ratios associated with a family history of breast cancer. For women in more-developed countries with zero, one, or two affected first-degree relatives, the estimated cumulative incidence of breast cancer up to age 50 was 1.7%, 3.7%, and 8.0%, respectively; corresponding estimates for incidence up to age 80 were 7.8%, 13.3%, and 21.1%. Corresponding estimates for death from breast cancer up to age 80 were 2.3%, 4.2%, and 7.6%. The age when the relative was diagnosed had only a moderate effect on these estimates.\n\nINTERPRETATION:\nEight out of nine women who develop breast cancer do not have an affected mother, sister, or daughter. Although women who have first-degree relatives with a history of breast cancer are at increased risk of the disease, most will never develop breast cancer, and most who do will be aged over 50 when their cancer is diagnosed. In countries where breast cancer is common, the lifetime excess incidence of breast cancer is 5.5% for women with one affected first-degree relative and 13.3% for women with two." + }, + "questions": [ + { + "id": "cbf00546-2597-43f6-9807-e7356451c22b", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1272, + "text": "increasing numbers of affected first-degree relatives" + }, + { + "answer_start": 1476, + "text": "one, two, and three or more affected first-degree relatives" + }, + { + "answer_start": 2842, + "text": "women with one affected first-degree relative" + }, + { + "answer_start": 2902, + "text": "women with two" + } + ] + } + ] +} \ No newline at end of file diff --git a/c629d7e6-cc55-4577-a462-523059efa933.json b/c629d7e6-cc55-4577-a462-523059efa933.json new file mode 100644 index 0000000000000000000000000000000000000000..20dea3bd63c8c5b2eeaf8f76d98ed6879c48c3fb --- /dev/null +++ b/c629d7e6-cc55-4577-a462-523059efa933.json @@ -0,0 +1,41 @@ +{ + "id": "c629d7e6-cc55-4577-a462-523059efa933", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "19932107", + "text": "BACKGROUND \u0026 AIMS:\nColorectal cancer (CRC) risk estimates based on family history typically include only close relatives. We report familial relative risk (FRR) in probands with various combinations, or constellations, of affected relatives, extending to third-degree.\n\nMETHODS:\nA population-based resource that includes a computerized genealogy linked to statewide cancer records was used to identify genetic relationships among CRC cases and their first-, second-, and third-degree relatives (FDRs, SDRs, and TDRs). FRRs were estimated by comparing the observed number of affected persons with a particular family history constellation to the expected number, based on cohort-specific CRC rates.\n\nRESULTS:\nA total of 2,327,327 persons included in \u003e or =3 generation family histories were analyzed; 10,556 had a diagnosis of CRC. The FRR for CRC in persons with \u003e or =1 affected FDR = 2.05 (95% CI, 1.96-2.14), consistent with published estimates. In the absence of a positive first-degree family history, considering both affected SDRs and TDRs, only 1 constellation had an FRR estimate that was significantly \u003e1.0 (0 affected FDRs, 1 affected SDR, 2 affected TDRs; FRR = 1.33; 95% CI, 1.13-1.55). The FRR for persons with 1 affected FDR, 1 affected SDR, and 0 affected TDRs was 1.88 (95% CI, 1.59-2.20), increasing to FRR = 3.28 (95% CI, 2.44-4.31) for probands with 1 affected FDR, 1 affected SDR, and \u003e or =3 affected TDRs.\n\nCONCLUSIONS:\nIncreased numbers of affected FDRs influences risk much more than affected SDRs or TDRs. However, when combined with a positive first-degree family history, a positive second- and third-degree family history can significantly increase risk." + }, + "questions": [ + { + "id": "1bf37888-cce0-4727-a622-3e2dc0a0cf4d", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1443, + "text": "Increased numbers of affected FDRs" + }, + { + "answer_start": 850, + "text": "persons with \u003e or =1 affected FDR" + } + ] + } + ] +} \ No newline at end of file diff --git a/c6f97b07-cc4f-4d44-95b7-aa604a6999ea.json b/c6f97b07-cc4f-4d44-95b7-aa604a6999ea.json new file mode 100644 index 0000000000000000000000000000000000000000..bd129b889d3e1a3d2c272053c3d68b55f38ad83d --- /dev/null +++ b/c6f97b07-cc4f-4d44-95b7-aa604a6999ea.json @@ -0,0 +1,44 @@ +{ + "id": "c6f97b07-cc4f-4d44-95b7-aa604a6999ea", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "33106845", + "text": "Risk of chronic obstructive pulmonary disease (COPD) is determined by both cigarette smoking and genetic susceptibility, but little is known about gene-by-smoking interactions. We performed a genome-wide association analysis of 179,689 controls and 21,077 COPD cases from UK Biobank subjects of European ancestry recruited from 2006 to 2010, considering genetic main effects and gene-by-smoking interaction effects simultaneously (2-degrees-of-freedom (df) test) as well as interaction effects alone (1-df interaction test). We sought to replicate significant results in COPDGene (United States, 2008-2010) and SpiroMeta Consortium (multiple countries, 1947-2015) data. We considered 2 smoking variables: 1) ever/never and 2) current/noncurrent. In the 1-df test, we identified 1 genome-wide significant locus on 15q25.1 (cholinergic receptor nicotinic β4 subunit, or CHRNB4) for ever- and current smoking and identified PI*Z allele (rs28929474) of serpin family A member 1 (SERPINA1) for ever-smoking and 3q26.2 (MDS1 and EVI1 complex locus, or MECOM) for current smoking in an analysis of previously reported COPD loci. In the 2-df test, most of the significant signals were also significant for genetic marginal effects, aside from 16q22.1 (sphingomyelin phosphodiesterase 3, or SMPD3) and 19q13.2 (Egl-9 family hypoxia inducible factor 2, or EGLN2). The significant effects at 15q25.1 and 19q13.2 loci, both previously described in prior genome-wide association studies of COPD or smoking, were replicated in COPDGene and SpiroMeta. We identified interaction effects at previously reported COPD loci; however, we failed to identify novel susceptibility loci." + }, + "questions": [ + { + "id": "507492d5-ffa1-402c-aee8-1699aa463a52", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 1381, + "text": "15q25.1" + }, + { + "answer_start": 1393, + "text": "19q13.2 loci" + }, + { + "answer_start": 778, + "text": "1 genome-wide significant locus on 15q25.1 (cholinergic receptor nicotinic β4 subunit, or CHRNB4)" + } + ] + } + ] +} \ No newline at end of file diff --git a/c727eb2b-3d96-4808-a9e7-b0eacacb838e.json b/c727eb2b-3d96-4808-a9e7-b0eacacb838e.json new file mode 100644 index 0000000000000000000000000000000000000000..b354abaaaec32011c08eb759864d3ae256c44cb7 --- /dev/null +++ b/c727eb2b-3d96-4808-a9e7-b0eacacb838e.json @@ -0,0 +1,38 @@ +{ + "id": "c727eb2b-3d96-4808-a9e7-b0eacacb838e", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "15562129", + "text": "CONTEXT:\nDespite reductions in cardiovascular disease (CVD) mortality over the past few decades, it is unclear whether adults with and without diabetes have experienced similar declines in CVD risk.\n\nOBJECTIVE:\nTo determine whether adults with and without diabetes experienced similar declines in incident CVD in 1950-1995.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nParticipants aged 45-64 years from the Framingham Heart Study original and offspring cohorts who attended examinations in 1950-1966 (\"earlier\" time period; 4118 participants, 113 with diabetes) and 1977-1995 (\"later\" time period; 4063 participants, 317 with diabetes). Incidence rates of CVD among those with and without diabetes were compared between the earlier and later periods.\n\nMAIN OUTCOME MEASURES:\nMyocardial infarction, coronary heart disease death, and stroke.\n\nRESULTS:\nAmong participants with diabetes, the age- and sex-adjusted CVD incidence rate was 286.4 per 10,000 person-years in the earlier period and 146.9 per 10,000 in the later period, a 49.3% (95% confidence interval [CI], 16.7%-69.4%) decline. Among participants without diabetes, the age- and sex-adjusted incidence rate was 84.6 per 10,000 person-years in the earlier period and 54.3 per 10,000 person-years in the later period, a 35.4% (95% CI, 25.3%-45.4%) decline. Hazard ratios for diabetes as a predictor of incident CVD were not different in the earlier vs later periods.\n\nCONCLUSIONS:\nWe report a 50% reduction in the rate of incident CVD events among adults with diabetes, although the absolute risk of CVD is 2-fold greater than among persons without diabetes. Adults with and without diabetes have benefited similarly during the decline in CVD rates over the last several decades. More aggressive treatment of CVD risk factors and further research on diabetes-specific factors contributing to CVD risk are needed to further reduce the high absolute risk of CVD still experienced by persons with diabetes." + }, + "questions": [ + { + "id": "a19d30f0-b910-4636-b28f-0a2d80580374", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 866, + "text": "diabetes" + }, + { + "answer_start": 1582, + "text": "persons without diabetes" + } + ] + } + ] +} \ No newline at end of file diff --git a/c7681a67-b2e2-435c-9304-eccc48b2edb2.json b/c7681a67-b2e2-435c-9304-eccc48b2edb2.json new file mode 100644 index 0000000000000000000000000000000000000000..fbf0e84d8d0e8d7fa69a144d68365b633162bc7b --- /dev/null +++ b/c7681a67-b2e2-435c-9304-eccc48b2edb2.json @@ -0,0 +1,38 @@ +{ + "id": "c7681a67-b2e2-435c-9304-eccc48b2edb2", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "9892589", + "text": "BACKGROUND:\nInflammatory reactions in coronary plaques play an important role in the pathogenesis of acute atherothrombotic events; inflammation elsewhere is also associated with both atherogenesis generally and its thrombotic complications. Recent studies indicate that systemic markers of inflammation can identify subjects at high risk of coronary events.\n\nMETHODS AND RESULTS:\nWe used a sensitive immunoradiometric assay to examine the association of serum C-reactive protein (CRP) with the incidence of first major coronary heart disease (CHD) event in 936 men 45 to 64 years of age. The subjects, who were sampled at random from the general population, participated in the first MONICA Augsburg survey (1984 to 1985) and were followed for 8 years. There was a positive and statistically significant unadjusted relationship, which was linear on the log-hazards scale, between CRP values and the incidence of CHD events (n=53). The hazard rate ratio (HRR) of CHD events associated with a 1-SD increase in log-CRP level was 1.67 (95% CI, 1.29 to 2. 17). After adjustment for age, the HRR was 1.60 (95% CI, 1.23 to 2. 08). Adjusting further for smoking behavior, the only variable selected from a variety of potential confounders by a forward stepping process with a 5% change in the relative risk of CRP as the selection criterion, yielded an HRR of 1.50 (95% CI, 1.14 to 1.97).\n\nCONCLUSIONS:\nThese results confirm the prognostic relevance of CRP, a sensitive systemic marker of inflammation, to the risk of CHD in a large, randomly selected cohort of initially healthy middle-aged men. They suggest that low-grade inflammation is involved in pathogenesis of atherosclerosis, especially its thrombo-occlusive complications." + }, + "questions": [ + { + "id": "dea483bd-9677-4950-9518-497cd9fe8248", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 992, + "text": "1-SD increase in log-CRP level" + }, + { + "answer_start": 1446, + "text": "CRP" + } + ] + } + ] +} \ No newline at end of file diff --git a/c8160351-888c-41be-98bb-1d5f4b6acf31.json b/c8160351-888c-41be-98bb-1d5f4b6acf31.json new file mode 100644 index 0000000000000000000000000000000000000000..351844ae2906631e6fa8a58331096bb4b25c2022 --- /dev/null +++ b/c8160351-888c-41be-98bb-1d5f4b6acf31.json @@ -0,0 +1,62 @@ +{ + "id": "c8160351-888c-41be-98bb-1d5f4b6acf31", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "34436608", + "text": "IMPORTANCE:\nBreast density is associated with breast cancer risk in women aged 40 to 65 years, but there is limited evidence of its association with risk of breast cancer among women aged 65 years or older.\n\nOBJECTIVE:\nTo compare the association between breast density and risk of invasive breast cancer among women aged 65 to 74 years vs women aged 75 years or older and to evaluate whether the association is modified by body mass index (BMI).\n\nDESIGN, SETTING, AND PARTICIPANTS:\nThis prospective cohort study used data from the Breast Cancer Surveillance Consortium from January 1, 1996, to December 31, 2012, for US women aged 65 years or older who underwent screening mammography. Data were analyzed from January 1, 2018, to December 31, 2020.\n\nEXPOSURES:\nBreast Imaging Reporting and Data System breast density category, age, and BMI.\n\nMAIN OUTCOMES AND MEASURES:\nThe 5-year cumulative incidence of invasive breast cancer by level of breast density (almost entirely fat, scattered fibroglandular densities, or heterogeneous or extreme density) and age (65-74 vs ≥75 years) was calculated using weighted means. Cox proportional hazards models were fit to estimate the association of breast density with invasive breast cancer risk. The likelihood ratio test was used to test the interaction between BMI and breast density.\n\nRESULTS:\nA total of 221 714 screening mammograms from 193 787 women were included in the study; a total of 38% of the study population was aged 75 years or older. Of the mammograms, most were from women aged 65 to 74 years (64.6%) and non-Hispanic White individuals (81.4%). The 5-year cumulative incidence of invasive breast cancer increased in association with increasing breast density among women aged 65 to 74 years (almost entirely fatty breasts: 11.3 per 1000 women [95% CI, 10.4-12.5 per 1000 women]; scattered fibroglandular densities: 17.2 per 1000 women [95% CI, 16.1-17.9 per 1000 women]; extremely or heterogeneously dense breasts: 23.7 per 1000 women [95% CI, 22.4-25.3 per 1000 women]) and among those aged 75 years or older (fatty breasts: 13.5 per 1000 women [95% CI, 11.6-15.5]; scattered fibroglandular densities: 18.4 per 1000 women [95% CI, 17.0-19.5 per 1000 women]; extremely or heterogeneously dense breasts: 22.5 per 1000 women [95% CI, 20.2-24.2 per 1000 women]). Extreme or heterogeneous breast density was associated with increased risk of breast cancer compared with scattered fibroglandular breast density in both age categories (65-74 years: hazard ratio [HR], 1.39 [95% CI, 1.28-1.50]; ≥75 years: HR, 1.23 [95% CI, 1.10-1.37]). Women with almost entirely fatty breasts had a decrease of approximately 30% (range, 27%-34%) in the risk of invasive breast cancer compared with women with scattered fibroglandular breast density (65-74 years: HR, 0.66 [95% CI, 0.58-0.75]; ≥75 years: HR, 0.73; 95% CI, 0.62-0.86). Associations between breast density and breast cancer risk were not significantly modified by BMI (for age 65-74 years: likelihood ratio test, 2.67; df, 2; P = .26; for age ≥75 years, 2.06; df, 2; P = .36).\n\nCONCLUSIONS AND RELEVANCE:\nThe findings suggest that breast density is associated with increased risk of invasive breast cancer among women aged 65 years or older. Breast density and life expectancy should be considered together when discussing the potential benefits vs harms of continued screening mammography in this population." + }, + "questions": [ + { + "id": "d18fe34e-24f4-4ea9-ade5-176818ee93fa", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1692, + "text": "increasing breast density among women aged 65 to 74 years" + }, + { + "answer_start": 1838, + "text": "scattered fibroglandular densities" + }, + { + "answer_start": 1930, + "text": "extremely or heterogeneously dense breasts" + }, + { + "answer_start": 2040, + "text": "those aged 75 years or older" + }, + { + "answer_start": 2126, + "text": "scattered fibroglandular densities" + }, + { + "answer_start": 2218, + "text": "extremely or heterogeneously dense breasts" + }, + { + "answer_start": 2319, + "text": "Extreme or heterogeneous breast density" + }, + { + "answer_start": 3132, + "text": "breast density" + } + ] + } + ] +} \ No newline at end of file diff --git a/c8c3950b-7101-4457-a22f-81730ed3c2a1.json b/c8c3950b-7101-4457-a22f-81730ed3c2a1.json new file mode 100644 index 0000000000000000000000000000000000000000..599dfbc168056b8d97b929b7d15df91cc1b33d09 --- /dev/null +++ b/c8c3950b-7101-4457-a22f-81730ed3c2a1.json @@ -0,0 +1,53 @@ +{ + "id": "c8c3950b-7101-4457-a22f-81730ed3c2a1", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "22665813", + "text": "BACKGROUND:\nChildhood cancer survivors develop gastrointestinal cancer more frequently and at a younger age than the general population, but the risk factors have not been well-characterized.\n\nOBJECTIVE:\nTo determine the risk and associated risk factors for gastrointestinal subsequent malignant neoplasms (SMNs) in childhood cancer survivors.\n\nDESIGN:\nRetrospective cohort study.\n\nSETTING:\nThe Childhood Cancer Survivor Study, a multicenter study of childhood cancer survivors diagnosed between 1970 and 1986.\n\nPATIENTS:\n14 358 survivors of cancer diagnosed when they were younger than 21 years of age who survived for 5 or more years after the initial diagnosis.\n\nMEASUREMENTS:\nStandardized incidence ratios (SIRs) for gastrointestinal SMNs were calculated by using age-specific population data. Multivariate Cox regression models identified associations between risk factors and gastrointestinal SMN development.\n\nRESULTS:\nAt median follow-up of 22.8 years (range, 5.5 to 30.2 years), 45 cases of gastrointestinal cancer were identified. The risk for gastrointestinal SMNs was 4.6-fold higher in childhood cancer survivors than in the general population (95% CI, 3.4 to 6.1). The SIR for colorectal cancer was 4.2 (CI, 2.8 to 6.3). The highest risk for gastrointestinal SMNs was associated with abdominal radiation (SIR, 11.2 [CI, 7.6 to 16.4]). However, survivors not exposed to radiation had a significantly increased risk (SIR, 2.4 [CI, 1.4 to 3.9]). In addition to abdominal radiation, high-dose procarbazine (relative risk, 3.2 [CI, 1.1 to 9.4]) and platinum drugs (relative risk, 7.6 [CI, 2.3 to 25.5]) independently increased the risk for gastrointestinal SMNs.\n\nLIMITATION:\nThis cohort has not yet attained an age at which risk for gastrointestinal cancer is greatest.\n\nCONCLUSION:\nChildhood cancer survivors, particularly those exposed to abdominal radiation, are at increased risk for gastrointestinal SMNs. These findings suggest that surveillance of at-risk childhood cancer survivors should begin at a younger age than that recommended for the general population.\n\nPRIMARY FUNDING SOURCE:\nNational Cancer Institute." + }, + "questions": [ + { + "id": "6e7100ec-1910-4b8d-bc6e-3ecf04c74a27", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1793, + "text": "Childhood cancer survivors, particularly those exposed to abdominal radiation" + }, + { + "answer_start": 1099, + "text": "childhood cancer survivors" + }, + { + "answer_start": 1358, + "text": "survivors not exposed to radiation" + }, + { + "answer_start": 1493, + "text": "high-dose procarbazine" + }, + { + "answer_start": 1558, + "text": "platinum drugs" + } + ] + } + ] +} \ No newline at end of file diff --git a/c8fd1337-431f-4655-8439-4af128c3fb55.json b/c8fd1337-431f-4655-8439-4af128c3fb55.json new file mode 100644 index 0000000000000000000000000000000000000000..5210a9ecd8973a617f6deb68c3594cfde29bba5c --- /dev/null +++ b/c8fd1337-431f-4655-8439-4af128c3fb55.json @@ -0,0 +1,42 @@ +{ + "id": "c8fd1337-431f-4655-8439-4af128c3fb55", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "28586371", + "text": "OBJECTIVE:\nThe association between opium use and bladder cancer has been investigated in many studies, with varying reporting results reported. This study aims to estimate the total odds ratio for the association between bladder cancer and opium consumption using meta-analysis.\n\nMETHODS:\nThe study was designed according to PRISMA guidelines. Two independent researchers searched for the relevant studies using PubMed, Web of Science, Scopus, OVID, Embase, and Google Scholar. After systematic screening of the studies identified during the first step, Cochrane risk of bias tool was determined for the selected studies. The case-control and the cohort studies were investigated to assess risk of bladder cancer due to opium use. In addition, the cross-sectional studies were analysed separately to assess frequency of opium consumption. These estimates were combined using the inverse variance method. Fixed or random effect models were applied to combine the point odds ratios. The heterogeneity between the primary results was assessed using the Cochran test and I-square index. The suspected factors for heterogeneity were investigated using meta-regression models. An Egger test was conducted to identify any probable publication bias. Forest plots illustrated the point and pooled estimates. All analyses were performed using Stata version 14 software and RevMan version 5.3.\n\nRESULTS:\nWe included 17 primary studies (11 case-control, one cohort and five cross-sectional) in the final meta-analysis. The total odds ratios (95% confidence intervals) for developing bladder cancer by opium use alone, and concurrent use of opium and cigarettes were estimated as 3.85 (3.05-4.87) and 5.7 (1.9-16.3) respectively. The odds ratio (95% confidence interval) for opium use with or without cigarette smoking was estimated as 5.3 (3.6-7.7).\n\nCONCLUSION:\nThis meta-analysis showed that opium use similar to cigarette smoking and maybe with similar mechanisms can be a risk factor for bladder cancer. It is therefore expected to be a risk factor for other cancers." + }, + "questions": [ + { + "id": "31cd77a1-5a20-46d8-a74f-f125e15e884e", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 1589, + "text": "opium use alone" + }, + { + "answer_start": 1610, + "text": "concurrent use of opium and cigarettes" + }, + { + "answer_start": 1762, + "text": "opium use with or without cigarette smoking" + } + ] + } + ] +} \ No newline at end of file diff --git a/c95141f1-79d2-42c5-b6e5-4a6383951350.json b/c95141f1-79d2-42c5-b6e5-4a6383951350.json new file mode 100644 index 0000000000000000000000000000000000000000..bd0055adb6f2f61a9349bda112892e0f37d654cb --- /dev/null +++ b/c95141f1-79d2-42c5-b6e5-4a6383951350.json @@ -0,0 +1,66 @@ +{ + "id": "c95141f1-79d2-42c5-b6e5-4a6383951350", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "15534160", + "text": "BACKGROUND:\nAlthough obesity is the most important risk factor for type 2 diabetes, evidence is emerging that certain foods and dietary factors may be associated with diabetes. To examine the association between major dietary patterns and risk of type 2 diabetes mellitus in a cohort of women.\n\nMETHODS:\nWe prospectively assessed the associations between major dietary patterns and risk of type 2 diabetes in women. Dietary information was collected in 1984, 1986, 1990, and 1994 from 69,554 women aged 38 to 63 years without a history of diabetes, cardiovascular disease, or cancer in 1984. We conducted factor analysis and identified 2 major dietary patterns: \"prudent\" and \"Western.\" We then calculated pattern scores for each participant and examined prospectively the associations between dietary pattern scores and type 2 diabetes risks.\n\nRESULTS:\nThe prudent pattern was characterized by higher intakes of fruits, vegetables, legumes, fish, poultry, and whole grains, while the Western pattern included higher intakes of red and processed meats, sweets and desserts, french fries, and refined grains. During 14 years of follow-up, we identified 2699 incident cases of type 2 diabetes. After adjusting for potential confounders, we observed a relative risk for diabetes of 1.49 (95% confidence interval [CI], 1.26-1.76, P for trend, \u003c.001) when comparing the highest to lowest quintiles of the Western pattern. Positive associations were also observed between type 2 diabetes and red meat and other processed meats. The relative risk for diabetes for every 1-serving increase in intake is 1.26 (95% CI, 1.21-1.42) for red meat, 1.38 (95% CI, 1.23-1.56) for total processed meats, 1.73 (95% CI, 1.39-2.16) for bacon, 1.49 (95% CI, 1.04-2.11) for hot dogs, and 1.43 (95% CI, 1.22-1.69) for processed meats.\n\nCONCLUSION:\nThe Western pattern, especially a diet higher in processed meats, may increase the risk of type 2 diabetes in women." + }, + "questions": [ + { + "id": "23b9da39-8213-419a-aae9-5b7b88c59221", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1824, + "text": "The Western pattern, especially a diet higher in processed meats" + }, + { + "answer_start": 985, + "text": "Western pattern included higher intakes of red and processed meats, sweets and desserts, french fries, and refined grains" + }, + { + "answer_start": 1486, + "text": "red meat and other processed meats" + }, + { + "answer_start": 1557, + "text": "every 1-serving increase in intake" + }, + { + "answer_start": 1624, + "text": "red meat" + }, + { + "answer_start": 1663, + "text": "total processed meats" + }, + { + "answer_start": 1715, + "text": "bacon" + }, + { + "answer_start": 1751, + "text": "hot dogs" + }, + { + "answer_start": 1794, + "text": "processed meats" + } + ] + } + ] +} \ No newline at end of file diff --git a/ca083607-dc75-4591-8287-175f9a2d2b2b.json b/ca083607-dc75-4591-8287-175f9a2d2b2b.json new file mode 100644 index 0000000000000000000000000000000000000000..03fb3b8ef1f5026061977b890a7a026711eb745f --- /dev/null +++ b/ca083607-dc75-4591-8287-175f9a2d2b2b.json @@ -0,0 +1,40 @@ +{ + "id": "ca083607-dc75-4591-8287-175f9a2d2b2b", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "8317812", + "text": "The object of this study was to assess the relationship between occupational dust exposure and chronic obstructive pulmonary disease (COPD). Studies were identified using MEDLINE (January 1966 to July 1991), SCISEARCH, manual review of reference lists, and personal contact with more than 30 international experts. Studies of COPD, lung function, emphysema, chronic bronchitis, or mortality in workers exposed to nonorganic dust were retrieved. Studies were included if dust exposure was measured quantitatively, and a quantitative relationship between dust exposure and one of the outcomes of interest was calculated while controlling at least for smoking and age. Methodological rigor was assessed, and data regarding the study populations, prognostic factors, and outcomes were extracted independently by two reviewers. Thirteen reports derived from four cohorts of workers met our inclusion criteria. Three of the cohorts were of coal miners and one was of gold miners. All of the studies found a statistically significant association between loss of lung function and cumulative respirable dust exposure. It was estimated that 80 (95% CI, 34 to 137) of 1,000 nonsmoking coal miners with a cumulative respirable dust exposure of 122.5 gh/m3 (considered equivalent to 35 years of work with a mean respirable dust level of 2 mg/m3) could be expected to develop a clinically important (\u003e 20%) loss of FEV1 attributable to dust. Among 1,000 smoking miners the comparable estimate was 66 (95% CI, 49 to 84). The risk of a clinically important loss of lung function attributable to dust among nonsmoking gold miners was estimated to be three times as large as for coal miners at less than one fifth of the cumulative respirable dust exposure (21.3 gh/m3), the maximal exposure observed among the cohort of gold miners. We conclude that occupational dust is an important cause of COPD, and the risk appears to be greater for gold miners than for coal miners. One possible explanation of the greater risk among gold miners is the higher silica content in gold mine dust." + }, + "questions": [ + { + "id": "62e36416-114c-48ae-a23c-16d6d4ed76b1", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 1834, + "text": "occupational dust" + }, + { + "answer_start": 1922, + "text": "gold miners" + } + ] + } + ] +} \ No newline at end of file diff --git a/cad34e15-0b77-4572-bfa5-02e4ea4681d5.json b/cad34e15-0b77-4572-bfa5-02e4ea4681d5.json new file mode 100644 index 0000000000000000000000000000000000000000..47ab828d84d218532e0c8b08d6d06ac0640c61d3 --- /dev/null +++ b/cad34e15-0b77-4572-bfa5-02e4ea4681d5.json @@ -0,0 +1,37 @@ +{ + "id": "cad34e15-0b77-4572-bfa5-02e4ea4681d5", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "15516844", + "text": "The observed increased incidence of colorectal cancer in Ashkenazi Jews compared to other populations is unexplained but likely has a genetic component. The I1307K APC polymorphism/mutation is carried by 6-8% of Ashkenazim and increases the risk of colorectal cancer 1.5-2 fold. There are few differences between the phenotype of colorectal cancer in I1307K carriers and sporadic cases. It is estimated that the mutation accounts for 6% of cases of colorectal cancer in Jews of Eastern European heritage. It should not be the subject of mass screening in Ashkenazi Jews, although it may be important in cases of familial colorectal cancer. Even rarer is the 1906G--\u003eC MSH2 mutation carried by less than 1% of Ashkenazim, but as with other HNPCC mutations likely associated with a high risk of malignancy. Mutations at 15q13-14 are associated with the colorectal adenoma and carcinoma syndrome (CRAC) described in Ashkenazi families. The prevalence of the mutation is not known, nor its significance as a cause of colorectal cancer. Despite the paucity of genetic explanations for the high risk of colorectal cancer in Ashkenazim, that risk warrants aggressive colorectal cancer screening and particular attention to family history of malignancy in all Jews of Ashkenazi descent." + }, + "questions": [ + { + "id": "95ea625b-f574-4219-b795-6017260e02ee", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 157, + "text": "I1307K APC polymorphism/mutation" + } + ] + } + ] +} \ No newline at end of file diff --git a/cb862db9-2475-4427-98ef-3bb5df729b4f.json b/cb862db9-2475-4427-98ef-3bb5df729b4f.json new file mode 100644 index 0000000000000000000000000000000000000000..ef0b51fedea97a086660de99a12947da208d96ed --- /dev/null +++ b/cb862db9-2475-4427-98ef-3bb5df729b4f.json @@ -0,0 +1,34 @@ +{ + "id": "cb862db9-2475-4427-98ef-3bb5df729b4f", + "disease": { + "id": "H00408", + "names": [ + "Type 1 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E10" + ], + "mesh": [ + "D003922" + ] + }, + "category": "Metabolic disease; Immune system disease; Endocrine disease" + }, + "article": { + "id": "1473616", + "text": "We studied the cumulative incidence, concordance rate and heritability for diabetes mellitus in a nationwide cohort of 13,888 Finnish twin pairs of the same sex. The twins were born before 1958 and both co-twins were alive in 1967. Data on diabetes were derived through computerized record linkage from death certificates, the National Hospital Discharge Register and the National Drug Register. Records were reviewed in order to assign a diagnostic category to the 738 diabetic patients identified. Of these patients 109 had Type 1 (insulin-dependent) diabetes, 505 Type 2 (non-insulin-dependent) diabetes, 46 gestational diabetes, 24 secondary diabetes, 38 impaired glucose tolerance and 16 remained unclassified. The cumulative incidence of diabetes was 1.4% in men and 1.3% in women aged 28-59 years and 9.3% and 7.0% in men and women aged 60 years and over, respectively. The cumulative incidence did not differ between monozygotic and dizygotic twins. The concordance rate for Type 1 diabetes was higher among monozygotic (23% probandwise and 13% pairwise) than dizygotic twins (5% probandwise and 3% pairwise). The probandwise and pairwise concordance rates for Type 2 diabetes were 34% and 20% among monozygotic twins and 16% and 9% in dizygotic twins, respectively. Heritability for Type 1 diabetes was greater than that for Type 2 where both genetic and environmental effects seemed to play a significant role." + }, + "questions": [ + { + "id": "9c8fe032-b8d6-43b7-89ab-54d4e0c2ebde", + "text": "What are the risk factors of Type 1 diabetes mellitus?", + "answers": [ + { + "answer_start": 1016, + "text": "monozygotic" + } + ] + } + ] +} \ No newline at end of file diff --git a/cbd88ed9-7422-4d18-b2d2-806e8916519d.json b/cbd88ed9-7422-4d18-b2d2-806e8916519d.json new file mode 100644 index 0000000000000000000000000000000000000000..c17fcdfdbefd08a62c77a091194e45dbbec94c44 --- /dev/null +++ b/cbd88ed9-7422-4d18-b2d2-806e8916519d.json @@ -0,0 +1,38 @@ +{ + "id": "cbd88ed9-7422-4d18-b2d2-806e8916519d", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "22422870", + "text": "OBJECTIVES:\nTo summarise evidence on the association between white rice consumption and risk of type 2 diabetes and to quantify the potential dose-response relation.\n\nDESIGN:\nMeta-analysis of prospective cohort studies.\n\nDATA SOURCES:\nSearches of Medline and Embase databases for articles published up to January 2012 using keywords that included both rice intake and diabetes; further searches of references of included original studies.\n\nSTUDY SELECTION:\nIncluded studies were prospective cohort studies that reported risk estimates for type 2 diabetes by rice intake levels.\n\nDATA SYNTHESIS:\nRelative risks were pooled using a random effects model; dose-response relations were evaluated using data from all rice intake categories in each study.\n\nRESULTS:\nFour articles were identified that included seven distinct prospective cohort analyses in Asian and Western populations for this study. A total of 13,284 incident cases of type 2 diabetes were ascertained among 352,384 participants with follow-up periods ranging from 4 to 22 years. Asian (Chinese and Japanese) populations had much higher white rice consumption levels than did Western populations (average intake levels were three to four servings/day versus one to two servings/week). The pooled relative risk was 1.55 (95% confidence interval 1.20 to 2.01) comparing the highest with the lowest category of white rice intake in Asian populations, whereas the corresponding relative risk was 1.12 (0.94 to 1.33) in Western populations (P for interaction=0.038). In the total population, the dose-response meta-analysis indicated that for each serving per day increment of white rice intake, the relative risk of type 2 diabetes was 1.11 (1.08 to 1.14) (P for linear trend\u003c0.001).\n\nCONCLUSION:\nHigher consumption of white rice is associated with a significantly increased risk of type 2 diabetes, especially in Asian (Chinese and Japanese) populations." + }, + "questions": [ + { + "id": "967977e8-095e-4079-9503-d03c752ca292", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1370, + "text": "white rice intake in Asian populations" + }, + { + "answer_start": 1755, + "text": "Higher consumption of white rice" + } + ] + } + ] +} \ No newline at end of file diff --git a/cc506bcc-a93f-433b-843d-1d1ee4ff82df.json b/cc506bcc-a93f-433b-843d-1d1ee4ff82df.json new file mode 100644 index 0000000000000000000000000000000000000000..0173026ea3e89b75dfc25bed5b8b3e5f32ba81a8 --- /dev/null +++ b/cc506bcc-a93f-433b-843d-1d1ee4ff82df.json @@ -0,0 +1,42 @@ +{ + "id": "cc506bcc-a93f-433b-843d-1d1ee4ff82df", + "disease": { + "id": "H00408", + "names": [ + "Type 1 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E10" + ], + "mesh": [ + "D003922" + ] + }, + "category": "Metabolic disease; Immune system disease; Endocrine disease" + }, + "article": { + "id": "10526738", + "text": "OBJECTIVE:\nTo explore whether perinatal factors are associated with the development of childhood type 1 diabetes.\n\nRESEARCH DESIGN AND METHODS:\nWe studied hospital records from 892 cases of childhood type 1 diabetes compared with 2,291 population-based control subjects in seven study centers in Europe.\n\nRESULTS:\nIn a pooled analysis incorporating stratification by center, we confirmed the previous findings that older maternal age, maternal preeclampsia, neonatal respiratory disease, and jaundice caused by blood group incompatibility are significant risk factors for type 1 diabetes, whereas being a firstborn child, having a low birth weight, or having a short birth length were protective. Cesarean section delivery and neonatal infectious diseases were not significantly associated with the risk of type 1 diabetes in this study. The strongest association was found for blood group incompatibility (AB0 and Rh factor) with an odds ratio (OR) of 2.96 (95% CI 1.88-4.65). AB0 incompatibility (OR = 3.92) was a more common and also a stronger risk factor than Rh incompatibility (OR = 1.62). The effect of AB0 blood group incompatibility was independent of treatment effects in logistical regression analysis.\n\nCONCLUSIONS:\nDifferent perinatal events are associated with an increased risk of type 1 diabetes. The effect of maternal-child blood group incompatibility is strong and indicates a true effect that must be further explored." + }, + "questions": [ + { + "id": "b110577a-2cb9-468f-b7f5-e8a232d552f3", + "text": "What are the risk factors of Type 1 diabetes mellitus?", + "answers": [ + { + "answer_start": 878, + "text": "blood group incompatibility (AB0 and Rh factor)" + }, + { + "answer_start": 978, + "text": "AB0 incompatibility" + }, + { + "answer_start": 1328, + "text": "maternal-child blood group incompatibility" + } + ] + } + ] +} \ No newline at end of file diff --git a/cc638060-ab23-4054-bed0-da18c350db76.json b/cc638060-ab23-4054-bed0-da18c350db76.json new file mode 100644 index 0000000000000000000000000000000000000000..82b5843328dc80a6b2aa0ef83d96371a030aeb2a --- /dev/null +++ b/cc638060-ab23-4054-bed0-da18c350db76.json @@ -0,0 +1,35 @@ +{ + "id": "cc638060-ab23-4054-bed0-da18c350db76", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "19052046", + "text": "BACKGROUND:\nCaesarean section might be a risk factor for asthma because of delayed microbial colonisation, but the association remains controversial. A study was undertaken to investigate prospectively whether children born by caesarean section are more at risk of having asthma in childhood and sensitisation at the age of 8 years, taking into account the allergic status of the parents.\n\nMETHODS:\n2917 children who participated in a birth cohort study were followed for 8 years. The definition of asthma included wheeze, dyspnoea and prescription of inhaled steroids. In a subgroup (n = 1454), serum IgE antibodies for inhalant and food allergens were measured at 8 years.\n\nRESULTS:\nIn the total study population, 12.4% (n = 362) of the children had asthma at the age of 8 years. Caesarean section, with a total prevalence of 8.5%, was associated with an increased risk of asthma (OR 1.79; 95% CI 1.27 to 2.51). This association was stronger among predisposed children (with two allergic parents: OR 2.91; 95% CI 1.20 to 7.05; with only one: OR 1.86; 95% CI 1.12 to 3.09) than in children with non-allergic parents (OR 1.36; 95% CI 0.77 to 2.42). The association between caesarean section and sensitisation at the age of 8 years was significant only in children of non-allergic parents (OR 2.14; 95% CI 1.16 to 3.98).\n\nCONCLUSIONS:\nChildren born by caesarean section have a higher risk of asthma than those born by vaginal delivery, particularly children of allergic parents. Caesarean section increases the risk for sensitisation to common allergens in children with non-allergic parents only." + }, + "questions": [ + { + "id": "36f62c52-f8d5-4635-8a44-705016060f65", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1334, + "text": "Children born by caesarean section" + } + ] + } + ] +} \ No newline at end of file diff --git a/cd724107-3f6a-46c8-8507-bf1606f5bfbd.json b/cd724107-3f6a-46c8-8507-bf1606f5bfbd.json new file mode 100644 index 0000000000000000000000000000000000000000..c2eda94bc2becc33f306a972a9419e634d9ee972 --- /dev/null +++ b/cd724107-3f6a-46c8-8507-bf1606f5bfbd.json @@ -0,0 +1,35 @@ +{ + "id": "cd724107-3f6a-46c8-8507-bf1606f5bfbd", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "10573048", + "text": "BACKGROUND:\nObesity and asthma are common disorders, and their prevalence rates continue to rise. Although individuals with asthma may gain weight as a result of activity limitations, the relationship between body mass index (BMI), which is calculated as weight in kilograms divided by the square of height in meters, and risk of developing asthma is not known.\n\nMETHODS:\nWe performed a prospective cohort study of female US registered nurses in the Nurses' Health Study II. In 1991, after excluding women who died with probable asthma or with incomplete data, there were 85911 participants, aged 26 to 46 years. The main outcome measure was self-report of physician-diagnosed asthma with recent use of an asthma medication.\n\nRESULTS:\nFrom 1991 to 1995, we identified 1596 incident cases of asthma. In a multivariate model controlling for 9 potential confounding factors (including age, race, smoking, physical activity, and energy intake), the relative risks of asthma for 6 increasing categories of BMI in 1991 were 0.9, 1.0 (reference), 1.1, 1.6, 1.7, and 2.7 (P for trend \u003c.001). Stronger associations were found using stricter definitions for asthma, and the finding was present in a variety of subgroups. In analyses controlling for the same variables, as well as BMI at age 18, women who gained weight after age 18 were at significantly increased risk of developing asthma during the 4-year follow-up period (P for trend \u003c.001).\n\nCONCLUSIONS:\nThe BMI has a strong, independent, and positive association with risk of adult-onset asthma. The increasing prevalence of obesity in developed nations may help explain concomitant increases in asthma prevalence." + }, + "questions": [ + { + "id": "074f4d4f-bc74-4f01-91cc-027d7b2ce522", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1572, + "text": "obesity" + } + ] + } + ] +} \ No newline at end of file diff --git a/cd8dd4ee-ed1c-45a0-8012-f0c39cdb5730.json b/cd8dd4ee-ed1c-45a0-8012-f0c39cdb5730.json new file mode 100644 index 0000000000000000000000000000000000000000..aaf65248c13064d384b48bff2abc57ed96491459 --- /dev/null +++ b/cd8dd4ee-ed1c-45a0-8012-f0c39cdb5730.json @@ -0,0 +1,37 @@ +{ + "id": "cd8dd4ee-ed1c-45a0-8012-f0c39cdb5730", + "disease": { + "id": "M2023_04_26_16_38_52", + "names": [ + "Migraine" + ], + "dbLinks": { + "icd10": [ + "G43" + ], + "icd11": [ + "8A80" + ], + "mesh": [ + "C10.228.140.546.399.750" + ] + }, + "description": "Migraine is a chronic neurological disorder characterized by recurrent episodes of unilateral, pulsatile headaches associated with autonomic symptoms such as nausea, vomiting, photophobia, and phonophobia. The pathophysiology of migraine is multifactorial and involves complex interactions between genetic, environmental, and neurochemical factors that modulate cerebral vascular tone and nociception. Migraine attacks can be triggered by a variety of factors, including stress, hormonal changes, sleep disturbances, and certain foods or medications. Treatment options for migraine include pharmacotherapy for acute attacks, preventive medications for frequent or severe headaches, and lifestyle modifications to avoid triggers. In refractory cases, interventional therapies such as nerve blocks or neuromodulation techniques may be considered." + }, + "article": { + "id": "22644169", + "text": "The burden of migraine strongly increases, considering its linkage with sleep disorders. Migraine is positively associated with many sleep-complaint disorders; some are confirmed by several studies, such as restless leg syndrome, whereas others still remain uncertain or controversial, e.g. narcolepsy. Many studies have investigated the association between headache and other sleep disturbances such as daytime sleepiness, insomnia, snoring and/or apnea, but only a few have focused on migraine. Highlighting the comorbidity between migraine and sleep disorders is important to improve treatment strategies and to extend the knowledge of migraine pathophysiology." + }, + "questions": [ + { + "id": "7dfe6fe8-a73a-4698-9311-4a078a19317c", + "text": "what are the risk factors of Migraine?", + "answers": [ + { + "answer_start": 291, + "text": "narcolepsy" + } + ] + } + ] +} \ No newline at end of file diff --git a/cda7956f-ea9a-46d9-87f1-0043bcbd47ad.json b/cda7956f-ea9a-46d9-87f1-0043bcbd47ad.json new file mode 100644 index 0000000000000000000000000000000000000000..cc9e156ddbd82fa6115d04c534950a5b2db392e7 --- /dev/null +++ b/cda7956f-ea9a-46d9-87f1-0043bcbd47ad.json @@ -0,0 +1,54 @@ +{ + "id": "cda7956f-ea9a-46d9-87f1-0043bcbd47ad", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "17684133", + "text": "The relationship between family history of cancer in first-degree relatives and risk of bladder cancer was examined in the Spanish Bladder Cancer Study. Information on family history of cancer was obtained for 1,158 newly diagnosed bladder cancer cases and 1,244 controls included in 18 hospitals between 1998 and 2001. A total of 464 (40.1%) cases and 436 (35.1%) controls reported a family history of cancer in \u003e/=1 relative [odds ratio (OR), 1.32; 95% confidence interval (95% CI), 1.11-1.59]; the OR was 1.23 (95% CI, 1.01-1.50) among those with only one relative affected and 1.67 (95% CI, 1.23-2.29) among those with \u003e/=2 affected relatives (P(trend) = 0.0004). A greater risk of bladder cancer was observed among those diagnosed at age \u003c/=45 years (OR, 2.67; 95% CI, 1.10-6.50) compared with those diagnosed over age 45 years (OR, 1.27; 95% CI, 1.06-1.52). The OR of bladder cancer among subjects reporting a family history of cancer of the bladder was 2.34 (95% CI, 0.95-5.77). Statistically significant associations emerged between bladder cancer risk and family history of cancer of the esophagus, lung, prostate, and brain. The OR of bladder cancer for those reporting family history of bladder cancer was 4.76 (95% CI, 1.25-18.09) among NAT2-slow acetylators and 1.17 (95% CI, 0.17-7.86) among NAT2-rapid/intermediate acetylators (P(interaction) = 0.609). Among individuals with GSTM1 null and present genotypes, the corresponding ORs were 2.91 (95% CI, 0.44-19.09) and 4.21 (95% CI, 1.26-14.14), respectively (P(interaction) = 0.712). Limitations of our study are small sample size in subgroup analyses, reliability of family history data, and possible residual confounding by shared environmental exposures. Overall, our findings support the hypothesis that genetic factors play a role in bladder cancer etiology. Whether these correspond to low-penetrance cancer-predisposing polymorphisms acting together and/or interacting with environmental factors warrants further research." + }, + "questions": [ + { + "id": "0ec767ad-f981-4c83-93e3-efc863981a5f", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 1065, + "text": "family history of cancer of the esophagus, lung, prostate, and brain" + }, + { + "answer_start": 1164, + "text": "those reporting family history of bladder cancer" + }, + { + "answer_start": 1249, + "text": "NAT2-slow acetylators" + }, + { + "answer_start": 385, + "text": "family history of cancer in \u003e/=1 relative" + }, + { + "answer_start": 539, + "text": "those with only one relative affected" + }, + { + "answer_start": 612, + "text": "those with \u003e/=2 affected relatives" + } + ] + } + ] +} \ No newline at end of file diff --git a/ce43f031-8066-4ea8-9191-cdea4edf7467.json b/ce43f031-8066-4ea8-9191-cdea4edf7467.json new file mode 100644 index 0000000000000000000000000000000000000000..b44c2b1f13a15d769d5d971b9e31ac668765912b --- /dev/null +++ b/ce43f031-8066-4ea8-9191-cdea4edf7467.json @@ -0,0 +1,34 @@ +{ + "id": "ce43f031-8066-4ea8-9191-cdea4edf7467", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "15138242", + "text": "CONTEXT:\nWhether parental cardiovascular disease confers increased risk independent of other risk factors remains controversial. Prior studies relied on offspring report, without complete validation of parental events.\n\nOBJECTIVE:\nTo determine whether parental cardiovascular disease predicts offspring events independent of traditional risk factors, using a prospective design for both parents and offspring, and uniform criteria to validate events.\n\nDESIGN:\nInception cohort study.\n\nSETTING:\nFramingham Heart Study, a US population-based epidemiologic cohort begun in 1948 with the offspring cohort established in 1971.\n\nPARTICIPANTS:\nAll Framingham Offspring Study participants (aged \u003e or =30 years) who were free of cardiovascular disease and both parents in the original Framingham cohort.\n\nMAIN OUTCOME MEASURES:\nWe examined the association of parental cardiovascular disease with 8-year risk of offspring cardiovascular disease, using pooled logistic regression.\n\nRESULTS:\nAmong 2302 men and women (mean age, 44 years), 164 men and 79 women had cardiovascular events during follow-up. Compared with participants with no parental cardiovascular disease, those with at least 1 parent with premature cardiovascular disease (onset age \u003c55 years in father, \u003c65 years in mother) had greater risk for events, with age-adjusted odds ratios of 2.6 (95% confidence interval [CI], 1.7-4.1) for men and 2.3 (95% CI, 1.3-4.3) for women. Multivariable adjustment resulted in odds ratios of 2.0 (95% CI, 1.2-3.1) for men and 1.7 (95% CI, 0.9-3.1) for women. Nonpremature parental cardiovascular disease and parental coronary disease were weaker predictors. Addition of parental information aided in discriminating event rates, notably among offspring with intermediate levels of cholesterol and blood pressure, as well as intermediate predicted multivariable risk.\n\nCONCLUSIONS:\nUsing validated events, we found that parental cardiovascular disease independently predicted future offspring events in middle-aged adults. Addition of parental information may help clinicians and patients with primary prevention of cardiovascular disease, when treatment decisions may be difficult in patients at intermediate risk based on levels of single or multiple risk factors. These data also support further research into genetic determinants of cardiovascular risk." + }, + "questions": [ + { + "id": "e180bfce-0058-4b09-b5f6-51ea64af0887", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1160, + "text": "those with at least 1 parent with premature cardiovascular disease (onset age \u003c55 years in father, \u003c65 years in mother)" + } + ] + } + ] +} \ No newline at end of file diff --git a/ce583409-108a-4d5f-81a1-a4abcc732736.json b/ce583409-108a-4d5f-81a1-a4abcc732736.json new file mode 100644 index 0000000000000000000000000000000000000000..d9155164ce15e16ee4a06e44357b0390c2c21895 --- /dev/null +++ b/ce583409-108a-4d5f-81a1-a4abcc732736.json @@ -0,0 +1,35 @@ +{ + "id": "ce583409-108a-4d5f-81a1-a4abcc732736", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "7742406", + "text": "Some studies indicate that children born to younger mothers are at higher risk for wheezing or asthma. I conducted a case-control study that included 457 new cases of asthma in 3- and 4-year-old children and an equal number of controls. I found that, in comparison with children of mothers 30 years of age or older, children of mothers age 26-30 years had an adjusted odd ratio (OR) of 1.16 [95% confidence interval (CI) = 0.73-1.85] of developing asthma; children of mothers between 21 and 25 years of age had an OR of 1.25 (95% CI = 0.76-2.07), and those whose mothers were 20 years of age or younger had an OR of 3.48 (95% CI = 1.08-11.22)." + }, + "questions": [ + { + "id": "dfa992f7-3511-4b7e-be72-c968317ecbe9", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 551, + "text": "those whose mothers were 20 years of age or younger" + } + ] + } + ] +} \ No newline at end of file diff --git a/ce98c566-916e-4a3d-8d17-1b2dd4508581.json b/ce98c566-916e-4a3d-8d17-1b2dd4508581.json new file mode 100644 index 0000000000000000000000000000000000000000..9ee7e8891926a27a3834a7eb68903d68985b17f6 --- /dev/null +++ b/ce98c566-916e-4a3d-8d17-1b2dd4508581.json @@ -0,0 +1,38 @@ +{ + "id": "ce98c566-916e-4a3d-8d17-1b2dd4508581", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "22956590", + "text": "OBJECTIVE:\nTo estimate the risk of breast cancer associated with diagnostic radiation in carriers of BRCA1/2 mutations.\n\nDESIGN:\nRetrospective cohort study (GENE-RAD-RISK).\n\nSETTING:\nThree nationwide studies (GENEPSO, EMBRACE, HEBON) in France, United Kingdom, and the Netherlands,\n\nPARTICIPANTS:\n1993 female carriers of BRCA1/2 mutations recruited in 2006-09.\n\nMAIN OUTCOME MEASURE:\nRisk of breast cancer estimated with a weighted Cox proportional hazards model with a time dependent individually estimated cumulative breast dose, based on nominal estimates of organ dose and frequency of self reported diagnostic procedures. To correct for potential survival bias, the analysis excluded carriers who were diagnosed more than five years before completion of the study questionnaire.\n\nRESULTS:\nIn carriers of BRCA1/2 mutations any exposure to diagnostic radiation before the age of 30 was associated with an increased risk of breast cancer (hazard ratio 1.90, 95% confidence interval 1.20 to 3.00), with a dose-response pattern. The risks by quarter of estimated cumulative dose \u003c0.0020 Gy, ≥ 0.0020-0.0065 Gy, ≥ 0.0066-0.0173 Gy, and ≥ 0.0174 Gy were 1.63 (0.96 to 2.77), 1.78 (0.88 to 3.58), 1.75 (0.72 to 4.25), and 3.84 (1.67 to 8.79), respectively. Analyses on the different types of diagnostic procedures showed a pattern of increasing risk with increasing number of radiographs before age 20 and before age 30 compared with no exposure. A history of mammography before age 30 was also associated with an increased risk of breast cancer (hazard ratio 1.43, 0.85 to 2.40). Sensitivity analysis showed that this finding was not caused by confounding by indication of family history.\n\nCONCLUSION:\nIn this large European study among carriers of BRCA1/2 mutations, exposure to diagnostic radiation before age 30 was associated with an increased risk of breast cancer at dose levels considerably lower than those at which increases have been found in other cohorts exposed to radiation. The results of this study support the use of non-ionising radiation imaging techniques (such as magnetic resonance imaging) as the main tool for surveillance in young women with BRCA1/2 mutations." + }, + "questions": [ + { + "id": "bf18c1bb-1ea6-47ec-acd6-8c66c282e3a4", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 794, + "text": "In carriers of BRCA1/2 mutations any exposure to diagnostic radiation before the age of 30" + }, + { + "answer_start": 1766, + "text": "exposure to diagnostic radiation before age 30" + } + ] + } + ] +} \ No newline at end of file diff --git a/cea6ba6d-0e90-4405-91b6-baf350248247.json b/cea6ba6d-0e90-4405-91b6-baf350248247.json new file mode 100644 index 0000000000000000000000000000000000000000..896059652129d1244e35ecd953adb227806bcb0d --- /dev/null +++ b/cea6ba6d-0e90-4405-91b6-baf350248247.json @@ -0,0 +1,55 @@ +{ + "id": "cea6ba6d-0e90-4405-91b6-baf350248247", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "22700840", + "text": "An association between preterm birth and an increased risk of childhood asthma has been demonstrated, but the importance of intrauterine growth retardation on asthma risk is unclear. Using data from Swedish health registers, infant characteristics and childhood asthma were studied. Analyses were made using Mantel-Haenszel methodology with adjustment for year of birth, maternal age, parity, smoking in early pregnancy and maternal body mass index. Preterm birth, birth weight and birth weight for gestational week were analysed and childhood asthma was evaluated from prescriptions of anti-asthmatic drugs. Neonatal respiratory problems and treatment for them were studied as mediating factors. Both short gestational duration and intrauterine growth retardation appeared to be risk factors and seemed to act separately. The largest effect was seen from short gestational duration. Use of mechanical ventilation in the newborn period and bronchopulmonary dysplasia were strong risk factors. A moderately increased risk was also seen in infants born large for gestational age. We conclude that preterm birth is a stronger risk factor for childhood asthma than intrauterine growth disturbances; however, the latter also affects the risk, and is also seen in infants born at term." + }, + "questions": [ + { + "id": "5a0581c2-1360-47d7-83eb-0d7f2a328a0f", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 702, + "text": "short gestational duration" + }, + { + "answer_start": 733, + "text": "intrauterine growth retardation" + }, + { + "answer_start": 884, + "text": "Use of mechanical ventilation in the newborn period" + }, + { + "answer_start": 940, + "text": "bronchopulmonary dysplasia" + }, + { + "answer_start": 1038, + "text": "infants born large for gestational age" + }, + { + "answer_start": 1095, + "text": "preterm birth" + } + ] + } + ] +} \ No newline at end of file diff --git a/cf4ef58d-9915-465b-b00a-7f7925899c66.json b/cf4ef58d-9915-465b-b00a-7f7925899c66.json new file mode 100644 index 0000000000000000000000000000000000000000..41246dfaaccba83c241b98a6f1e1f6420ea535d5 --- /dev/null +++ b/cf4ef58d-9915-465b-b00a-7f7925899c66.json @@ -0,0 +1,39 @@ +{ + "id": "cf4ef58d-9915-465b-b00a-7f7925899c66", + "disease": { + "id": "H00056", + "names": [ + "Alzheimer disease", + "Dementia due to Alzheimer disease" + ], + "dbLinks": { + "icd10": [ + "G30" + ], + "mesh": [ + "D000544" + ] + }, + "category": "Neurodegenerative disease" + }, + "article": { + "id": "18779424", + "text": "OBJECTIVE:\nTo determine if baseline measurements of cerebral atrophy and severity of white matter hyperintensity (WMH) predict the rate of future cognitive decline in patients with Alzheimer disease (AD).\n\nDESIGN:\nData were drawn from the Predictors Study, a longitudinal study that enrolls patients with mild AD and reassesses them every 6 months with use of the Columbia modified Mini-Mental State (mMMS) examination (score range, 0-57). Magnetic resonance images were analyzed to determine the severity of WMH, using the Scheltens scale, and the degree of atrophy, using the bicaudate ratio. Generalized estimating equations were used to determine whether severity of baseline magnetic resonance image measurements and their interaction predicted the rate of mMMS score decline at subsequent visits.\n\nSETTING:\nThree university-based AD centers in the United States.\n\nPARTICIPANTS:\nAt baseline, 84 patients with AD from the Predictors Study received structural magnetic resonance imaging and were selected for analysis. They had a mean of 6 follow-up evaluations. Main Outcome Measure The mMMS score.\n\nRESULTS:\nGeneralized estimating equation models demonstrated that the degree of baseline atrophy (beta = -0.316; P = .04), the severity of WMH (beta = -0.173; P = .03), and their interaction (beta = -6.061; P = .02) predicted the rate of decline in mMMS scores.\n\nCONCLUSIONS:\nBoth degree of cerebral atrophy and severity of WMH are associated with the rapidity of cognitive decline in AD. Atrophy and WMH may have a synergistic effect on future decline in AD, such that patients with a high degree of both have a particularly precipitous cognitive course. These findings lend further support to the hypothesis that cerebrovascular pathological abnormalities contribute to the clinical syndrome of AD." + }, + "questions": [ + { + "id": "13f8b777-c746-4e67-93d2-3100380b7fea", + "text": "What are the risk factors of Alzheimer disease?", + "answers": [ + { + "answer_start": 1385, + "text": "degree of cerebral atrophy" + }, + { + "answer_start": 1416, + "text": "severity of WMH" + } + ] + } + ] +} \ No newline at end of file diff --git a/cf72dfbe-5b74-43cb-b10a-7205c30264e2.json b/cf72dfbe-5b74-43cb-b10a-7205c30264e2.json new file mode 100644 index 0000000000000000000000000000000000000000..c67fc498f16a2801ff8e4dfadf0c7360e1a8acb5 --- /dev/null +++ b/cf72dfbe-5b74-43cb-b10a-7205c30264e2.json @@ -0,0 +1,42 @@ +{ + "id": "cf72dfbe-5b74-43cb-b10a-7205c30264e2", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "16626308", + "text": "OBJECTIVE:\nTo determine if bladder cancer diagnosed after prostatic radiation therapy (RT) differs in behaviour from bladder cancer diagnosed after prostate cancer not treated with RT, as such bladder cancer is thought to be more aggressive than de novo bladder cancer, and epidemiological studies show a higher rate of bladder cancer in patients after irradiation.\n\nPATIENTS AND METHODS:\nWe reviewed our records to identify patients who had a diagnosis of bladder cancer with a previous diagnosis of prostate cancer. Patient age, date of diagnosis of prostate cancer, date of diagnosis of bladder cancer, symptoms, clinical stage, initial pathology, definitive therapy, definitive pathological stage, and disease status were recorded.\n\nRESULTS:\nIn all, 100 patients were identified who had a diagnosis of bladder cancer after a diagnosis of prostate cancer between January 1992 and August 2003; 58 had had RT for prostate cancer. The mean time between a diagnosis of bladder cancer and prostate cancer was 62 months in the RT group and 34 months in the unirradiated group (P = 0.002) At diagnosis of bladder cancer, 56 (97%) of the patients who received RT had high-grade urothelial carcinoma, vs 27 (64%) of those not irradiated (P \u003c 0.001). Thirty (52%) of the patients with RT had muscle-invasive bladder cancer, vs 17 (40%) of those not irradiated (P = 0.3). The survival rate was similar for both groups.\n\nCONCLUSIONS:\nBladder cancer is diagnosed later, and is of higher grade, in patients who are irradiated for prostate cancer than in those treated with other methods. Patients with prostate cancer who are treated with RT should be monitored closely for the presence of bladder cancer." + }, + "questions": [ + { + "id": "2907fb33-bb49-4c23-bbca-9fae72e1b57b", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 1487, + "text": "patients who are irradiated for prostate cancer" + }, + { + "answer_start": 1577, + "text": "Patients with prostate cancer who are treated with RT" + }, + { + "answer_start": 1133, + "text": "patients who received RT had high-grade urothelial carcinoma" + } + ] + } + ] +} \ No newline at end of file diff --git a/cff369cf-1b42-4b80-852e-73893ac23f76.json b/cff369cf-1b42-4b80-852e-73893ac23f76.json new file mode 100644 index 0000000000000000000000000000000000000000..e218c91c4eaafa7d15a6be30fd1e58bc661c61d5 --- /dev/null +++ b/cff369cf-1b42-4b80-852e-73893ac23f76.json @@ -0,0 +1,34 @@ +{ + "id": "cff369cf-1b42-4b80-852e-73893ac23f76", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "21474041", + "text": "OBJECTIVES:\nThe purpose of this study was to determine the association between fitness and lifetime risk for cardiovascular disease (CVD).\n\nBACKGROUND:\nHigher levels of traditional risk factors are associated with marked differences in lifetime risks for CVD. However, data are sparse regarding the association between fitness and the lifetime risk for CVD.\n\nMETHODS:\nWe followed up 11,049 men who underwent clinical examination at the Cooper Institute in Dallas, Texas, before 1990 until the occurrence of CVD death, non-CVD death, or attainment of age 90 years (281,469 person-years of follow-up, median follow-up 25.3 years, 1,106 CVD deaths). Fitness was measured by the Balke protocol and categorized according to treadmill time into low, moderate, and high fitness, with further stratification by CVD risk factor burden. Lifetime risk for CVD death determined by the National Death Index was estimated for fitness levels measured at ages 45, 55, and 65 years, with non-CVD death as the competing event.\n\nRESULTS:\nDifferences in fitness levels (low fitness vs. high fitness) were associated with marked differences in the lifetime risks for CVD death at each index age: age 45 years, 13.7% versus 3.4%; age 55 years, 34.2% versus 15.3%; and age 65 years, 35.6% versus 17.1%. These associations were strongest among persons with CVD risk factors.\n\nCONCLUSIONS:\nA single measurement of low fitness in mid-life was associated with higher lifetime risk for CVD death, particularly among persons with a high burden of CVD risk factors." + }, + "questions": [ + { + "id": "3bb656bc-869c-472d-86ca-1a9130b70c83", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1365, + "text": "A single measurement of low fitness in mid-life" + } + ] + } + ] +} \ No newline at end of file diff --git a/d0090833-30cf-4abb-a106-b146322defe7.json b/d0090833-30cf-4abb-a106-b146322defe7.json new file mode 100644 index 0000000000000000000000000000000000000000..0ba62aa01469e0b2fd445d8ffe30753e7a469707 --- /dev/null +++ b/d0090833-30cf-4abb-a106-b146322defe7.json @@ -0,0 +1,39 @@ +{ + "id": "d0090833-30cf-4abb-a106-b146322defe7", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "9739976", + "text": "CONTEXT:\nCancer registries have reported an increased incidence of melanoma and certain noncutaneous cancers following nonmelanoma skin cancer (NMSC). Whether these findings were attributable to intensified surveillance, shared risk factors, or increased cancer susceptibility remains unclear.\n\nOBJECTIVE:\nTo determine whether a history of NMSC predicts cancer mortality.\n\nDESIGN:\nProspective cohort with 12-year mortality follow-up adjusted for multiple risk factors.\n\nSETTING:\nCancer Prevention Study II, United States and Puerto Rico.\n\nPARTICIPANTS:\nNearly 1.1 million adult volunteers who completed a baseline questionnaire in 1982.\n\nMAIN OUTCOME MEASURE:\nDeaths due to all cancers and common cancers.\n\nRESULTS:\nAfter adjusting for age, race, education, smoking, obesity, alcohol use, and other conventional risk factors, a baseline history of NMSC was associated with increased total cancer mortality (men's relative risk [RR], 1.30; 95% confidence interval [CI], 1.23-1.36; women's RR, 1.26; 95% CI, 1.17-1.35). Exclusion of deaths due to melanoma reduced these RRs only slightly. Mortality was increased for the following cancers: melanoma (RR, 3.36 in men, 3.52 in women); pharynx (RR, 2.77 in men, 2.81 in women); lung (RR, 1.37 in men, 1.46 in women); non-Hodgkin lymphoma (RR, 1.32 in men, 1.50 in women); in men only, salivary glands (RR, 2.96), prostate (RR, 1.28), testis (RR, 12.7), urinary bladder (RR, 1.41), and leukemia (RR, 1.37); and in women only, breast (RR, 1.34). All-cause mortality was slightly increased (adjusted men's RR, 1.03 [95% CI, 1.00-1.06]; women's RR, 1.04 [95% CI, 1.00-1.09]).\n\nCONCLUSIONS:\nPersons with a history of NMSC are at increased risk of cancer mortality. Although the biological mechanisms are unknown, a history of NMSC should increase the clinician's alertness for certain noncutaneous cancers as well as melanoma." + }, + "questions": [ + { + "id": "3aa1eb8f-0b04-4e6e-807c-4f7e7d709da6", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 118, + "text": " nonmelanoma skin cancer (NMSC)" + }, + { + "answer_start": 828, + "text": "baseline history of NMSC" + } + ] + } + ] +} \ No newline at end of file diff --git a/d0da6110-14a2-4961-ada8-fc3241330309.json b/d0da6110-14a2-4961-ada8-fc3241330309.json new file mode 100644 index 0000000000000000000000000000000000000000..bf41028320f76b1ad0774c77502e934eb1c21960 --- /dev/null +++ b/d0da6110-14a2-4961-ada8-fc3241330309.json @@ -0,0 +1,38 @@ +{ + "id": "d0da6110-14a2-4961-ada8-fc3241330309", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "16527694", + "text": "BACKGROUND \u0026 AIMS:\nCeliac disease (CD) is a common gluten-sensitive enteropathy associated with human leukocyte antigen (HLA)-DQ2 and HLA-DQ8. The aim of this study was to determine if a particular HLA-DQ subtype predisposes to complications such as refractory CD with (RCD II) or without aberrant T cells (RCD I), and enteropathy-associated T-cell lymphomas (EATL).\n\nMETHODS:\nMolecular HLA-DQ typing was performed on 43 RCD I, 43 RCD II, and 30 EATL patients, and compared with age-matched groups of 121 patients with histologically defined uncomplicated CD and 183 healthy controls. All individuals were Dutch Caucasians and were at least 21 years of age.\n\nRESULTS:\nHLA-DQ2 was present in 79% of RCD I, 97.7% of RCD II, and 96.6% of EATL patients. The differences were significant when compared with 28.9% in controls but not with 91.7% in uncomplicated CD. Homozygosity for HLA-DQ2 was observed in 25.5% of RCD I, 44.1% of RCD II, and 53.3% of EATL patients vs 20.7% of uncomplicated CD patients and 2.1% of controls. HLA-DQ8 was present in 10.7% of CD, 16.2% of RCD I, 9.3% of RCD II, and 6.6% of EATL patients vs 20.2% of controls.\n\nCONCLUSIONS:\nHomozygosity for HLA-DQ2 is associated with RCD II and EATL. Early identification of HLA-DQ2 homozygous CD patients may help to recognize CD patients at risk for developing these severe complications." + }, + "questions": [ + { + "id": "7161fefe-4885-4d64-b59b-ea8f35adc960", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 668, + "text": "HLA-DQ2" + }, + { + "answer_start": 860, + "text": "Homozygosity for HLA-DQ2" + } + ] + } + ] +} \ No newline at end of file diff --git a/d12eb338-33e6-4df0-a274-7cc2c9f581ea.json b/d12eb338-33e6-4df0-a274-7cc2c9f581ea.json new file mode 100644 index 0000000000000000000000000000000000000000..01cb4e7fb5a9ab0ee87ff43c573b469ef470c4a3 --- /dev/null +++ b/d12eb338-33e6-4df0-a274-7cc2c9f581ea.json @@ -0,0 +1,43 @@ +{ + "id": "d12eb338-33e6-4df0-a274-7cc2c9f581ea", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "15814575", + "text": "OBJECTIVE:\nRheumatoid arthritis (RA) has a complex and multifactorial aetiology. Infectious agents could start this disease. The majority of the characteristics of this infirmity can be observed in chronic arthritis produced by mycoplasmas in animals. In this study the association between Mycoplasma pneumoniae and RA has been evaluated.\n\nMETHODS:\nA case-control study was performed. Sera taken from 78 RA patients and from 156 controls were analysed to ascertain the levels of immunoglobulin G (IgG) against M. pneumoniae. Other variables, like age, gender, work status, history of pneumonia, etc., were recorded in a questionnaire.\n\nRESULTS:\nThe presence of antibodies against M. pneumoniae was associated with RA (odds ratio=2.34, P\u003c0.001).\n\nCONCLUSIONS:\nThe results suggest that M. pneumoniae could be a cofactor in the pathogenesis of RA; however, more studies need to be done." + }, + "questions": [ + { + "id": "b8ec5d27-c5bf-4e47-8e5b-e0ed9940586f", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 661, + "text": "antibodies against M. pneumoniae" + }, + { + "answer_start": 290, + "text": "Mycoplasma pneumoniae" + }, + { + "answer_start": 784, + "text": "M. pneumoniae" + } + ] + } + ] +} \ No newline at end of file diff --git a/d153d030-c91f-4d43-ae48-b9448448ad98.json b/d153d030-c91f-4d43-ae48-b9448448ad98.json new file mode 100644 index 0000000000000000000000000000000000000000..1cc3f0b8a675ecd4aed8338da8967151a268d364 --- /dev/null +++ b/d153d030-c91f-4d43-ae48-b9448448ad98.json @@ -0,0 +1,46 @@ +{ + "id": "d153d030-c91f-4d43-ae48-b9448448ad98", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "24101761", + "text": "OBJECTIVES:\nTiming of gluten introduction has been associated with the risk of celiac disease (CD) in children, but the optimal time window is unknown. We aimed to study the effect of age of gluten introduction on the risk of CD, adjusting for continued breastfeeding.\n\nMETHODS:\nIn The Norwegian Mother and Child Cohort Study, a prospective birth cohort including 107,000 children, CD was identified by questionnaires and by linkage to the Norwegian Patient Register. Gluten introduction was reported monthly from 0 to 6 months of age, and breastfeeding from 0 to 18 months.\n\nRESULTS:\nAfter exclusion of cases with insufficient information, 324 children with CD in a cohort of 82,167 were used in the analyses. Gluten was introduced before or at 4 months in 8.0%, 5 to 6 months in 45.3%, and after 6 months in 46.6%, whereas continued breastfeeding was stable at ≈ 78% at 6 months age. CD was diagnosed in 3.68/1000 of the infants with gluten introduction at 5 to 6 months compared with 4.15/1000 with late and 4.24/1000 with early gluten introduction. After adjustment for the child's age and gender, breastfeeding, and maternal CD, delayed gluten introduction was associated with an increased risk of CD (adjusted odds ratio, 1.27 [95% confidence interval, 1.01-1.65], P = .045). Breastfeeding \u003e12 months was also associated with increased risk (adjusted odds ratio, 1.49 [95% confidence interval, 1.01-2.21], P = .046).\n\nCONCLUSIONS:\nWe found an increased risk of CD in children introduced to gluten after 6 months and a higher risk in children breastfed after 12 months age." + }, + "questions": [ + { + "id": "f7398ed5-9b75-459a-b14f-e8a64a25dcdb", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 1473, + "text": "children introduced to gluten after 6 months" + }, + { + "answer_start": 1539, + "text": "children breastfed after 12 months age" + }, + { + "answer_start": 1134, + "text": "delayed gluten introduction" + }, + { + "answer_start": 1282, + "text": "Breastfeeding \u003e12 months" + } + ] + } + ] +} \ No newline at end of file diff --git a/d1716498-9fe8-492d-940e-bfcb17c15839.json b/d1716498-9fe8-492d-940e-bfcb17c15839.json new file mode 100644 index 0000000000000000000000000000000000000000..1d6f650af15157f2498dd2634f956f04668c5326 --- /dev/null +++ b/d1716498-9fe8-492d-940e-bfcb17c15839.json @@ -0,0 +1,42 @@ +{ + "id": "d1716498-9fe8-492d-940e-bfcb17c15839", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "23620057", + "text": "AIMS/HYPOTHESIS:\nConsumption of sugar-sweetened beverages has been shown, largely in American populations, to increase type 2 diabetes incidence. We aimed to evaluate the association of consumption of sweet beverages (juices and nectars, sugar-sweetened soft drinks and artificially sweetened soft drinks) with type 2 diabetes incidence in European adults.\n\nMETHODS:\nWe established a case-cohort study including 12,403 incident type 2 diabetes cases and a stratified subcohort of 16,154 participants selected from eight European cohorts participating in the European Prospective Investigation into Cancer and Nutrition (EPIC) study. After exclusions, the final sample size included 11,684 incident cases and a subcohort of 15,374 participants. Cox proportional hazards regression models (modified for the case-cohort design) and random-effects meta-analyses were used to estimate the association between sweet beverage consumption (obtained from validated dietary questionnaires) and type 2 diabetes incidence.\n\nRESULTS:\nIn adjusted models, one 336 g (12 oz) daily increment in sugar-sweetened and artificially sweetened soft drink consumption was associated with HRs for type 2 diabetes of 1.22 (95% CI 1.09, 1.38) and 1.52 (95% CI 1.26, 1.83), respectively. After further adjustment for energy intake and BMI, the association of sugar-sweetened soft drinks with type 2 diabetes persisted (HR 1.18, 95% CI 1.06, 1.32), but the association of artificially sweetened soft drinks became statistically not significant (HR 1.11, 95% CI 0.95, 1.31). Juice and nectar consumption was not associated with type 2 diabetes incidence.\n\nCONCLUSIONS/INTERPRETATION:\nThis study corroborates the association between increased incidence of type 2 diabetes and high consumption of sugar-sweetened soft drinks in European adults." + }, + "questions": [ + { + "id": "7514c366-645a-40e4-b9f1-2a5f79fd31ee", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1041, + "text": "one 336 g (12 oz) daily increment in sugar-sweetened and artificially sweetened soft drink consumption" + }, + { + "answer_start": 1331, + "text": "sugar-sweetened soft drinks" + }, + { + "answer_start": 1745, + "text": "high consumption of sugar-sweetened soft drinks in European adults" + } + ] + } + ] +} \ No newline at end of file diff --git a/d1b422c6-202c-42d3-8b8d-16d4920976d2.json b/d1b422c6-202c-42d3-8b8d-16d4920976d2.json new file mode 100644 index 0000000000000000000000000000000000000000..fbc680b3349450cc72cd55ea499828426ff44f84 --- /dev/null +++ b/d1b422c6-202c-42d3-8b8d-16d4920976d2.json @@ -0,0 +1,46 @@ +{ + "id": "d1b422c6-202c-42d3-8b8d-16d4920976d2", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "11063954", + "text": "PURPOSE:\nTo determine the association between cigarette smoking and the incidence of type 2 diabetes mellitus.\n\nSUBJECTS AND METHODS:\nWe studied 21,068 US male physicians aged 40 to 84 years in the Physicians' Health Study who were initially free of diagnosed diabetes mellitus, cardiovascular disease, and cancer. Information about cigarette smoking and other risk indicators was obtained at baseline. The primary outcome was reported diagnosis of type 2 diabetes mellitus.\n\nRESULTS:\nDuring 255,830 person-years of follow-up, 770 new cases of type 2 diabetes mellitus were identified. Smokers had a dose-dependent increased risk of developing type 2 diabetes mellitus: compared with never smokers, the age-adjusted relative risk was 2.1 (95% confidence interval [CI]: 1.7 to 2.6) for current smokers of \u003e or = 20 cigarettes per day, 1.4 (95% CI: 1.0 to 2.0) for current smokers of \u003c20 cigarettes per day, and 1.2 (95% CI: 1.0 to 1.4) for past smokers. After multivariate adjustment for body mass index, physical activity, and other risk factors, the relative risks were 1.7 (95% CI: 1.3 to 2.3) for current smokers of \u003e or = 20 cigarettes per day, 1.5 (95% CI: 1.0 to 2.2) for current smokers of \u003c20 cigarettes per day, and 1.1 (95% CI: 1.0 to 1.4) for past smokers. Total pack-years of cigarette smoking was also associated with the risk of type 2 diabetes mellitus (P for trend \u003c0.001).\n\nCONCLUSIONS:\nThese prospective data support the hypothesis that cigarette smoking is an independent and modifiable determinant of type 2 diabetes mellitus." + }, + "questions": [ + { + "id": "872cecc1-c4e7-43a1-b162-80f2489cf498", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 586, + "text": "Smokers" + }, + { + "answer_start": 786, + "text": "urrent smokers of \u003e or = 20 cigarettes per day" + }, + { + "answer_start": 863, + "text": "current smokers of \u003c20 cigarettes per day" + }, + { + "answer_start": 1455, + "text": "cigarette smoking" + } + ] + } + ] +} \ No newline at end of file diff --git a/d1e304fd-d568-49fa-89fa-d51a16626e6b.json b/d1e304fd-d568-49fa-89fa-d51a16626e6b.json new file mode 100644 index 0000000000000000000000000000000000000000..fc5e09a94d05c01da3aee603d40e25d4d86f9376 --- /dev/null +++ b/d1e304fd-d568-49fa-89fa-d51a16626e6b.json @@ -0,0 +1,39 @@ +{ + "id": "d1e304fd-d568-49fa-89fa-d51a16626e6b", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "28712803", + "text": "BACKGROUND:\nSevere and uncontrolled asthma during pregnancy has been linked to several unfavorable perinatal outcomes. However, current knowledge on the association between the severity and control of maternal asthma and offspring asthma is sparse.\n\nOBJECTIVE:\nWe sought to investigate the extent to which offspring asthma is influenced by maternal asthma severity and control during pregnancy.\n\nMETHODS:\nWe performed a prospective population-based cohort study. Using linkage of Danish national registers, we constructed a cohort of 675,379 singletons, of which 15,014 children were born to asthmatic mothers. Among them, 7,188 children were born to mothers with active asthma during pregnancy. We categorized mothers with active asthma into 4 groups based on dispensed antiasthma prescriptions and on use of medical services: mild controlled, mild uncontrolled, moderate-to-severe controlled, and moderate-to-severe uncontrolled asthma. The outcomes were offspring early-onset transient, early-onset persistent, and late-onset asthma. We estimated prevalence ratios (PRs) of each phenotype of asthma using a log-binomial model with 95% CIs.\n\nRESULTS:\nHigher prevalence of early-onset persistent asthma was observed among children of asthmatic mothers with mild uncontrolled (PR, 1.19; 95% CI, 1.05-1.35), moderate-to-severe controlled (PR, 1.33; 95% CI, 1.09-1.63), and moderate-to-severe uncontrolled asthma (PR, 1.37; 95% CI, 1.17-1.61) compared with those of mothers with mild controlled asthma. A borderline increased prevalence of early-onset transient asthma was observed among children of mothers with uncontrolled asthma.\n\nCONCLUSION:\nMaternal uncontrolled asthma increases the risk of early-onset persistent and transient asthma. If replicated, this could suggest that maintaining asthma control in pregnancy is an area for possible prevention of specific phenotypes of offspring asthma." + }, + "questions": [ + { + "id": "4649fd6f-a004-4615-9d8d-1a4461f0e440", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1223, + "text": "children of asthmatic mothers with mild uncontrolled (PR, 1.19; 95% CI, 1.05-1.35), moderate-to-severe controlled (PR, 1.33; 95% CI, 1.09-1.63), and moderate-to-severe uncontrolled asthma (PR, 1.37; 95% CI, 1.17-1.61)" + }, + { + "answer_start": 1645, + "text": "Maternal uncontrolled asthma" + } + ] + } + ] +} \ No newline at end of file diff --git a/d23e1bc3-1b57-4fb8-8013-ad69938d8615.json b/d23e1bc3-1b57-4fb8-8013-ad69938d8615.json new file mode 100644 index 0000000000000000000000000000000000000000..375ddcd85dca5965652b232eb97158e80f96e137 --- /dev/null +++ b/d23e1bc3-1b57-4fb8-8013-ad69938d8615.json @@ -0,0 +1,34 @@ +{ + "id": "d23e1bc3-1b57-4fb8-8013-ad69938d8615", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "8178795", + "text": "A modification of the model of Pike et al. (Nature 1983;303: 767-70) was applied to 91,523 women in the Nurses' Health Study who did not report prevalent cancer initially and who were followed for 14 years (1,212,855 person-years and 2,341 incident breast cancers). The model took into account current age, age at all births, age at menopause, and age at menarche in predicting the annual and cumulative incidence of breast cancer. The authors found that ages both at first birth and at subsequent births have long-term influence on breast cancer incidence. The incidence density for parous women was greater than for nulliparous women for 20-30 years after the time of the first birth. However, cumulative incidence up to age 70 years was about 20% lower, 10% lower, or 5% higher for parous versus nulliparous women if their first birth was at age 20, 25, or 35 years, respectively. The authors also observed a significantly lower incidence after each additional birth as well as after menopause for women of the same age. Overall, the effect of reproductive factors (other than age at menarche) appears to influence cumulative incidence to age 70 years by a maximum of approximately 50% when women with multiple births with an early age at first birth are compared with women with a single birth at a late age." + }, + "questions": [ + { + "id": "7bd66cb0-d1d6-4b02-ad67-eaf8bb0f96a1", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 584, + "text": "parous women" + } + ] + } + ] +} \ No newline at end of file diff --git a/d2c632ce-63ba-4864-870a-75351d6e4687.json b/d2c632ce-63ba-4864-870a-75351d6e4687.json new file mode 100644 index 0000000000000000000000000000000000000000..abefbe9f37c61a92aa5c88eea00106b350357581 --- /dev/null +++ b/d2c632ce-63ba-4864-870a-75351d6e4687.json @@ -0,0 +1,39 @@ +{ + "id": "d2c632ce-63ba-4864-870a-75351d6e4687", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "18980776", + "text": "BACKGROUND:\nEvidence from prospective studies consistently links obesity to asthma onset in white women, although there is controversy as to whether the association is causal. There are few data on this topic in black women, among whom the prevalence of obesity and asthma is high.\n\nOBJECTIVE:\nWe prospectively assessed the relation of body mass index (BMI) to asthma incidence in the Black Women's Health Study.\n\nMETHODS:\nWe followed 46,435 women from 1995 through 2005 with biennial mailed questionnaires. Cox regression models were used to estimate incidence rate ratios and 95% CIs.\n\nRESULTS:\nDuring 403,394 person-years of follow-up, 1068 participants reported physician-diagnosed asthma and concurrent use of asthma medication. Compared with women with BMIs of 20 to 24, the multivariate incidence rate ratios for higher categories of BMI increased from 1.26 (95% CI, 1.05-1.51) for BMIs of 25 to 29 to 2.85 (95% CI, 2.19-3.72) for BMIs of 40 or greater, with a significant trend. The association of BMI with asthma risk was consistent across strata of smoking status, age, presence of sleep apnea, parental history of asthma, BMI at age 18 years, and energy expenditure and intake.\n\nCONCLUSION:\nIn this large cohort of African American women, there was a positive association between BMI and asthma risk that was similar in magnitude to those observed in longitudinal studies of white women." + }, + "questions": [ + { + "id": "a265bf4f-a36e-4d46-8ab9-aa0a4ac8b92b", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1291, + "text": "BMI" + }, + { + "answer_start": 820, + "text": "higher categories of BMI" + } + ] + } + ] +} \ No newline at end of file diff --git a/d3eef280-ca38-4207-a162-4a0707f18def.json b/d3eef280-ca38-4207-a162-4a0707f18def.json new file mode 100644 index 0000000000000000000000000000000000000000..6a6be8e129141d8e0a36123d0d2ec70ff4bdb5a1 --- /dev/null +++ b/d3eef280-ca38-4207-a162-4a0707f18def.json @@ -0,0 +1,38 @@ +{ + "id": "d3eef280-ca38-4207-a162-4a0707f18def", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "9920077", + "text": "Women with polycystic ovary syndrome (PCOS) are insulin resistant, have insulin secretory defects, and are at high risk for glucose intolerance. We performed this study to determine the prevalence of glucose intolerance and parameters associated with risk for this in PCOS women. Two-hundred and fifty-four PCOS women, aged 14-44 yr, were prospectively evaluated at 2 centers, 1 urban and ethnically diverse (n = 110) and 1 rural and ethnically homogeneous (n = 144). The rural PCOS women were compared to 80 control women of similar weight, ethnicity, and age. A 75-g oral glucose challenge was administered after a 3-day 300-g carbohydrate diet and an overnight fast with 0 and 2 h blood samples for glucose levels. Diabetes was categorized according to WHO criteria. The prevalence of glucose intolerance was 31.1% impaired glucose intolerance (IGT) and 7.5% diabetes. In nonobese PCOS women (body mass index, \u003c27 kg/m2), 10.3% IGT and 1.5% diabetes were found. The prevalence of glucose intolerance was significantly higher in PCOS vs. control women (chi2 = 7.0; P = 0.01; odds ratio = 2.76; 95% confidence interval = 1.23-6.57). Variables most associated with postchallenge glucose levels were fasting glucose levels (P \u003c 0.0001), PCOS status (P = 0.002), waist/hip ratio (P = 0.01), and body mass index (P = 0.021). The American Diabetes Association criteria applied to fasting glucose significantly underdiagnosed diabetes compared to the WHO criteria (3.2% vs. 7.5%; chi2 = 4.7; P = 0.046; odds ratio = 2.48; 95% confidence interval = 1.01-6.69). We conclude that 1) PCOS women are at significantly increased risk for IGT and type 2 diabetes mellitus at all weights and at a young age; 2) these prevalence rates are similar in 2 different populations of PCOS women, suggesting that PCOS may be a more important risk factor than ethnicity or race for glucose intolerance in young women; and 3) the American Diabetes Association diabetes diagnostic criteria failed to detect a significant number of PCOS women with diabetes by postchallenge glucose values." + }, + "questions": [ + { + "id": "c0032415-38df-4421-927c-e56db7db94c1", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 0, + "text": "Women with polycystic ovary syndrome (PCOS)" + }, + { + "answer_start": 1575, + "text": "PCOS women" + } + ] + } + ] +} \ No newline at end of file diff --git a/d47d57f5-5114-40ad-8ee0-2671d96ddfcb.json b/d47d57f5-5114-40ad-8ee0-2671d96ddfcb.json new file mode 100644 index 0000000000000000000000000000000000000000..1ec3c67de1a8649ecbbb81f322775e226bad4553 --- /dev/null +++ b/d47d57f5-5114-40ad-8ee0-2671d96ddfcb.json @@ -0,0 +1,43 @@ +{ + "id": "d47d57f5-5114-40ad-8ee0-2671d96ddfcb", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "10750668", + "text": "Ultraviolet B (UVB) radiation exposure increases the risk of skin cancer in whites. Motivated by indications that United States geographic variation of relative skin cancer risk in blacks approaches that in whites, we used Poisson regression to estimate the risk of skin cancer in blacks as a function of average annual surface-levels of UVB radiation, measured by Robertson-Berger meters. United States data were used on deaths in 506 state economic areas, 1970-1994, and on incident cases in the nine areas of the Surveillance, Epidemiology, and End Results Program, 1973-1994. For black males, the age-adjusted relative risk of mortality for a 50% increase in UVB radiation was significantly above one for malignant melanoma, 1970-1994 (1.16; 95% confidence interval, 1.02-1.32) and nearly so for nonmelanoma skin cancer, 1970-1981 (1.18; 95% confidence interval, 1.00-1.39), for which the time period was chosen to avoid AIDS-related deaths from Kaposi's sarcoma. However, for black females, the relative risk of mortality was not significantly elevated for either skin cancer, and, for both black males and females, the relative risk of incidence was not significantly elevated for melanoma in the period 1973-1994. Incidence data on nonmelanoma skin cancer were not available. Although the public health implication is uncertain because of the much lower absolute risk of skin cancer in blacks compared with whites, the findings suggest that sunlight exposure increases skin cancer risk in blacks." + }, + "questions": [ + { + "id": "5c8d703c-7f5c-40d6-a3c9-f9755534128c", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 1448, + "text": "sunlight exposure" + }, + { + "answer_start": 663, + "text": "UVB radiation" + }, + { + "answer_start": 0, + "text": "Ultraviolet B (UVB) radiation exposure" + } + ] + } + ] +} \ No newline at end of file diff --git a/d499544a-e3c3-4414-b017-ec3fb0e0d99e.json b/d499544a-e3c3-4414-b017-ec3fb0e0d99e.json new file mode 100644 index 0000000000000000000000000000000000000000..ff21e3c74876b1087acef8dfce26f53a7e439c59 --- /dev/null +++ b/d499544a-e3c3-4414-b017-ec3fb0e0d99e.json @@ -0,0 +1,39 @@ +{ + "id": "d499544a-e3c3-4414-b017-ec3fb0e0d99e", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "25769192", + "text": "BACKGROUND:\nPatients with melanoma in situ are at an increased risk of subsequent melanoma compared with the general population, but the risk of subsequent melanoma after initial melanoma in situ versus after initial invasive melanoma is not known.\n\nOBJECTIVE:\nWe sought to compare the risk of subsequent melanoma in the cohort whose first cancer was melanoma in situ to the risk in the cohort whose first cancer was invasive melanoma.\n\nMETHODS:\nIn this cohort study, we identified individuals whose first cancer was either melanoma in situ or invasive melanoma from the Surveillance, Epidemiology, and End Results (SEER) program between 1973 and 2011 and used Cox proportional hazards models for comparison.\n\nRESULTS:\nCompared with the invasive melanoma cohort, the melanoma in situ cohort was more likely to develop subsequent melanoma of any stage after 2 years, subsequent invasive melanoma after 10 years, and subsequent melanoma in situ at all the time points (P \u003c .001, P = .003, P \u003c .001, respectively).\n\nLIMITATIONS:\nUnderreporting of melanomas, particularly melanoma in situ cases, and missing cases of subsequent melanomas as a result of patient migration from the SEER registry areas could affect results.\n\nCONCLUSION:\nGiven the increased long-term risk of subsequent melanoma in the melanoma in situ cohort, the patients with melanoma in situ diagnosis may benefit from a long-term surveillance for subsequent melanomas." + }, + "questions": [ + { + "id": "c9095517-1567-4b6e-abc1-0bd2cfb21a17", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 1325, + "text": "patients with melanoma in situ diagnosis" + }, + { + "answer_start": 767, + "text": "melanoma in situ" + } + ] + } + ] +} \ No newline at end of file diff --git a/d4ad3c7b-a887-4019-ad07-aacee26d7467.json b/d4ad3c7b-a887-4019-ad07-aacee26d7467.json new file mode 100644 index 0000000000000000000000000000000000000000..2ba8830d74e492650d5ae2a8a8a9682621ae2e81 --- /dev/null +++ b/d4ad3c7b-a887-4019-ad07-aacee26d7467.json @@ -0,0 +1,34 @@ +{ + "id": "d4ad3c7b-a887-4019-ad07-aacee26d7467", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "10990078", + "text": "AIMS/HYPOTHESIS:\nThe aim of this study was to determine the frequency and temporal development of antibodies related to celiac disease in offspring of parents with Type I (insulin-dependent) diabetes mellitus.\n\nMETHODS:\nSera from 913 offspring of parents with Type I diabetes prospectively followed from birth to the age of 8 years were tested for IgG-transglutaminase antibodies (IgG-tTGCAs), endomysial IgA antibodies (EMA) and gliadin antibodies.\n\nRESULTS:\nWe found tTGCAs in 32 (3.5%) of the 913 relatives. Prevalence was related to age and reached 6.5% at age 8 years. Endomysial IgA antibodies were detected in 44% of the relatives with tTGCAs and 0.6% of tTGCA negative relatives and were also most prevalent (5 %) in those aged 8 years. Both tTGCAs and EMAs were more frequent in relatives with the HLA DRB1*03 DQA1*0501 DQB1*02 haplotype (7.1% and 7.2%, respectively; p \u003c 0.005). Antigliadin antibodies were common in both tTGCA positive (42%) and negative (23%) relatives, did not show a relation with age and were less prevalent in relatives with HLA DR3 (p \u003c 0.05). There was no association between the presence of antibodies associated with celiac disease and islet autoantibodies in these relatives. Of the relatives 15 (1.6%) had tTGCAs plus EMAs. In two of these, anti-gliadin antibodies were detected before the detection of tTGCAs and EMAs at the age of 9 months whereas none of the remainder had any antibodies associated with celiac disease before age 2 years. In three there were no detectable antigliadin antibodies in any of the samples tested. Celiac disease without clinical symptoms was diagnosed in 9 of 12 by intestinal biopsy. CONCLUSION/INTERPRETATION. A statistically significant proportion of relatives of patients with Type I diabetes have celiac disease-associated autoimmunity and the silent form of celiac disease early in life. These relatives should, therefore, be considered for celiac antibody screening." + }, + "questions": [ + { + "id": "b9b41856-2d6d-4c7c-902f-eb0eda4ac309", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 1725, + "text": "relatives of patients with Type I diabetes" + } + ] + } + ] +} \ No newline at end of file diff --git a/d54b60ed-1d11-48aa-aece-0ef84b849914.json b/d54b60ed-1d11-48aa-aece-0ef84b849914.json new file mode 100644 index 0000000000000000000000000000000000000000..61b5a08c3f0508f5b7ad80edd427467dcc653e12 --- /dev/null +++ b/d54b60ed-1d11-48aa-aece-0ef84b849914.json @@ -0,0 +1,50 @@ +{ + "id": "d54b60ed-1d11-48aa-aece-0ef84b849914", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "2589303", + "text": "The association between classical cardiovascular risk factors, including diet, and the 25-year incidence of non-insulin-dependent diabetes mellitus was examined in 841 middle-aged men within the Zutphen Study. The incidence rate was 3.8/1,000 person-years. In univariate analyses, baseline measurements of subscapular and tricipital skinfold thicknesses, body mass index (weight (kg)/height (m)2), cigarette use, resting heart rate, and systolic blood pressure were significantly associated with diabetes incidence. In multivariate survival analyses also taking age, energy intake, and alcohol consumption into account, subscapular skinfold thickness, resting heart rate, and cigarette use were independently related to diabetes incidence. The effect of subscapular skinfold thickness was shown among subjects free of cardiovascular disease at baseline and during follow-up and among cases who developed cardiovascular disease. Cigarette smoking was an independent risk factor only in men who remained free of cardiovascular disease, while the effect of resting heart rate was stronger within incident cases of cardiovascular disease. No associations were found between dietary factors and diabetes incidence." + }, + "questions": [ + { + "id": "7bbdf8dc-037f-4462-8f09-36db0d79f6e2", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 306, + "text": "subscapular and tricipital skinfold thicknesses" + }, + { + "answer_start": 355, + "text": "body mass index (weight (kg)/height (m)2)" + }, + { + "answer_start": 398, + "text": "cigarette use" + }, + { + "answer_start": 413, + "text": "resting heart rate" + }, + { + "answer_start": 437, + "text": "systolic blood pressure" + } + ] + } + ] +} \ No newline at end of file diff --git a/d5a98391-e90b-4fa7-8811-c134ca6ab7c6.json b/d5a98391-e90b-4fa7-8811-c134ca6ab7c6.json new file mode 100644 index 0000000000000000000000000000000000000000..c677a9acfda6f506e1a9007df1b22450b223494a --- /dev/null +++ b/d5a98391-e90b-4fa7-8811-c134ca6ab7c6.json @@ -0,0 +1,38 @@ +{ + "id": "d5a98391-e90b-4fa7-8811-c134ca6ab7c6", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "21846855", + "text": "CONTEXT:\nPrevious studies indicate that the population attributable risk (PAR) of bladder cancer for tobacco smoking is 50% to 65% in men and 20% to 30% in women and that current cigarette smoking triples bladder cancer risk relative to never smoking. During the last 30 years, incidence rates have remained stable in the United States in men (123.8 per 100,000 person-years to 142.2 per 100,000 person-years) and women (32.5 per 100,000 person-years to 33.2 per 100,000 person-years); however, changing smoking prevalence and cigarette composition warrant revisiting risk estimates for smoking and bladder cancer.\n\nOBJECTIVE:\nTo evaluate the association between tobacco smoking and bladder cancer.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nMen (n = 281,394) and women (n = 186,134) of the National Institutes of Health-AARP (NIH-AARP) Diet and Health Study cohort completed a lifestyle questionnaire and were followed up between October 25, 1995, and December 31, 2006. Previous prospective cohort studies of smoking and incident bladder cancer were identified by systematic review and relative risks were estimated from fixed-effects models with heterogeneity assessed by the I(2) statistic.\n\nMAIN OUTCOME MEASURES:\nHazard ratios (HRs), PARs, and number needed to harm (NNH).\n\nRESULTS:\nDuring 4,518,941 person-years of follow-up, incident bladder cancer occurred in 3896 men (144.0 per 100,000 person-years) and 627 women (34.5 per 100,000 person-years). Former smokers (119.8 per 100,000 person-years; HR, 2.22; 95% confidence interval [CI], 2.03-2.44; NNH, 1250) and current smokers (177.3 per 100,000 person-years; HR, 4.06; 95% CI, 3.66-4.50; NNH, 727) had higher risks of bladder cancer than never smokers (39.8 per 100,000 person-years). In contrast, the summary risk estimate for current smoking in 7 previous studies (initiated between 1963 and 1987) was 2.94 (95% CI, 2.45-3.54; I(2) = 0.0%). The PAR for ever smoking in our study was 0.50 (95% CI, 0.45-0.54) in men and 0.52 (95% CI, 0.45-0.59) in women.\n\nCONCLUSION:\nCompared with a pooled estimate of US data from cohorts initiated between 1963 and 1987, relative risks for smoking in the more recent NIH-AARP Diet and Health Study cohort were higher, with PARs for women comparable with those for men." + }, + "questions": [ + { + "id": "8b0192c0-16da-4a8c-aa51-5fd5b9c853ee", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 1451, + "text": "Former smokers" + }, + { + "answer_start": 1565, + "text": "current smokers" + } + ] + } + ] +} \ No newline at end of file diff --git a/d5f07c99-7a6b-4003-9793-9160c5a8f04b.json b/d5f07c99-7a6b-4003-9793-9160c5a8f04b.json new file mode 100644 index 0000000000000000000000000000000000000000..40d3fe3d2e102f86ee9355f1cedca452e5883192 --- /dev/null +++ b/d5f07c99-7a6b-4003-9793-9160c5a8f04b.json @@ -0,0 +1,39 @@ +{ + "id": "d5f07c99-7a6b-4003-9793-9160c5a8f04b", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "15843455", + "text": "OBJECTIVE:\nTo study whether formal education and occupational class are associated with incidence of rheumatoid arthritis overall and with the incidence of the two major subgroups of rheumatoid arthritis-seropositive (RF+) and seronegative (RF-) disease.\n\nMETHODS:\n930 cases and 1126 controls participated in a population based case-control study using incident cases of rheumatoid arthritis, carried out in Sweden during the period May 1996 to June 2001. The relative risk (RR) of developing rheumatoid arthritis with 95% confidence interval (CI) was calculated for different levels of formal education compared with university degree and for different occupational classes compared with higher non-manual employees.\n\nSUBJECTS:\nwithout a university degree had an increased risk of rheumatoid arthritis compared with those with a university degree (RR = 1.4 (95% CI, 1.2 to 1.8)). For manual employees, assistant and intermediate non-manual employees together, the risk of developing rheumatoid arthritis was about 20% more than for non-manual employees. These increased risks were more pronounced for RF+ than for RF- rheumatoid arthritis and were mainly confined to women. Smoking could not of its own explain the observed associations between risk of rheumatoid arthritis in different socioeconomic groups in Sweden.\n\nCONCLUSIONS:\nThere was an association between high socioeconomic status and lower risk of rheumatoid arthritis in a population based investigation that was representative for the Swedish population. The study shows that as yet unexplained environmental or lifestyle factors, or both, influence the risk of rheumatoid arthritis, even in the relatively egalitarian Swedish society." + }, + "questions": [ + { + "id": "844688f2-d7e0-46ea-98c5-e233922e1c59", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 729, + "text": "without a university degree" + }, + { + "answer_start": 885, + "text": "manual employees, assistant and intermediate non-manual employees together" + } + ] + } + ] +} \ No newline at end of file diff --git a/d6324cb0-fd01-4fbc-b77b-30b123f7d9c4.json b/d6324cb0-fd01-4fbc-b77b-30b123f7d9c4.json new file mode 100644 index 0000000000000000000000000000000000000000..3d387a5840c39c207da68304f8c5f7e91436a85c --- /dev/null +++ b/d6324cb0-fd01-4fbc-b77b-30b123f7d9c4.json @@ -0,0 +1,39 @@ +{ + "id": "d6324cb0-fd01-4fbc-b77b-30b123f7d9c4", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "8664138", + "text": "The atypical mole syndrome (AMS) phenotype, characterised by a large number of common naevi as well as atypical naevi, has been described in families with a genetic susceptibility to melanoma. However, the importance of this phenotype for melanoma in the general population has not been conclusively determined. This study was designed to examine the types and distribution of naevi as well as the prevalence of the AMS phenotype in melanoma patients in England compared with controls. A total of 426 cutaneous melanoma cases (61% of all incident cases) aged 16-75 years were recruited between 1989 and 1993 from the north-east Thames region of the UK and 416 controls from the same age group were recruited over the same period and from the same region. Each subject answered a questionnaire covering demographic details, sun exposure history and other risk factors and underwent a skin examination with total body naevus count performed by a dermatologist. The AMS phenotype was defined using a scoring system. Atypical naevi gave the highest relative risk for cutaneous melanoma, with an odds ratio (OR) of 28.7 (P \u003c 0.0001) for four or more atypical naevi compared with none. Many common naevi were also an important risk factor: the OR for 100 or more naevi 2 mm or above in diameter compared with 0-4 naevi was 7.7 (P \u003c 0.0001). Melanoma was also associated with naevi on sun-exposed sites but also with naevi on non-sun-exposed sites such as the dorsum of the feet, buttocks and anterior scalp. Sixteen per cent of the cases had the AMS phenotype compared with 2% of the controls (OR 10.4, P \u003c 0.0001). The AMS phenotype was more common in males than females (P = 0.008). The odds ratio for the presence of the AMS phenotype was dependent on age, with an odds ratio of 16.1 (95% CI 4.6-57.5) for the presence of the AMS phenotype if aged less than 40 compared with an odds ratio of 6.9 (95% CI 2.9-16.6) if aged 40 or more. The AMS phenotype was strongly predictive of an increased risk of melanoma outside the familial context." + }, + "questions": [ + { + "id": "1e43d768-c810-49ce-94d5-fe888ebc82c0", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 1935, + "text": "AMS phenotype" + }, + { + "answer_start": 4, + "text": "atypical mole syndrome (AMS) phenotype" + } + ] + } + ] +} \ No newline at end of file diff --git a/d682bff4-7f46-4ce5-ba52-cd0d38b9b298.json b/d682bff4-7f46-4ce5-ba52-cd0d38b9b298.json new file mode 100644 index 0000000000000000000000000000000000000000..2671b1190212ac2c8d661fde847a20f06bd197e3 --- /dev/null +++ b/d682bff4-7f46-4ce5-ba52-cd0d38b9b298.json @@ -0,0 +1,43 @@ +{ + "id": "d682bff4-7f46-4ce5-ba52-cd0d38b9b298", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "19789839", + "text": "Although the risk for most cancers appears to be relatively low in patients with Parkinson's disease (PD), skin cancers and melanomas occur more frequently in the PD population as compared to controls. This article summarizes the findings of cohort studies on skin cancer in Parkinson's disease. Given that melanoma may precede use of L-dopa, the increased risk of melanoma for PD patients cannot be attributed to L-dopa. On the basis of these observations it may be reasonable to recommend that all patients with PD, whether treated with L-dopa or not, should undergo regular dermatological screening for neoplastic or pre-neoplastic skin lesions, especially melanoma." + }, + "questions": [ + { + "id": "7f52e09b-6c3d-4cb7-ac4d-972a701c9f7e", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 81, + "text": "Parkinson's disease (PD)" + }, + { + "answer_start": 378, + "text": "PD patients" + }, + { + "answer_start": 163, + "text": "PD population" + } + ] + } + ] +} \ No newline at end of file diff --git a/d70e21a4-76fc-45a2-9b5b-08adc9442e20.json b/d70e21a4-76fc-45a2-9b5b-08adc9442e20.json new file mode 100644 index 0000000000000000000000000000000000000000..4a78e824010d70cdf9e3f352365591fcaa125f83 --- /dev/null +++ b/d70e21a4-76fc-45a2-9b5b-08adc9442e20.json @@ -0,0 +1,39 @@ +{ + "id": "d70e21a4-76fc-45a2-9b5b-08adc9442e20", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "18579547", + "text": "Studies from the UK and USA suggest that frequent use of paracetamol (acetaminophen) may increase the risk of asthma, but data across Europe are lacking. As part of a multicentric case-control study organised by the Global Allergy and Asthma European Network (GA(2)LEN), it was examined whether or not frequent paracetamol use is associated with adult asthma across Europe. The network compared 521 cases with a diagnosis of asthma and reporting of asthma symptoms within the last 12 months with 507 controls with no diagnosis of asthma and no asthmatic symptoms within the last 12 months across 12 European centres. All cases and controls were selected from the same population, defined by age (20-45 yrs) and place of residence. In a random effects meta-analysis, weekly use of paracetamol, compared with less frequent use, was strongly positively associated with asthma after controlling for confounders. There was no evidence for heterogeneity across centres. No association was seen between use of other analgesics and asthma. These data add to the increasing and consistent epidemiological evidence implicating frequent paracetamol use in asthma in diverse populations." + }, + "questions": [ + { + "id": "76c8209c-4192-4e5f-903c-27bd97554293", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 766, + "text": "weekly use of paracetamol" + }, + { + "answer_start": 1117, + "text": "frequent paracetamol use" + } + ] + } + ] +} \ No newline at end of file diff --git a/d843a3b1-1703-4394-81aa-5b595375a7f0.json b/d843a3b1-1703-4394-81aa-5b595375a7f0.json new file mode 100644 index 0000000000000000000000000000000000000000..b4b936a1a64bb73119fdba8c54cf9d240d85d288 --- /dev/null +++ b/d843a3b1-1703-4394-81aa-5b595375a7f0.json @@ -0,0 +1,37 @@ +{ + "id": "d843a3b1-1703-4394-81aa-5b595375a7f0", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "21193451", + "text": "BACKGROUND:\nSurgical management of colon cancer for patients with Lynch syndrome who carry a mismatch repair (MMR) gene mutation is controversial. The decision to remove more or less of the colon involves the consideration of a relatively high risk of metachronous colorectal cancer (CRC) with the impact of more extensive surgery.\n\nOBJECTIVE:\nTo estimate and compare the risks of metachronous CRC for patients with Lynch syndrome undergoing either segmental or extensive (subtotal or total) resection for first colon cancer.\n\nDESIGN:\nRisk of metachronous CRC was estimated for 382 MMR gene mutation carriers (172 MLH1, 167 MSH2, 23 MSH6 and 20 PMS2) from the Colon Cancer Family Registry, who had surgery for their first colon cancer, using retrospective cohort analysis. Age-dependent cumulative risks of metachronous CRC were calculated using the Kaplan-Meier method. Risk factors for metachronous CRC were assessed by a Cox proportional hazards regression.\n\nRESULTS:\nNone of 50 subjects who had extensive colectomy was diagnosed with metachronous CRC (incidence rate 0.0; 95% CI 0.0 to 7.2 per 1000 person-years). Of 332 subjects who had segmental resections, 74 (22%) were diagnosed with metachronous CRC (incidence rate 23.6; 95% CI 18.8 to 29.7 per 1000 person-years). For those who had segmental resections, incidence was statistically higher than for those who had extensive surgery (P \u003c0.001). Cumulative risk of metachronous CRC was 16% (95% CI 10% to 25%) at 10 years, 41% (95% CI 30% to 52%) at 20 years and 62% (95% CI 50% to 77%) at 30 years after segmental colectomy. Risk of metachronous CRC reduced by 31% (95% CI 12% to 46%; p=0.002) for every 10 cm of bowel removed.\n\nCONCLUSIONS:\nPatients with Lynch syndrome with first colon cancer treated with more extensive colonic resection have a lower risk of metachronous CRC than those receiving less extensive surgery. This finding will better inform decision-making about the extent of primary surgical resection." + }, + "questions": [ + { + "id": "64ef03f6-b596-42d9-8a7a-3b47e9756a8d", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1701, + "text": "Patients with Lynch syndrome with first colon cancer treated with more extensive colonic resection" + } + ] + } + ] +} \ No newline at end of file diff --git a/d852b992-a8dd-41a9-b2ba-e982a05e590e.json b/d852b992-a8dd-41a9-b2ba-e982a05e590e.json new file mode 100644 index 0000000000000000000000000000000000000000..4cdd11427ef864941a43f0da0f4e39db982400a5 --- /dev/null +++ b/d852b992-a8dd-41a9-b2ba-e982a05e590e.json @@ -0,0 +1,35 @@ +{ + "id": "d852b992-a8dd-41a9-b2ba-e982a05e590e", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "20530047", + "text": "The impact of single exposures on asthma development is better understood than the effect of multiple exposures. The objective of the present study was to evaluate the effect of combined early exposure to dog allergen (Can-f1) plus indoor nitrogen dioxide (NO₂) or environmental tobacco smoke (ETS) on asthma and bronchial hyperreactivity (BHR) in a high-risk birth cohort. We also aimed to assess atopy's impact on the effects of these exposures. Peri-birth ETS exposure was measured using cord blood cotinine (CCot). During year 1, atopy, NO₂, Can-f1, and urinary cotinine (UCot) were measured. At 7 yrs of age, 380 children were assessed for asthma and BHR. Exposure effects were determined using stepwise multiple linear regression. Co-exposure to elevated Can-f1 and NO₂, or Can-f1 and ETS (CCot), increased risk for asthma, relative to having neither such exposure (OR 4.8 (95% CI 1.1-21.5) and 2.7 (1.1-7.1), respectively); similar risks resulted when substituting dog ownership for allergen. Atopy increased asthma and BHR risk associated with several exposures; notably, atopy with elevated UCot, relative to atopy without such exposure, increased risk of BHR (OR 3.1 (95% CI 1.1-8.6)). In a high-risk birth cohort, early co-exposure to Can-f1 and NO₂ or ETS increased the risk of incident asthma. Atopy increased the risk of asthma and BHR associated with ETS." + }, + "questions": [ + { + "id": "b123689a-9f10-42d8-9816-e7b1e6d30dd0", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1225, + "text": "early co-exposure to Can-f1 and NO₂ or ETS" + } + ] + } + ] +} \ No newline at end of file diff --git a/d860a9b0-8475-46e7-bcb6-bab19e0b14fc.json b/d860a9b0-8475-46e7-bcb6-bab19e0b14fc.json new file mode 100644 index 0000000000000000000000000000000000000000..903ccbc0e289b3d91cabfd98453cd8a6aafd26a6 --- /dev/null +++ b/d860a9b0-8475-46e7-bcb6-bab19e0b14fc.json @@ -0,0 +1,47 @@ +{ + "id": "d860a9b0-8475-46e7-bcb6-bab19e0b14fc", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "26426533", + "text": "BACKGROUND:\nThe risk of periodontitis (PD) is increased in the patient group of rheumatoid arthritis (RA). RA and PD also shared some pathological mechanism. The aim of this study is to investigate the risk of RA associated with PD exposure.\n\nMETHODS AND FINDINGS:\nThis study identified 3 mutually exclusive cohorts using the 1999-2010 Taiwanese National Health Insurance Research Database (NHIRD) to investigate the association between PD and the risk of incident RA. All patients with PD in 2000 were identified from the database of all enrollees as the PD cohort. From the representative database of 1,000,000 enrollees randomly selected in 2010 (LHID2010), individuals without any periodontal disease (PO) during 1999-2010 were selected as the non-PO cohort. Individuals who were not included in the non-PO cohort and received dental scaling (DS) no more than two times per year during 1999-2010 were selected as the DS cohort from LHID2010. Using cox proportional regression analysis, hazard ratios (HRs) with 95% confidence intervals (Cis) were calculated to quantify the association between PD exposure and RA development. In the three-group comparison using the non-PO cohort as reference, we found that the risk of RA was higher in the PD and DS cohorts (HRs, 1.89 and 1.43; 95% CIs, 1.56-2.29 and 1.09-1.87, respectively). For comparisons between two cohorts, the PD cohort had a higher risk of RA than the non-PO and DS cohorts (HRs, 1.91 and 1.35; 95% CIs, 1.57-2.30 and 1.09-1.67, respectively).\n\nCONCLUSION:\nPD was associated with an increased risk of RA development." + }, + "questions": [ + { + "id": "d091e539-2bf0-462b-b2e6-c510812d413c", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 1522, + "text": "PD" + }, + { + "answer_start": 24, + "text": "periodontitis (PD)" + }, + { + "answer_start": 1245, + "text": "PD " + }, + { + "answer_start": 1252, + "text": "DS" + } + ] + } + ] +} \ No newline at end of file diff --git a/d88e4cf3-3d5b-4f7d-8e07-a36bfc02a537.json b/d88e4cf3-3d5b-4f7d-8e07-a36bfc02a537.json new file mode 100644 index 0000000000000000000000000000000000000000..4f56b90a73ae4b43be06fda0021334548aa31bf9 --- /dev/null +++ b/d88e4cf3-3d5b-4f7d-8e07-a36bfc02a537.json @@ -0,0 +1,54 @@ +{ + "id": "d88e4cf3-3d5b-4f7d-8e07-a36bfc02a537", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "18666209", + "text": "BACKGROUND:\nThe Gail model has been commonly used to estimate a woman's risk of breast cancer within a certain time period. High bone mineral density (BMD) is also a significant risk factor for breast cancer, but it appears to play no role in the Gail model. The objective of the current study was to investigate whether hip BMD predicts postmenopausal breast cancer risk independently of the Gail score.\n\nMETHODS:\nIn this prospective study, 9941 postmenopausal women who had a baseline hip BMD and Gail score from the Women's Health Initiative were included in the analysis. Their average age was 63.0 +/- 7.4 years at baseline.\n\nRESULTS:\nAfter an average of 8.43 years of follow-up, 327 incident breast cancer cases were reported and adjudicated. In a multivariate Cox proportional hazards model, the hazards ratios (95% confidence interval [95% CI]) for incident breast cancer were 1.35 (95% CI, 1.05-1.73) for high Gail score (\u003eor=1.67%) and 1.25 (95% CI, 1.11-1.40) for each unit of increase in the total hip BMD T-score. Restricting the analysis to women with both BMD and a Gail score above the median, a sharp increase in incident breast cancer for women with the highest BMD and Gail scores was found (P \u003c .05).\n\nCONCLUSIONS:\nThe contribution of BMD to the prediction of incident postmenopausal breast cancer across the entire population was found to be independent of the Gail score. However, among women with both high BMD and a high Gail score, there appears to be an interaction between these 2 factors. These findings suggest that BMD and Gail score may be used together to better quantify the risk of breast cancer." + }, + "questions": [ + { + "id": "485dc71e-b683-4140-b5ff-e07c809b014f", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 914, + "text": "high Gail score (\u003eor=1.67%)" + }, + { + "answer_start": 975, + "text": "each unit of increase in the total hip BMD T-score" + }, + { + "answer_start": 1172, + "text": "highest BMD and Gail scores" + }, + { + "answer_start": 1425, + "text": "high BMD" + }, + { + "answer_start": 1440, + "text": "high Gail score" + }, + { + "answer_start": 124, + "text": "High bone mineral density (BMD)" + } + ] + } + ] +} \ No newline at end of file diff --git a/d9059abc-3349-450c-b302-1ef4cf76eb5c.json b/d9059abc-3349-450c-b302-1ef4cf76eb5c.json new file mode 100644 index 0000000000000000000000000000000000000000..e84524312b69c01e846a160cc4fea78d298b5240 --- /dev/null +++ b/d9059abc-3349-450c-b302-1ef4cf76eb5c.json @@ -0,0 +1,43 @@ +{ + "id": "d9059abc-3349-450c-b302-1ef4cf76eb5c", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "11897985", + "text": "BACKGROUND:\nFor many years, the association between asthma and rhinitis has primarily been attributed to a common allergic background. Recently, it has been suggested that asthma and rhinitis are associated in the absence of atopy. The nature of this association is not well known.\n\nOBJECTIVE:\nThe purpose of this study, which was performed in a large, longitudinal community population, was to determine the extent to which rhinitis is an independent risk factor for adult-onset asthma.\n\nMETHODS:\nWe carried out a nested case-control study from the longitudinal cohort of the Tucson Epidemiologic Study of Obstructive Lung Diseases. One hundred seventy-three incident patients with physician-confirmed asthma were compared with 2177 subjects who reported no asthma or shortness of breath with wheezing. Potential risk factors, including the presence of rhinitis, were assessed before the onset of asthma (patients) or before the last completed survey (control subjects).\n\nRESULTS:\nRhinitis was a significant risk factor for asthma (crude odds ratio, 4.13; 95% confidence interval, 2.88-5.92). After adjustment for years of follow-up, age, sex, atopic status, smoking status, and presence of chronic obstructive pulmonary disease, the magnitude of the association was reduced but still highly significant (adjusted odds ratio, 3.21; 95% confidence interval, 2.19-4.71). After stratification, rhinitis increased the risk of development of asthma by about 3 times both among atopic and nonatopic patients and by more than 5 times among patients in the highest IgE tertile. Patients with rhinitis with persistent and severe nasal symptoms and a personal history of physician-confirmed sinusitis had an additional increased risk of asthma development.\n\nCONCLUSION:\nWe conclude that rhinitis is a significant risk factor for adult-onset asthma in both atopic and nonatopic subjects. The nature of the association between rhinitis and asthma is open to interpretation." + }, + "questions": [ + { + "id": "e69f2294-e6ec-4fad-9c70-62b42989c948", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1392, + "text": "rhinitis" + }, + { + "answer_start": 982, + "text": "Rhinitis" + }, + { + "answer_start": 1571, + "text": "Patients with rhinitis with persistent and severe nasal symptoms and a personal history of physician-confirmed sinusitis" + } + ] + } + ] +} \ No newline at end of file diff --git a/d98a9673-2760-4fc7-9ab0-c0baafbbfadb.json b/d98a9673-2760-4fc7-9ab0-c0baafbbfadb.json new file mode 100644 index 0000000000000000000000000000000000000000..83f6a81f680ca19c5d2ed4085882cf55b466d13e --- /dev/null +++ b/d98a9673-2760-4fc7-9ab0-c0baafbbfadb.json @@ -0,0 +1,41 @@ +{ + "id": "d98a9673-2760-4fc7-9ab0-c0baafbbfadb", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "9663397", + "text": "Colon cancer has been associated with several nutrients and foods. The authors used data from a population-based study conducted in Northern California, Utah, and Minnesota to examine associations between dietary eating patterns and risk of developing colon cancer. Through factor analysis, detailed dietary intake data obtained from 1,993 cases (diagnosed in 1991-1994) and 2,410 controls were grouped into factors that were evaluated for relations with lifestyle characteristics and colon cancer risk. Several dietary patterns emerged. The dietary patterns with the most variation were labeled \"Western,\" \"prudent,\" \"high fat/sugar dairy,\" \"substituters,\" and \"drinkers.\" The \"Western\" dietary pattern was associated with a higher body mass index and a greater intake of total energy and dietary cholesterol. The \"prudent\" pattern was associated with higher levels of vigorous leisure time physical activity, smaller body size, and higher intakes of dietary fiber and folate. Persons who had high scores on the \"drinker\" pattern were also more likely to smoke cigarettes. The \"Western\" dietary pattern was associated with an increased risk of colon cancer in both men and women. The association was strongest among people diagnosed prior to age 67 years (for men, odds ratio (OR)=1.96, 95% confidence interval (CI) 1.22-3.15; for women, OR=2.02, 95% CI 1.21-3.36) and among men with distal tumors (OR=2.25, 95% CI 1.47-3.46). The \"prudent\" diet was protective, with the strongest associations being observed among people diagnosed prior to age 67 years (men: OR=0.63, 95% CI 0.43-0.92; women: OR=0.58, 95% CI 0.38-0.87); associations with this dietary pattern were also strong among persons with proximal tumors (men: OR=0.55, 95% CI 0.38-0.80; women: OR=0.64, 95% CI 0.45-0.92). Although \"substituters\" (people who substituted low fat dairy products for high fat dairy products, margarine for butter, poultry for red meat, and whole grains for refined grains) were at reduced risk of colon cancer, the reduction in risk was not statistically significant. These data support the hypothesis that overall dietary intake pattern is associated with colon cancer, and that the dietary pattern associated with the greatest increase in risk is the one which typifies a Western-style diet." + }, + "questions": [ + { + "id": "43bf88e4-f9f0-4caa-ac65-50c3a9d56ecd", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 2264, + "text": "Western-style diet" + }, + { + "answer_start": 1078, + "text": "\"Western\" dietary pattern" + } + ] + } + ] +} \ No newline at end of file diff --git a/d9bf682f-13a6-46f0-bfd1-7b0a629bfa6e.json b/d9bf682f-13a6-46f0-bfd1-7b0a629bfa6e.json new file mode 100644 index 0000000000000000000000000000000000000000..6ef1732691963300b4e206b1d4b9949d7b0fe0fc --- /dev/null +++ b/d9bf682f-13a6-46f0-bfd1-7b0a629bfa6e.json @@ -0,0 +1,57 @@ +{ + "id": "d9bf682f-13a6-46f0-bfd1-7b0a629bfa6e", + "disease": { + "id": "M2023_04_26_16_38_52", + "names": [ + "Migraine" + ], + "dbLinks": { + "icd10": [ + "G43" + ], + "icd11": [ + "8A80" + ], + "mesh": [ + "C10.228.140.546.399.750" + ] + }, + "description": "Migraine is a chronic neurological disorder characterized by recurrent episodes of unilateral, pulsatile headaches associated with autonomic symptoms such as nausea, vomiting, photophobia, and phonophobia. The pathophysiology of migraine is multifactorial and involves complex interactions between genetic, environmental, and neurochemical factors that modulate cerebral vascular tone and nociception. Migraine attacks can be triggered by a variety of factors, including stress, hormonal changes, sleep disturbances, and certain foods or medications. Treatment options for migraine include pharmacotherapy for acute attacks, preventive medications for frequent or severe headaches, and lifestyle modifications to avoid triggers. In refractory cases, interventional therapies such as nerve blocks or neuromodulation techniques may be considered." + }, + "article": { + "id": "17040332", + "text": "Review of epidemiological and clinical studies suggests that sleep disorders are disproportionately observed in specific headache diagnoses (eg, migraine, tension-type, cluster) and other nonspecific headache patterns (ie, chronic daily headache, \"awakening\" or morning headache). Interestingly, the sleep disorders associated with headache are of varied types, including obstructive sleep apnea (OSA), periodic limb movement disorder, circadian rhythm disorder, insomnia, and hypersomnia. Headache, particularly morning headache and chronic headache, may be consequent to, or aggravated by, a sleep disorder, and management of the sleep disorder may improve or resolve the headache. Sleep-disordered breathing is the best example of this relationship. Insomnia is the sleep disorder most often cited by clinical headache populations. Depression and anxiety are comorbid with both headache and sleep disorders (especially insomnia) and consideration of the full headache-sleep-affective symptom constellation may yield opportunities to maximize treatment. This paper reviews the comorbidity of headache and sleep disorders (including coexisting psychiatric symptoms where available). Clinical implications for headache evaluation are presented. Sleep screening strategies conducive to headache practice are described. Consideration of the spectrum of sleep-disordered breathing is encouraged in the headache population, including awareness of potential upper airway resistance syndrome in headache patients lacking traditional risk factors for OSA. Pharmacologic and behavioral sleep regulation strategies are offered that are also compatible with treatment of primary headache." + }, + "questions": [ + { + "id": "39225c47-d0f9-4e65-b8ed-3becd12e34a0", + "text": "what are the risk factors of Migraine?", + "answers": [ + { + "answer_start": 61, + "text": "sleep disorders" + }, + { + "answer_start": 372, + "text": "obstructive sleep apnea (OSA)" + }, + { + "answer_start": 403, + "text": "periodic limb movement disorder" + }, + { + "answer_start": 436, + "text": "circadian rhythm disorder" + }, + { + "answer_start": 463, + "text": "insomnia" + }, + { + "answer_start": 477, + "text": "hypersomnia" + } + ] + } + ] +} \ No newline at end of file diff --git a/da03c559-18e9-4667-827f-408970286757.json b/da03c559-18e9-4667-827f-408970286757.json new file mode 100644 index 0000000000000000000000000000000000000000..4413e5af58af080333767d1343c355e4443a05e7 --- /dev/null +++ b/da03c559-18e9-4667-827f-408970286757.json @@ -0,0 +1,39 @@ +{ + "id": "da03c559-18e9-4667-827f-408970286757", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "23553100", + "text": "OBJECTIVES:\nRheumatoid arthritis (RA) is less common among men than women, and sex hormones have been suggested to play a part in the pathogenesis. Lower levels of testosterone have been demonstrated in men with RA, but it is not known if these changes precede the disease.\n\nMETHODS:\nIn a nested case-control study, using information and blood samples from a population-based health survey, we identified incident cases of RA by linking the cohort to local and national RA registers. Two controls for each validated case, matched for age, sex and year of screening, were selected from the health survey. Using stored blood samples, collected between 08:00 and 10:00 am after an overnight fast, we analysed levels of testosterone and other reproductive hormones.\n\nRESULTS:\nSerum was available from 104 cases (median time from screening to RA diagnosis 12.7 years (range 1-28); 73% rheumatoid factor (RF) positive at diagnosis or later) and 174 matched controls. In conditional logistic regression models, adjusted for smoking and body mass index, lower levels of testosterone were associated with subsequent development of RF-negative RA (OR 0.31 per SD, 95% CI 0.12 to 0.85), with a weaker association with RF-positive RA (OR 0.87 per SD; 95% CI 0.53 to 1.43). Levels of follicle-stimulating hormone were significantly increased in pre-RF-negative RA (p=0.02), but decreased in pre-RF-positive RA (p=0.02).\n\nCONCLUSIONS:\nLower levels of testosterone were predictive of RF-negative RA, suggesting that hormonal changes precede the onset of RA and affect the disease phenotype." + }, + "questions": [ + { + "id": "98f09998-78fe-496b-8f9b-29053f47f0ef", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 1421, + "text": "Lower levels of testosterone" + }, + { + "answer_start": 1046, + "text": "lower levels of testosterone" + } + ] + } + ] +} \ No newline at end of file diff --git a/da142303-2802-448c-ae14-7bb77d6e979e.json b/da142303-2802-448c-ae14-7bb77d6e979e.json new file mode 100644 index 0000000000000000000000000000000000000000..869993de58000a3f3153448809e785b99e9775f1 --- /dev/null +++ b/da142303-2802-448c-ae14-7bb77d6e979e.json @@ -0,0 +1,40 @@ +{ + "id": "da142303-2802-448c-ae14-7bb77d6e979e", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "15218992", + "text": "Genetic susceptibility to the development of chronic obstructive pulmonary disease (COPD) might depend on variation in the activities of enzymes that detoxify cigarette smoke products, such as microsomal epoxide hydrolase (mEPHX) and glutathione S-transferase (GST). It was investigated whether polymorphisms in these genes had any association with susceptibility to COPD and COPD severity. The genotypes of 184 patients with COPD and 212 control subjects were determined by polymerase chain reaction followed by restriction fragment length polymorphism analysis of the mEPHX, GSTM1, GSTT1 and GSTP1 genes. All subjects were smokers or exsmokers. The proportion of GSTM1-null genotypes was significantly higher in patients with COPD than in control subjects (61.4 versus 42.5%). No differences were observed in the frequency of polymorphic genotypes for mEPHX, GSTT1 and GSTP1. During combined analysis of genetic polymorphisms for mEPHX, GSTM1 and GSTP1, it was found that there are strong indicators for susceptibility to COPD (genotype combination with at least one mutant mEPHX exon-3 allele (histidine 113), GSTM1 null and homozygous for the GSTPI isoleucine 105 allele). The frequencies of homozygous mutant alleles of mEPHX exon 3 and the GSTMI-null genotype were significantly higher in patients with severe COPD (forced expiratory volume in one second of \u003c35% of the predicted value). It is proposed that the combination of genetic variants including at least one mutant microsomal epoxide hydrolase exon-3 allele and glutathione S-transferase M1-null and homozygous isoleucine 105 glutathione S-transferase P1 genotypes are significant indicators of susceptibility to chronic obstructive pulmonary disease in the Taiwanese population. In addition, the homozygous variant of microsomal epoxide hydrolase exon 3 and the glutathione S-transferase M1-null genotype are independent risk factors for developing severe chronic obstructive pulmonary disease." + }, + "questions": [ + { + "id": "d2c4b7f2-eda4-46e8-a211-69c092c547fc", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 1196, + "text": "homozygous mutant alleles of mEPHX exon 3" + }, + { + "answer_start": 1246, + "text": "GSTMI-null genotype" + } + ] + } + ] +} \ No newline at end of file diff --git a/da5e7a3c-8183-48df-8e6c-85ca2a62acd2.json b/da5e7a3c-8183-48df-8e6c-85ca2a62acd2.json new file mode 100644 index 0000000000000000000000000000000000000000..358fdb324d085465fa4202ada20d47270a76f3e4 --- /dev/null +++ b/da5e7a3c-8183-48df-8e6c-85ca2a62acd2.json @@ -0,0 +1,35 @@ +{ + "id": "da5e7a3c-8183-48df-8e6c-85ca2a62acd2", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "12758050", + "text": "The development and phenotypic expression of allergic airway disease depends on a complex interaction between genetic and several environmental factors, such as exposure to food, inhalant allergens and non-specific adjuvant factors (e.g. tobacco smoke, air pollution and infections). The first months of life seem to be a particularly vulnerable period and there is evidence that sensitisation is related to the level of allergen exposure during early life. At present, the combination of atopic heredity and elevated cord-blood IgE seems to result in the best predictive discrimination as regards development of allergic disease at birth. Early sensitisation, cow's milk allergy and atopic eczema are predictors for later development of allergic airway disease. Exposure to indoor allergens, especially house dust mite allergens, is a risk factor for sensitisation and development of asthma later in childhood in high-risk infants and infants with early atopic manifestations." + }, + "questions": [ + { + "id": "42e8d3ab-d2e9-426e-ae00-09606e89536d", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 763, + "text": "Exposure to indoor allergens, especially house dust mite allergens" + } + ] + } + ] +} \ No newline at end of file diff --git a/da6b0acf-b303-4b46-a83a-d53206d83e37.json b/da6b0acf-b303-4b46-a83a-d53206d83e37.json new file mode 100644 index 0000000000000000000000000000000000000000..b97671cf59dfce2bef76d238a4725e12adb491fe --- /dev/null +++ b/da6b0acf-b303-4b46-a83a-d53206d83e37.json @@ -0,0 +1,42 @@ +{ + "id": "da6b0acf-b303-4b46-a83a-d53206d83e37", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "31408136", + "text": "IMPORTANCE:\nHigh gluten intake during childhood may confer risk of celiac disease.\n\nOBJECTIVES:\nTo investigate if the amount of gluten intake is associated with celiac disease autoimmunity and celiac disease in genetically at-risk children.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nThe participants in The Environmental Determinants of Diabetes in the Young (TEDDY), a prospective observational birth cohort study designed to identify environmental triggers of type 1 diabetes and celiac disease, were followed up at 6 clinical centers in Finland, Germany, Sweden, and the United States. Between 2004 and 2010, 8676 newborns carrying HLA antigen genotypes associated with type 1 diabetes and celiac disease were enrolled. Screening for celiac disease with tissue transglutaminase autoantibodies was performed annually in 6757 children from the age of 2 years. Data on gluten intake were available in 6605 children (98%) by September 30, 2017.\n\nEXPOSURES:\nGluten intake was estimated from 3-day food records collected at ages 6, 9, and 12 months and biannually thereafter until the age of 5 years.\n\nMAIN OUTCOMES AND MEASURES:\nThe primary outcome was celiac disease autoimmunity, defined as positive tissue transglutaminase autoantibodies found in 2 consecutive serum samples. The secondary outcome was celiac disease confirmed by intestinal biopsy or persistently high tissue transglutaminase autoantibody levels.\n\nRESULTS:\nOf the 6605 children (49% females; median follow-up: 9.0 years [interquartile range, 8.0-10.0 years]), 1216 (18%) developed celiac disease autoimmunity and 447 (7%) developed celiac disease. The incidence for both outcomes peaked at the age of 2 to 3 years. Daily gluten intake was associated with higher risk of celiac disease autoimmunity for every 1-g/d increase in gluten consumption (hazard ratio [HR], 1.30 [95% CI, 1.22-1.38]; absolute risk by the age of 3 years if the reference amount of gluten was consumed, 28.1%; absolute risk if gluten intake was 1-g/d higher than the reference amount, 34.2%; absolute risk difference, 6.1% [95% CI, 4.5%-7.7%]). Daily gluten intake was associated with higher risk of celiac disease for every 1-g/d increase in gluten consumption (HR, 1.50 [95% CI, 1.35-1.66]; absolute risk by age of 3 years if the reference amount of gluten was consumed, 20.7%; absolute risk if gluten intake was 1-g/d higher than the reference amount, 27.9%; absolute risk difference, 7.2% [95% CI, 6.1%-8.3%]).\n\nCONCLUSIONS AND RELEVANCE:\nHigher gluten intake during the first 5 years of life was associated with increased risk of celiac disease autoimmunity and celiac disease among genetically predisposed children." + }, + "questions": [ + { + "id": "3f810b7e-919f-4115-a42e-30b4ec6bc3cd", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 2477, + "text": "Higher gluten intake during the first 5 years of life" + }, + { + "answer_start": 1677, + "text": "Daily gluten intake" + }, + { + "answer_start": 2153, + "text": "every 1-g/d increase in gluten consumption" + } + ] + } + ] +} \ No newline at end of file diff --git a/db362e4f-2b69-45de-b718-fcba19505959.json b/db362e4f-2b69-45de-b718-fcba19505959.json new file mode 100644 index 0000000000000000000000000000000000000000..1ae8fa2c6573d55e10d6323130f1dfebc46d4215 --- /dev/null +++ b/db362e4f-2b69-45de-b718-fcba19505959.json @@ -0,0 +1,34 @@ +{ + "id": "db362e4f-2b69-45de-b718-fcba19505959", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "26286216", + "text": "OBJECTIVES:\nTo quantify risk of overall cancer across all levels of alcohol consumption among women and men separately, with a focus on light to moderate drinking and never smokers; and assess the influence of drinking patterns on overall cancer risk.\n\nDESIGN:\nTwo prospective cohort studies.\n\nSETTING:\nHealth professionals in the United States.\n\nPARTICIPANTS:\n88,084 women and 47,881 men participating in the Nurses' Health Study (from 1980) and Health Professionals Follow-up Study (from 1986), followed until 2010.\n\nMAIN OUTCOMES AND MEASURES:\nRelative risks of cancer.\n\nRESULTS:\n19,269 and 7571 (excluding non-advanced prostate cancers) incident cancers were documented among women and men, respectively, over 3,144,853 person years. Compared with non-drinkers, light to moderate drinkers had relative risks of total cancer of 1.02 (95% confidence interval 0.98 to 1.06) and 1.04 (1.00 to 1.09; P(trend) = 0.12) for alcohol intake of 0.1-4.9 and 5-14.9 g/day among women, respectively. Corresponding values for men were 1.03 (0.96 to 1.11), 1.05 (0.97 to 1.12), and 1.06 (0.98 to 1.15; P(trend) = 0.31) for alcohol intake of 0.1-4.9, 5-14.9, and 15-29.9 g/day, respectively. Associations for light to moderate drinking and total cancer were similar among ever or never smokers, although alcohol consumption above moderate levels (in particular ≥ 30 g/day) was more strongly associated with risk of total cancer among ever smokers than never smokers. For a priori defined alcohol related cancers in men, risk was not appreciably increased for light and moderate drinkers who never smoked (P(trend) = 0.18). However, for women, even an alcohol consumption of 5-14.9 g/day was associated with increased risk of alcohol related cancer (relative risk 1.13 (95% confidence interval 1.06 to 1.20)), driven by breast cancer. More frequent and heavy episodic drinking was not further associated with risk of total cancer after adjusting for total alcohol intake.\n\nCONCLUSION:\nLight to moderate drinking is associated with minimally increased risk of overall cancer. For men who have never smoked, risk of alcohol related cancers is not appreciably increased for light and moderate drinking (up to two drinks per day). However, for women who have never smoked, risk of alcohol related cancers (mainly breast cancer) increases even within the range of up to one alcoholic drink a day." + }, + "questions": [ + { + "id": "76385d9f-d285-445e-af8f-97b2e5c09a0e", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1638, + "text": "alcohol consumption of 5-14.9 g/day" + } + ] + } + ] +} \ No newline at end of file diff --git a/dbba74a0-9620-4038-a3ee-c10759b3ea93.json b/dbba74a0-9620-4038-a3ee-c10759b3ea93.json new file mode 100644 index 0000000000000000000000000000000000000000..369c969984680be676eda934c2d532b16ef6aa40 --- /dev/null +++ b/dbba74a0-9620-4038-a3ee-c10759b3ea93.json @@ -0,0 +1,35 @@ +{ + "id": "dbba74a0-9620-4038-a3ee-c10759b3ea93", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "32934151", + "text": "OBJECTIVES:\nAlthough the airway microbiota is a highly dynamic ecology, the role of longitudinal changes in airway microbiota during early childhood in asthma development is unclear. We aimed to investigate the association of longitudinal changes in early nasal microbiota with the risk of developing asthma.\n\nMETHODS:\nIn this prospective, population-based birth cohort study, we followed children from birth to age 7 years. The nasal microbiota was tested by using 16S ribosomal RNA gene sequencing at ages 2, 13, and 24 months. We applied an unsupervised machine learning approach to identify longitudinal nasal microbiota profiles during age 2 to 13 months (the primary exposure) and during age 2 to 24 months (the secondary exposure) and examined the association of these profiles with the risk of physician-diagnosed asthma at age 7 years.\n\nRESULTS:\nOf the analytic cohort of 704 children, 57 (8%) later developed asthma. We identified 4 distinct longitudinal nasal microbiota profiles during age 2 to 13 months. In the multivariable analysis, compared with the persistent dominance profile during age 2 to 13 months, the persistent sparsity profile was associated with a significantly higher risk of asthma (adjusted odds ratio, 2.74; 95% confidence interval, 1.20-6.27). Similar associations were observed between the longitudinal changes in nasal microbiota during age 2 to 24 months and risk of asthma.\n\nCONCLUSIONS:\nChildren with an altered longitudinal pattern in the nasal microbiota during early childhood had a high risk of developing asthma. Our data guide the development of primary prevention strategies (eg, early identification of children at high risk and modification of microbiota) for childhood asthma. These observations present a new avenue for risk modification for asthma (eg, microbiota modification)." + }, + "questions": [ + { + "id": "892ea583-6706-4bf8-a7f6-94f8775ec65f", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1443, + "text": "altered longitudinal pattern in the nasal microbiota during early childhood" + } + ] + } + ] +} \ No newline at end of file diff --git a/dc5eb1cb-0dd2-40de-955a-e74cf67adf77.json b/dc5eb1cb-0dd2-40de-955a-e74cf67adf77.json new file mode 100644 index 0000000000000000000000000000000000000000..eb265857089036741c8db08e53e102b85a6e5f5f --- /dev/null +++ b/dc5eb1cb-0dd2-40de-955a-e74cf67adf77.json @@ -0,0 +1,42 @@ +{ + "id": "dc5eb1cb-0dd2-40de-955a-e74cf67adf77", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "23863325", + "text": "OBJECTIVES:\nThe aim of this study was to describe the occurrence of clinically diagnosed coeliac disease in children ages 0 to 12 years in Norway, including regional variation and coexisting type 1 diabetes mellitus, thyroid disease, and Down syndrome.\n\nMETHODS:\nThe Norwegian Patient Register (NPR) contains individual-level hospital data from 2008 onward. Small-bowel biopsies for establishing the coeliac disease diagnosis are only performed at public hospitals reporting to the NPR. Data on all hospital contacts during 2008-2011 when a diagnosis of coeliac disease was registered were retrieved from the NPR for patients born between 1999 and 2011, allowing estimation of the proportion registered with coeliac disease at ages 0 to 12 years in a cohort study.\n\nRESULTS:\nA total of 3006 individuals (58.2% girls) were recorded as having coeliac disease among 797,360 children, corresponding to a proportion of 3.8/1000 (95% confidence interval [CI] 3.7-3.9/1000) children, 4.5 (CI 4.3-4.7) among girls and 3.1 (CI 2.9-3.3/1000) among boys (P \u003c 0.001). The proportion increased with age up to approximately 6 years and was 5.0/1000 (CI 4.5-5.6) at the age of 12 years, and was slightly higher in the south/west (3.9/1000) as compared to the middle/north (3.5/1000) regions of Norway (P = 0.013). A total of 214 of 3006 (7.1%) patients with coeliac disease were registered with coexisting conditions: type 1 diabetes mellitus (n = 142, 4.7%), Down syndrome (n = 47, 1.6%), or thyroid disease (n = 41, 1.4%).\n\nCONCLUSIONS:\nIn this first nationwide study of clinically diagnosed coeliac disease in Norwegian children, we found a high occurrence, comparable with that in Sweden. Comorbidity was common, but routine screening of high-risk groups contributed to a limited number of cases." + }, + "questions": [ + { + "id": "eb1de214-71de-48e5-97bc-e7e15666cd2a", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 1403, + "text": "type 1 diabetes mellitus" + }, + { + "answer_start": 1445, + "text": "Down syndrome" + }, + { + "answer_start": 1478, + "text": "thyroid disease" + } + ] + } + ] +} \ No newline at end of file diff --git a/dc64534a-afbd-4067-ba56-62d0f5ec7dda.json b/dc64534a-afbd-4067-ba56-62d0f5ec7dda.json new file mode 100644 index 0000000000000000000000000000000000000000..9e64c466554dc849e556c95aac54a33005f8e938 --- /dev/null +++ b/dc64534a-afbd-4067-ba56-62d0f5ec7dda.json @@ -0,0 +1,34 @@ +{ + "id": "dc64534a-afbd-4067-ba56-62d0f5ec7dda", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "16775176", + "text": "Mammographic features are associated with breast cancer risk, but estimates of the strength of the association vary markedly between studies, and it is uncertain whether the association is modified by other risk factors. We conducted a systematic review and meta-analysis of publications on mammographic patterns in relation to breast cancer risk. Random effects models were used to combine study-specific relative risks. Aggregate data for \u003e 14,000 cases and 226,000 noncases from 42 studies were included. Associations were consistent in studies conducted in the general population but were highly heterogeneous in symptomatic populations. They were much stronger for percentage density than for Wolfe grade or Breast Imaging Reporting and Data System classification and were 20% to 30% stronger in studies of incident than of prevalent cancer. No differences were observed by age/menopausal status at mammography or by ethnicity. For percentage density measured using prediagnostic mammograms, combined relative risks of incident breast cancer in the general population were 1.79 (95% confidence interval, 1.48-2.16), 2.11 (1.70-2.63), 2.92 (2.49-3.42), and 4.64 (3.64-5.91) for categories 5% to 24%, 25% to 49%, 50% to 74%, and \u003e or = 75% relative to \u003c 5%. This association remained strong after excluding cancers diagnosed in the first-year postmammography. This review explains some of the heterogeneity in associations of breast density with breast cancer risk and shows that, in well-conducted studies, this is one of the strongest risk factors for breast cancer. It also refutes the suggestion that the association is an artifact of masking bias or that it is only present in a restricted age range." + }, + "questions": [ + { + "id": "d4c2ac57-f325-47cc-aa70-0452edd84ca2", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1429, + "text": "breast density" + } + ] + } + ] +} \ No newline at end of file diff --git a/dd2c8516-0926-4a06-b0f5-fc5a2b9443e6.json b/dd2c8516-0926-4a06-b0f5-fc5a2b9443e6.json new file mode 100644 index 0000000000000000000000000000000000000000..ab5990b00d7c198e9df6546e3d5fe46a9d461c64 --- /dev/null +++ b/dd2c8516-0926-4a06-b0f5-fc5a2b9443e6.json @@ -0,0 +1,42 @@ +{ + "id": "dd2c8516-0926-4a06-b0f5-fc5a2b9443e6", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "12351457", + "text": "The combination of insulin resistance, dyslipidemia, hypertension, and obesity has been described as a \"metabolic syndrome\" that is a strong determinant of type 2 diabetes. Factor analysis was used to identify components of this syndrome in 1,918 Pima Indians. Prospective analyses were conducted to evaluate associations of identified factors with incidence of diabetes. Factor analysis identified 4 factors that accounted for 79% of the variance in the original 10 variables. Each of these factors reflected a proposed component of the metabolic syndrome: insulinemia, body size, blood pressure, and lipid metabolism. Among 890 originally nondiabetic participants with follow-up data, 144 developed diabetes in a median follow-up of 4.1 years. The insulinemia factor was strongly associated with diabetes incidence (incidence rate ratio [IRR] for a 1-SD difference in factor scores = 1.81, P \u003c 0.01). The body size and lipids factors also significantly predicted diabetes (IRR 1.52 and 1.37, respectively, P \u003c 0.01 for both), whereas the blood pressure factor did not (IRR 1.11, P = 0.20). Identification of four unique factors with different associations with incidence of diabetes suggests that the correlations among these variables reflect distinct metabolic processes, about which substantial information may be lost in the attempt to combine them into a single entity." + }, + "questions": [ + { + "id": "d0df9cef-7652-4c33-b79d-1b3777fe2278", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 750, + "text": "insulinemia" + }, + { + "answer_start": 903, + "text": "The body size" + }, + { + "answer_start": 921, + "text": "lipids" + } + ] + } + ] +} \ No newline at end of file diff --git a/dd3d8d6d-7793-410f-b587-dc8b690dc503.json b/dd3d8d6d-7793-410f-b587-dc8b690dc503.json new file mode 100644 index 0000000000000000000000000000000000000000..beae82e1138e2c17274a530d8623c123520441d1 --- /dev/null +++ b/dd3d8d6d-7793-410f-b587-dc8b690dc503.json @@ -0,0 +1,39 @@ +{ + "id": "dd3d8d6d-7793-410f-b587-dc8b690dc503", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "11817612", + "text": "OBJECTIVE:\nTo evaluate whether coffee, tea, and caffeine consumption are risk factors for rheumatoid arthritis (RA) onset among older women.\n\nMETHODS:\nThese factors were evaluated in a prospective cohort study that was initiated in 1986 and that included 31,336 women ages 55-69 years without a history of RA. Risk factor data were self-reported using a mailed questionnaire. Through 1997, 158 cases of RA were identified and validated against medical records. The relative risk (RR) and 95% confidence interval (95% CI) were used as the measures of association and were adjusted for age, alcohol use, smoking history, age at menopause, marital status, and the use of hormone replacement therapy.\n\nRESULTS:\nCompared with those reporting no use, subjects drinking \u003e or =4 cups/day of decaffeinated coffee were at increased risk of RA (RR 2.58, 95% CI 1.63-4.06). In contrast, women consuming \u003e3 cups/day of tea displayed a decreased risk of RA (RR 0.39, 95% CI 0.16-0.97) compared with women who never drank tea. Caffeinated coffee and daily caffeine intake were not associated with the development of RA. Multivariable adjustment for a number of potential confounders did not alter these results. The associations of RA onset with the highest categories of decaffeinated coffee consumption (RR 3.10, 95% CI 1.75-5.48) and tea consumption (RR 0.24, 95% CI 0.06-0.98) were stronger in women with seropositive disease compared with those with seronegative disease (RR 1.54, 95% CI 0.62-3.84 and RR 0.93, 95% CI 0.27-3.20, respectively).\n\nCONCLUSION:\nDecaffeinated coffee intake is independently and positively associated with RA onset, while tea consumption shows an inverse association with disease onset. Further investigations of decaffeinated coffee and tea intake as arthritis risk factors are needed to verify these findings and explore their biologic basis." + }, + "questions": [ + { + "id": "c6eea785-480e-4726-a8d5-750741af8699", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 745, + "text": "subjects drinking \u003e or =4 cups/day of decaffeinated coffee" + }, + { + "answer_start": 1547, + "text": "Decaffeinated coffee intake" + } + ] + } + ] +} \ No newline at end of file diff --git a/dda98c8c-6afa-4743-9c40-62d85047e731.json b/dda98c8c-6afa-4743-9c40-62d85047e731.json new file mode 100644 index 0000000000000000000000000000000000000000..a76395993f71c22775a39ece193844c70b9b61cd --- /dev/null +++ b/dda98c8c-6afa-4743-9c40-62d85047e731.json @@ -0,0 +1,40 @@ +{ + "id": "dda98c8c-6afa-4743-9c40-62d85047e731", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "29720562", + "text": "BACKGROUND:\nIt has been debated, but not yet established, whether increased airway responsiveness can predict COPD. Recognising this link may help in identifying subjects at risk.\n\nOBJECTIVE:\nWe studied prospectively whether airway responsiveness is associated with the risk of developing COPD.\n\nMETHODS:\nWe pooled data from two multicentre cohort studies that collected data from three time points using similar methods (European Community Respiratory Health Survey and Swiss Cohort Study on Air Pollution and Lung and Heart Diseases in Adults). We classified subjects (median age 37 years, 1st-3rd quartiles: 29-44) by their level of airway responsiveness using quintiles of methacholine dose-response slope at the first examination (1991-1994). Then, we excluded subjects with airflow obstruction at the second examination (1999-2003) and analysed incidence of COPD (postbronchodilator FEV/FVC below the lower limit of normal) at the third examination (2010-2014) as a function of responsiveness, adjusting for sex, age, education, body mass index, history of asthma, smoking, occupational exposures and indicators of airway calibre.\n\nRESULTS:\nWe observed 108 new cases of COPD among 4205 subjects during a median time of 9 years. Compared with the least responsive group (incidence rate 0.6 per 1000/year), adjusted incidence rate ratios for COPD ranged from 1.79 (95% CI 0.52 to 6.13) to 8.91 (95% CI 3.67 to 21.66) for increasing airway responsiveness. Similar dose-response associations were observed between smokers and non-smokers, and stronger associations were found among subjects without a history of asthma or asthma-like symptoms.\n\nCONCLUSIONS:\nOur study suggests that increased airway responsiveness is an independent risk factor for COPD. Further research should clarify whether early treatment in patients with high responsiveness can slow down disease progression." + }, + "questions": [ + { + "id": "19a30c6c-1ace-4766-b3d4-1d1ec323b436", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 1425, + "text": "increasing airway responsiveness" + }, + { + "answer_start": 1684, + "text": "increased airway responsiveness" + } + ] + } + ] +} \ No newline at end of file diff --git a/de7257c9-5b62-4b76-83f9-4dd50a661c2e.json b/de7257c9-5b62-4b76-83f9-4dd50a661c2e.json new file mode 100644 index 0000000000000000000000000000000000000000..25a57079053aded16702de5b9d9b1efd9c0d47a8 --- /dev/null +++ b/de7257c9-5b62-4b76-83f9-4dd50a661c2e.json @@ -0,0 +1,38 @@ +{ + "id": "de7257c9-5b62-4b76-83f9-4dd50a661c2e", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "12503980", + "text": "CONTEXT:\nObesity and diabetes are increasing in the United States.\n\nOBJECTIVE:\nTo estimate the prevalence of obesity and diabetes among US adults in 2001.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nRandom-digit telephone survey of 195 005 adults aged 18 years or older residing in all states participating in the Behavioral Risk Factor Surveillance System in 2001.\n\nMAIN OUTCOME MEASURES:\nBody mass index, based on self-reported weight and height and self-reported diabetes.\n\nRESULTS:\nIn 2001 the prevalence of obesity (BMI \u003e or =30) was 20.9% vs 19.8% in 2000, an increase of 5.6%. The prevalence of diabetes increased to 7.9% vs 7.3% in 2000, an increase of 8.2%. The prevalence of BMI of 40 or higher in 2001 was 2.3%. Overweight and obesity were significantly associated with diabetes, high blood pressure, high cholesterol, asthma, arthritis, and poor health status. Compared with adults with normal weight, adults with a BMI of 40 or higher had an odds ratio (OR) of 7.37 (95% confidence interval [CI], 6.39-8.50) for diagnosed diabetes, 6.38 (95% CI, 5.67-7.17) for high blood pressure, 1.88 (95% CI,1.67-2.13) for high cholesterol levels, 2.72 (95% CI, 2.38-3.12) for asthma, 4.41 (95% CI, 3.91-4.97) for arthritis, and 4.19 (95% CI, 3.68-4.76) for fair or poor health.\n\nCONCLUSIONS:\nIncreases in obesity and diabetes among US adults continue in both sexes, all ages, all races, all educational levels, and all smoking levels. Obesity is strongly associated with several major health risk factors." + }, + "questions": [ + { + "id": "2ae2d1a2-4b21-4d75-9628-e27d89c1dc66", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 905, + "text": " adults with a BMI of 40 or higher" + }, + { + "answer_start": 1428, + "text": "Obesity" + } + ] + } + ] +} \ No newline at end of file diff --git a/dee5fc24-ec23-4319-9984-6300638c6759.json b/dee5fc24-ec23-4319-9984-6300638c6759.json new file mode 100644 index 0000000000000000000000000000000000000000..81fd6fd19a6255652c970e3f4840dd870c6e7106 --- /dev/null +++ b/dee5fc24-ec23-4319-9984-6300638c6759.json @@ -0,0 +1,38 @@ +{ + "id": "dee5fc24-ec23-4319-9984-6300638c6759", + "disease": { + "id": "H00408", + "names": [ + "Type 1 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E10" + ], + "mesh": [ + "D003922" + ] + }, + "category": "Metabolic disease; Immune system disease; Endocrine disease" + }, + "article": { + "id": "17327312", + "text": "OBJECTIVE:\nWe sought to assess the long-term trends in the incidence of type 1 diabetes among non-Hispanic white and Hispanic youth aged 0-17 years from Colorado using data from the Colorado IDDM Study Registry (1978-1988) and SEARCH for Diabetes in Youth (2002-2004).\n\nRESEARCH DESIGN AND METHODS:\nCases of diabetes were ascertained through physician reporting and hospital databases. Type 1 diabetes was defined as use of insulin within 2 weeks from diagnosis. Completeness of ascertainment was estimated as 97%. Annual average incidence rates (per 100,000/year) and 95% CIs for the time periods were computed. Trends in incidence were assessed by Poisson regression.\n\nRESULTS:\nThe incidence of type 1 diabetes was 14.8 (95% CI 14.0-15.6) in 1978-1988 and 23.9 (22.2-25.6) in 2002-2004 for the state of Colorado (P \u003c 0.0001). From 1978 to 2004, the incidence of type 1 diabetes increased by 2.3% (1.6-3.1) per year (P \u003c 0.0001). The increase in incidence was significant for both non-Hispanic white (2.7% [95% CI 1.9-3.6] per year, P \u003c 0.0001) and Hispanic youth (1.6% [0.2-3.1] per year, P = 0.013).\n\nCONCLUSIONS:\nThe incidence of type 1 diabetes has increased 1.6-fold among Colorado youth from 1978-1988 to 2002-2004, and both non-Hispanic white and Hispanic youth are affected by this trend." + }, + "questions": [ + { + "id": "32b47887-a6c4-4e3e-b339-62f93cd2d84f", + "text": "What are the risk factors of Type 1 diabetes mellitus?", + "answers": [ + { + "answer_start": 982, + "text": "non-Hispanic white" + }, + { + "answer_start": 1050, + "text": "Hispanic youth" + } + ] + } + ] +} \ No newline at end of file diff --git a/dfac69f1-ef64-4df2-ab2d-48f73d8aecb4.json b/dfac69f1-ef64-4df2-ab2d-48f73d8aecb4.json new file mode 100644 index 0000000000000000000000000000000000000000..f2b79d3db978390813f0a4fad5be60236b33ea53 --- /dev/null +++ b/dfac69f1-ef64-4df2-ab2d-48f73d8aecb4.json @@ -0,0 +1,38 @@ +{ + "id": "dfac69f1-ef64-4df2-ab2d-48f73d8aecb4", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "16434451", + "text": "CONTEXT:\nPolycystic ovary syndrome (PCOS) is associated with menstrual and reproductive abnormalities, insulin resistance, and obesity.\n\nOBJECTIVE:\nThe objective of this study was to determine the prevalence of diagnosed PCOS and its association with cardiovascular risk factors.\n\nSETTING:\nThe study is set in an integrated health care delivery system in northern California.\n\nPATIENTS:\nA total of 11,035 women with PCOS were identified by one or more outpatient diagnoses of PCOS using health plan databases. An age-matched sample of women without PCOS was also selected.\n\nOUTCOME MEASURES:\nPrevalence of PCOS and targeted cardiovascular risk factors [hypertension, dyslipidemia, diabetes mellitus, and body mass index (BMI)] were measured.\n\nRESULTS:\nDuring 2002-2004, the prevalence of diagnosed PCOS among female members aged 25-34 yr was 2.6% (95% confidence interval 1.6-1.7%). Women with diagnosed PCOS were more likely than those without PCOS to be obese [BMI \u003e or = 30 mg/m(2); odds ratio (OR) 4.21, 3.96-4.47]. Furthermore, PCOS was associated with diabetes (OR 2.45, confidence interval 2.16-2.79), hypertension (OR 1.41, 1.31-1.51) and known dyslipidemia (OR 1.53, 1.39-1.68), even after adjusting for BMI and known confounders. Among women with PCOS, compared with whites, Blacks and Hispanics were more likely and Asians less likely to be obese; Asians and Hispanics were more likely to have diabetes; and Blacks were more likely and Hispanics less likely to have hypertension.\n\nCONCLUSIONS:\nWithin a large, community-based population receiving health care, diagnosed PCOS was highly prevalent and associated with a much higher frequency of cardiovascular risk factors that varied by race/ethnicity. Our prevalence estimates likely underestimate the true prevalence of PCOS. Further studies are needed to explore racial/ethnic differences and the extent to which PCOS contributes to future cardiovascular risk." + }, + "questions": [ + { + "id": "4e6ee33a-dc03-42d0-b611-698d8846a190", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 9, + "text": "Polycystic ovary syndrome (PCOS)" + }, + { + "answer_start": 1033, + "text": "PCOS" + } + ] + } + ] +} \ No newline at end of file diff --git a/dfca6bac-bca4-4b17-aa48-0e0171c2301f.json b/dfca6bac-bca4-4b17-aa48-0e0171c2301f.json new file mode 100644 index 0000000000000000000000000000000000000000..73e24b489ac12eb690a1d302983a2a30c326ec59 --- /dev/null +++ b/dfca6bac-bca4-4b17-aa48-0e0171c2301f.json @@ -0,0 +1,38 @@ +{ + "id": "dfca6bac-bca4-4b17-aa48-0e0171c2301f", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "15770008", + "text": "BACKGROUND:\nThe lower breast cancer incidence in minority women and the higher breast cancer mortality in African American women than in white women are largely unexplained. The influence of breast cancer risk factors on these differences has received little attention.\n\nMETHODS:\nRacial/ethnic differences in breast cancer incidence and outcome were examined in 156,570 postmenopausal women participating in the Women's Health Initiative. Detailed information on breast cancer risk factors including mammography was collected, and participants were followed prospectively for breast cancer incidence, pathological breast cancer characteristics, and breast cancer mortality. Comparisons of breast cancer incidence and mortality across racial/ethnic groups were estimated as hazard ratios (HRs) and 95% confidence intervals (CIs) from Cox proportional hazard models. Tumor characteristics were compared as odds ratios (ORs) and 95% confidence intervals in logistic regression models.\n\nRESULTS:\nAfter median follow-up of 6.3 years, 3938 breast cancers were diagnosed. Age-adjusted incidences for all minority groups (i.e., African American, Hispanic, American Indian/Alaskan Native, and Asian/Pacific Islander) were lower than for white women, but adjustment for breast cancer risk factors accounted for the differences for all but African Americans (HR = 0.75, 95% CI = 0.61 to 0.92) corresponding to 29 cases and 44 cases per 10,000 person years for African American and white women, respectively. Breast cancers in African American women had unfavorable characteristics; 32% of those in African Americans but only 10% in whites were both high grade and estrogen receptor negative (adjusted OR = 4.70, 95% CI = 3.12 to 7.09). Moreover, after adjustment for prognostic factors, African American women had higher mortality after breast cancer than white women (HR = 1.79, 95% CI = 1.05 to 3.05) corresponding to nine and six deaths per 10 000 person-years from diagnosis in African American and white women, respectively.\n\nCONCLUSION:\nDifferences in breast cancer incidence rates between most racial/ethnic groups were largely explained by risk factor distribution except in African Americans. However, breast cancers in African American women more commonly had characteristics of poor prognosis, which may contribute to their increased mortality after diagnosis." + }, + "questions": [ + { + "id": "9ab59afc-2d57-44fa-b047-98f708350f80", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1776, + "text": "African American women" + }, + { + "answer_start": 2172, + "text": "African Americans" + } + ] + } + ] +} \ No newline at end of file diff --git a/dfeec45e-5cfe-44f1-91c0-ba41e7db0478.json b/dfeec45e-5cfe-44f1-91c0-ba41e7db0478.json new file mode 100644 index 0000000000000000000000000000000000000000..359355d0909be759c5ae43eee73ba4b9b79386f1 --- /dev/null +++ b/dfeec45e-5cfe-44f1-91c0-ba41e7db0478.json @@ -0,0 +1,50 @@ +{ + "id": "dfeec45e-5cfe-44f1-91c0-ba41e7db0478", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "17406351", + "text": "We performed a survival analysis to assess the effect of meat consumption and meat type on the risk of breast cancer in the UK Women's Cohort Study. Between 1995 and 1998 a cohort of 35 372 women was recruited, aged between 35 and 69 years with a wide range of dietary intakes, assessed by a 217-item food frequency questionnaire. Hazard ratios (HRs) were estimated using Cox regression adjusted for known confounders. High consumption of total meat compared with none was associated with premenopausal breast cancer, HR=1.20 (95% CI: 0.86-1.68), and high non-processed meat intake compared with none, HR=1.20 (95% CI: 0.86-1.68). Larger effect sizes were found in postmenopausal women for all meat types, with significant associations with total, processed and red meat consumption. Processed meat showed the strongest HR=1.64 (95% CI: 1.14-2.37) for high consumption compared with none. Women, both pre- and postmenopausal, who consumed the most meat had the highest risk of breast cancer." + }, + "questions": [ + { + "id": "4a6d1063-49ff-4f7d-bab7-6a9c9eb60c0e", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 551, + "text": "high non-processed meat intake compared with none" + }, + { + "answer_start": 419, + "text": "High consumption of total meat compared with none" + }, + { + "answer_start": 690, + "text": "all meat types, with significant associations with total, processed and red meat consumption" + }, + { + "answer_start": 784, + "text": "Processed meat" + }, + { + "answer_start": 889, + "text": "Women, both pre- and postmenopausal, who consumed the most meat" + } + ] + } + ] +} \ No newline at end of file diff --git a/dff94248-1423-4ab8-ac6c-1cbf00e19a1f.json b/dff94248-1423-4ab8-ac6c-1cbf00e19a1f.json new file mode 100644 index 0000000000000000000000000000000000000000..218cdda6b90a5cc1c6f5b65950fd8eb1ebcf63c1 --- /dev/null +++ b/dff94248-1423-4ab8-ac6c-1cbf00e19a1f.json @@ -0,0 +1,35 @@ +{ + "id": "dff94248-1423-4ab8-ac6c-1cbf00e19a1f", + "disease": { + "id": "H00056", + "names": [ + "Alzheimer disease", + "Dementia due to Alzheimer disease" + ], + "dbLinks": { + "icd10": [ + "G30" + ], + "mesh": [ + "D000544" + ] + }, + "category": "Neurodegenerative disease" + }, + "article": { + "id": "25341874", + "text": "Drugs that modify the risk of dementia in the elderly are of potential interest for dementia prevention. Proton pump inhibitors (PPIs) are widely used to reduce gastric acid production, but information on the risk of dementia is lacking. We assessed association between the use of PPIs and the risk of dementia in elderly people. Data were derived from a longitudinal, multicenter cohort study in elderly primary care patients, the German Study on Aging, Cognition and Dementia in Primary Care Patients (AgeCoDe), including 3,327 community-dwelling persons aged ≥ 75 years. From follow-up 1 to follow-up 4 (follow-up interval 18 months), we identified a total of 431 patients with incident any dementia, including 260 patients with Alzheimer's disease. We used time-dependent Cox regression to estimate hazard ratios of incident any dementia and Alzheimer's disease. Potential confounders included in the analysis comprised age, sex, education, the Apolipoprotein E4 (ApoE4) allele status, polypharmacy, and the comorbidities depression, diabetes, ischemic heart disease, and stroke. Patients receiving PPI medication had a significantly increased risk of any dementia [Hazard ratio (HR) 1.38, 95% confidence interval (CI) 1.04-1.83] and Alzheimer's disease (HR 1.44, 95% CI 1.01-2.06) compared with nonusers. Due to the major burden of dementia on public health and the lack of curative medication, this finding is of high interest to research on dementia and provides indication for dementia prevention." + }, + "questions": [ + { + "id": "52b0ca5d-d001-46d1-b1b3-75b4d2f1cb32", + "text": "What are the risk factors of Alzheimer disease?", + "answers": [ + { + "answer_start": 1084, + "text": "Patients receiving PPI medication" + } + ] + } + ] +} \ No newline at end of file diff --git a/e035f911-c11b-4c66-990c-1eba6eb1e47a.json b/e035f911-c11b-4c66-990c-1eba6eb1e47a.json new file mode 100644 index 0000000000000000000000000000000000000000..cfa29fa08602965569adb27adf4934f6e28a477e --- /dev/null +++ b/e035f911-c11b-4c66-990c-1eba6eb1e47a.json @@ -0,0 +1,34 @@ +{ + "id": "e035f911-c11b-4c66-990c-1eba6eb1e47a", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "22238330", + "text": "AIMS:\nTo evaluate the association between occupational and leisure-time physical activity (PA), ownership of goods promoting sedentary behaviour, and the risk of myocardial infarction (MI) in different socio-economic populations of the world. Studies in developed countries have found low PA as a risk factor for cardiovascular disease; however, the protective effect of occupational PA is less certain. Moreover, ownership of goods promoting sedentary behaviour may be associated with an increased risk.\n\nMETHODS:\nIn INTERHEART, a case-control study of 10 043 cases of first MI and 14 217 controls who did not report previous angina or physical disability completed a questionnaire on work and leisure-time PA.\n\nRESULTS:\nSubjects whose occupation involved either light [multivariable-adjusted odds ratio (OR) 0.78, confidence interval (CI) 0.71-0.86] or moderate (OR 0.89, CI 0.80-0.99) PA were at a lower risk of MI, whereas those who did heavy physical labour were not (OR 1.02, CI 0.88-1.19), compared with sedentary subjects. Mild exercise (OR 0.87, CI 0.81-0.93) as well as moderate or strenuous exercise (OR 0.76, CI 0.69-0.82) was protective. The effect of PA was observed across countries with low, middle, and high income. Subjects who owned both a car and a television (TV) (multivariable-adjusted OR 1.27, CI 1.05-1.54) were at higher risk of MI compared with those who owned neither.\n\nCONCLUSION:\nLeisure-time PA and mild-to-moderate occupational PA, but not heavy physical labour, were associated with a reduced risk, while ownership of a car and TV was associated with an increased risk of MI across all economic regions." + }, + "questions": [ + { + "id": "368f4937-4fd3-40f6-80da-2569cd8e815e", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1538, + "text": "ownership of a car and TV" + } + ] + } + ] +} \ No newline at end of file diff --git a/e0ea2e67-798b-43e7-8a6b-a241d49a1593.json b/e0ea2e67-798b-43e7-8a6b-a241d49a1593.json new file mode 100644 index 0000000000000000000000000000000000000000..6c7ffbb712893e13f2b82dfc9c0a5122bea6905c --- /dev/null +++ b/e0ea2e67-798b-43e7-8a6b-a241d49a1593.json @@ -0,0 +1,38 @@ +{ + "id": "e0ea2e67-798b-43e7-8a6b-a241d49a1593", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "20026811", + "text": "BACKGROUND:\nConsumption of Chinese herbs that contain aristolochic acid (eg, Mu Tong) has been associated with an increased risk of urinary tract cancer.\n\nMETHODS:\nWe conducted a population-based case-control study in Taiwan to examine the association between prescribed Chinese herbal products that contain aristolochic acid and urinary tract cancer. All patients newly diagnosed with urinary tract cancer (case subjects) from January 1, 2001, to December 31, 2002, and a random sample of the entire insured population from January 1, 1997, to December 31, 2002 (control subjects), were selected from the National Health Insurance reimbursement database. Subjects who were ever prescribed more than 500 pills of nonsteroidal anti-inflammatory drugs and/or acetaminophen were excluded, leaving 4594 case patients and 174,701 control subjects in the final analysis. Adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by using multivariable logistic regression models for the association between prescribed Chinese herbs containing aristolochic acid and the occurrence of urinary tract cancer. Models were adjusted for age, sex, residence in a township where black foot disease was endemic (an indicator of chronic arsenic exposure from drinking water [a risk factor for urinary tract cancer]), and history of chronic urinary tract infection. Statistical tests were two-sided.\n\nRESULTS:\nHaving been prescribed more than 60 g of Mu Tong and an estimated consumption of more than 150 mg of aristolochic acid were independently associated with an increased risk for urinary tract cancer in multivariable analyses (Mu Tong: at 61-100 g, OR = 1.6, 95% CI = 1.3 to 2.1, and at \u003e200 g, OR = 2.1, 95% CI = 1.3 to 3.4; aristolochic acid: at 151-250 mg, OR = 1.4, 95% CI = 1.1 to 1.8, and at \u003e500 mg, OR = 2.0, 95% CI = 1.4 to 2.9). A statistically significant linear dose-response relationship was observed between the prescribed dose of Mu Tong or the estimated cumulative dose of aristolochic acid and the risk of urinary tract cancer (P \u003c .001 for both).\n\nCONCLUSIONS:\nConsumption of aristolochic acid-containing Chinese herbal products is associated with an increased risk of cancer of the urinary tract in a dose-dependent manner that is independent of arsenic exposure." + }, + "questions": [ + { + "id": "92c424f7-f860-48ff-93d4-b6fccd48ba15", + "text": "What are the risk factors of Bladder Cancer?", + "answers": [ + { + "answer_start": 2087, + "text": "Consumption of aristolochic acid-containing Chinese herbal products" + }, + { + "answer_start": 1411, + "text": "Having been prescribed more than 60 g of Mu Tong and an estimated consumption of more than 150 mg of aristolochic acid" + } + ] + } + ] +} \ No newline at end of file diff --git a/e0f578a1-165b-4123-8229-1abd54e08250.json b/e0f578a1-165b-4123-8229-1abd54e08250.json new file mode 100644 index 0000000000000000000000000000000000000000..efe500008c340510d9103d289e44133116b4846e --- /dev/null +++ b/e0f578a1-165b-4123-8229-1abd54e08250.json @@ -0,0 +1,35 @@ +{ + "id": "e0f578a1-165b-4123-8229-1abd54e08250", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "8345417", + "text": "Information on long-term respiratory symptoms in prematurely born children is scanty. We studied an unselected population of 9- to 11-year-old schoolchildren. A self-administered questionnaire was distributed to the parents. Children underwent lung function testing, cold air challenge, and skin prick tests. A gestational age \u003c 37 weeks in children with a birth weight \u003c or = 2500 gm was reported by 5% of the parents. Premature girls had significantly more current asthma (odds ratio (OR) 2.6; 95% confidence interval (CI) 1.4, 4.7; p \u003c 0.05), recurrent wheezing (OR 1.7; 95% CI 1.1, 2.7; p \u003c 0.001), recurrent shortness of breath (OR 2.4; 95% CI 1.5, 3.9; p \u003c 0.001), and frequent cough with exercise (OR 1.8; 95% CI 1.1, 2.9; p \u003c 0.05) than term girls, especially if they required mechanical ventilation after birth. No such differences could be shown in boys. More prematurely born children who required mechanical ventilation (OR 3.7; 95% CI 2.2, 6.4; p \u003c 0.0001) had a family history of asthma than children born at term. Significant decrements could be demonstrated for different measurements of lung function in premature girls. These results remained significant after control for confounders in a multivariate regression analysis. No difference was found between groups for bronchial hyperresponsiveness to cold, dry air or for atopic sensitization. We conclude that a family history of asthma may predispose premature children to more severe respiratory disease. Respiratory symptoms and decrements in lung function seen in girls may reflect abnormalities of lung function in survivors of severe neonatal respiratory disease." + }, + "questions": [ + { + "id": "bcc4b290-8661-4ba8-84bc-67482ebc7872", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 420, + "text": "Premature girls" + } + ] + } + ] +} \ No newline at end of file diff --git a/e19409c0-fe7c-4caf-9019-602d48f98fc8.json b/e19409c0-fe7c-4caf-9019-602d48f98fc8.json new file mode 100644 index 0000000000000000000000000000000000000000..9f65118f432b1961418cb8ca4fa8e08719aad3b9 --- /dev/null +++ b/e19409c0-fe7c-4caf-9019-602d48f98fc8.json @@ -0,0 +1,39 @@ +{ + "id": "e19409c0-fe7c-4caf-9019-602d48f98fc8", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "24164287", + "text": "BACKGROUND:\nRecent studies reported increased risks for the development of asthma in children after prenatal exposure to acid-suppressive drugs. As a result of common pathogenesis, associations could also be present for other allergic diseases.\n\nMETHODS:\nUsing the prescription database IADB.nl, we conducted a cohort study amongst 33 536 children in the Netherlands, with a maximum follow-up of 8 years. Maternal exposure was defined as ≥1 dispensed prescription for proton pump inhibitors (PPIs) and/or Histamine 2-antagonists (H2As) during pregnancy. Children were considered to have a drug-treated allergic disease if they received either ≥2 prescriptions for dermal (atopic dermatitis), inhaled (asthma) or nasal (allergic rhinitis) steroids within a 12-month period. Clustered Cox proportional hazard regression was used to estimate crude and adjusted hazard ratios (aHR) with 95% confidence intervals (95% CI).\n\nRESULTS:\nThe aHR for the development of any allergic disease was 1.37 (95% CI: 1.14-1.66) for children exposed to PPIs or H2As. Prenatal exposure to PPIs and/or H2As was associated with atopic dermatitis, asthma and allergic rhinitis with aHRs of 1.32 (95% CI 1.06-1.64), 1.57 (95% CI 1.20-2.05) and 2.40 (95% CI 1.42-4.04), respectively. The aHR for the development of two or more (aHR 2.13 95% CI: 1.43-3.19) and three allergic diseases (aHR 5.18 95% CI: 2.16-12.42) were even more elevated after prenatal exposure to PPIs or H2As.\n\nCONCLUSION:\nPrenatal exposure to PPIs and H2As appeared associated with an increased risk for the development of atopic dermatitis, asthma and allergic rhinitis in the offspring, especially with the development of multiple allergic diseases. Because our study has limitations inherent to observational studies, prospective studies are now warranted to confirm our findings." + }, + "questions": [ + { + "id": "1e3a1c07-4699-4e53-a9c9-327a222187a2", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1466, + "text": "Prenatal exposure to PPIs and H2As" + }, + { + "answer_start": 1047, + "text": "Prenatal exposure to PPIs and/or H2As" + } + ] + } + ] +} \ No newline at end of file diff --git a/e1a65cc2-2866-4980-9e62-53b855cf9e58.json b/e1a65cc2-2866-4980-9e62-53b855cf9e58.json new file mode 100644 index 0000000000000000000000000000000000000000..031d7b117eb74827960d8d63d4dea0505a9c8b64 --- /dev/null +++ b/e1a65cc2-2866-4980-9e62-53b855cf9e58.json @@ -0,0 +1,45 @@ +{ + "id": "e1a65cc2-2866-4980-9e62-53b855cf9e58", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "18420544", + "text": "Colorectal cancer is an alcohol-related malignancy; however, the association appears to be stronger among Asian populations with a relatively high prevalence of the slow-metabolizing aldehyde dehydrogenase variant. To examine the association between alcohol consumption and colorectal cancer in Japanese, the authors analyzed original data from five cohort studies that measured alcohol intake using validated questionnaires at baseline. Hazard ratios were calculated in the individual studies, with adjustment for a common set of variables, and then combined using a random-effects model. During 2,231,010 person-years of follow-up (ranging variously from 1988 to 2004), 2,802 colorectal cancer cases were identified. In men, multivariate-adjusted pooled hazard ratios for alcohol intakes of 23-45.9 g/day, 46-68.9 g/day, 69-91.9 g/day, and \u003e or =92 g/day, compared with nondrinking, were 1.42 (95% confidence interval (CI): 1.21, 1.66), 1.95 (95% CI: 1.53, 2.49), 2.15 (95% CI: 1.74, 2.64), and 2.96 (95% CI: 2.27, 3.86), respectively (p for trend \u003c 0.001). The association was evident for both the colon and the rectum. A significant positive association was also observed in women. One fourth of colorectal cancer cases in men were attributable to an alcohol intake of \u003e or =23 g/day. An alcohol-colorectal cancer association seems to be more apparent in Japanese than in Western populations. Whether this difference can be ascribed to genetic or environmental factors needs to be clarified." + }, + "questions": [ + { + "id": "4ccf567e-09f9-44e6-b26b-430e65ab14fd", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 24, + "text": "alcohol-related malignancy" + }, + { + "answer_start": 774, + "text": "alcohol intakes of 23-45.9 g/day, 46-68.9 g/day, 69-91.9 g/day, and \u003e or =92 g/day" + }, + { + "answer_start": 1255, + "text": "alcohol intake of \u003e or =23 g/day" + } + ] + } + ] +} \ No newline at end of file diff --git a/e1baf6d4-af00-4574-b13d-276bd89cb2c7.json b/e1baf6d4-af00-4574-b13d-276bd89cb2c7.json new file mode 100644 index 0000000000000000000000000000000000000000..769f0ae3fd2607d87aa1185e16a904bf7f046dc9 --- /dev/null +++ b/e1baf6d4-af00-4574-b13d-276bd89cb2c7.json @@ -0,0 +1,43 @@ +{ + "id": "e1baf6d4-af00-4574-b13d-276bd89cb2c7", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "15998953", + "text": "BACKGROUND:\nMelanoma risk factors include fair pigmentation, multiple nevi, low DNA repair capacity, and CDKN2A or CDK4 mutations. Variants of the melanocortin-1 receptor (MC1R) gene have been associated with fair pigmentation and melanoma risk, and a polymorphism of the Agouti Signaling Protein (ASIP) gene has been associated with dark pigmentation. We examined MC1R and ASIP genotypes in relation to phenotypic characteristics, sporadic and familial melanoma risk, and melanoma thickness as an indicator of disease progression in a Mediterranean population.\n\nMETHODS:\nWe studied 267 melanoma patients and 382 control subjects from a case-control study and a family study in northeastern Italy. Host factors were assessed by physical examination, questionnaire, spectrophotometer, and minimal erythema dose measurement. MC1R was sequenced, ASIP was genotyped, and DNA repair capacity was measured by the host-cell reactivation assay. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated by logistic regression models. Effect modification of the association between MC1R and melanoma risk by phenotypic characteristics and DNA repair capacity was also assessed. All statistical tests were two-sided.\n\nRESULTS:\nCarrying MC1R variant alleles was associated with a two- to fourfold increase in risk of both sporadic and familial melanoma compared with carrying wild-type MC1R, particularly in individuals carrying multiple variant alleles (OR = 3.9; 95% CI = 3.3 to 4.6). This association was stronger in individuals with fewer additional risk factors (those with dark skin or few nevi). MC1R variant allele carriers were also three to four times more likely than were non-carriers to have thick melanomas. The ASIP polymorphism was not associated with pigmentation, nevi, or melanoma risk.\n\nCONCLUSIONS:\nMC1R was associated with melanoma risk and progression in a Mediterranean population, particularly in the absence of other strong risk factors, such as freckling or many nevi." + }, + "questions": [ + { + "id": "919278f5-fdc9-4231-8548-0434e04aebab", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 1227, + "text": "Carrying MC1R variant alleles" + }, + { + "answer_start": 1602, + "text": "MC1R variant allele carriers" + }, + { + "answer_start": 1819, + "text": "MC1R" + } + ] + } + ] +} \ No newline at end of file diff --git a/e2875222-989c-498b-a900-f358d5e8908d.json b/e2875222-989c-498b-a900-f358d5e8908d.json new file mode 100644 index 0000000000000000000000000000000000000000..4ce28c9708b9a12d5848c272585ee086c348ac5f --- /dev/null +++ b/e2875222-989c-498b-a900-f358d5e8908d.json @@ -0,0 +1,38 @@ +{ + "id": "e2875222-989c-498b-a900-f358d5e8908d", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "17229950", + "text": "BACKGROUND:\nExtensive mammographic density is associated with an increased risk of breast cancer and makes the detection of cancer by mammography difficult, but the influence of density on risk according to method of cancer detection is unknown.\n\nMETHODS:\nWe carried out three nested case-control studies in screened populations with 1112 matched case-control pairs. We examined the association of the measured percentage of density in the baseline mammogram with risk of breast cancer, according to method of cancer detection, time since the initiation of screening, and age.\n\nRESULTS:\nAs compared with women with density in less than 10% of the mammogram, women with density in 75% or more had an increased risk of breast cancer (odds ratio, 4.7; 95% confidence interval [CI], 3.0 to 7.4), whether detected by screening (odds ratio, 3.5; 95% CI, 2.0 to 6.2) or less than 12 months after a negative screening examination (odds ratio, 17.8; 95% CI, 4.8 to 65.9). Increased risk of breast cancer, whether detected by screening or other means, persisted for at least 8 years after study entry and was greater in younger than in older women. For women younger than the median age of 56 years, 26% of all breast cancers and 50% of cancers detected less than 12 months after a negative screening test were attributable to density in 50% or more of the mammogram.\n\nCONCLUSIONS:\nExtensive mammographic density is strongly associated with the risk of breast cancer detected by screening or between screening tests. A substantial fraction of breast cancers can be attributed to this risk factor." + }, + "questions": [ + { + "id": "5fa798f4-db12-4367-bcdb-b6b1e429ec2f", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 658, + "text": "women with density in 75% or more" + }, + { + "answer_start": 1372, + "text": "Extensive mammographic density" + } + ] + } + ] +} \ No newline at end of file diff --git a/e2d87680-e627-4abd-952f-2af3bcbd0297.json b/e2d87680-e627-4abd-952f-2af3bcbd0297.json new file mode 100644 index 0000000000000000000000000000000000000000..be4824a7253e60839efd2836fb0ad4841d021185 --- /dev/null +++ b/e2d87680-e627-4abd-952f-2af3bcbd0297.json @@ -0,0 +1,38 @@ +{ + "id": "e2d87680-e627-4abd-952f-2af3bcbd0297", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "23779232", + "text": "IMPORTANCE:\nRed meat consumption has been consistently associated with an increased risk of type 2 diabetes mellitus (T2DM). However, whether changes in red meat intake are related to subsequent T2DM risk remains unknown.\n\nOBJECTIVE:\nTo evaluate the association between changes in red meat consumption during a 4-year period and subsequent 4-year risk of T2DM in US adults.\n\nDESIGN AND SETTING:\nThree prospective cohort studies in US men and women.\n\nPARTICIPANTS:\nWe followed up 26,357 men in the Health Professionals Follow-up Study (1986-2006), 48,709 women in the Nurses' Health Study (1986-2006), and 74,077 women in the Nurses' Health Study II (1991-2007). Diet was assessed by validated food frequency questionnaires and updated every 4 years. Time-dependent Cox proportional hazards regression models were used to calculate hazard ratios with adjustment for age, family history, race, marital status, initial red meat consumption, smoking status, and initial and changes in other lifestyle factors (physical activity, alcohol intake, total energy intake, and diet quality). Results across cohorts were pooled by an inverse variance-weighted, fixed-effect meta-analysis.\n\nMAIN OUTCOMES AND MEASURES:\nIncident T2DM cases validated by supplementary questionnaires.\n\nRESULTS:\nDuring 1,965,824 person-years of follow-up, we documented 7540 incident T2DM cases. In the multivariate-adjusted models, increasing red meat intake during a 4-year interval was associated with an elevated risk of T2DM during the subsequent 4 years in each cohort (all P \u003c .001 for trend). Compared with the reference group of no change in red meat intake, increasing red meat intake of more than 0.50 servings per day was associated with a 48% (pooled hazard ratio, 1.48; 95% CI, 1.37-1.59) elevated risk in the subsequent 4-year period, and the association was modestly attenuated after further adjustment for initial body mass index and concurrent weight gain (1.30; 95% CI, 1.21-1.41). Reducing red meat consumption by more than 0.50 servings per day from baseline to the first 4 years of follow-up was associated with a 14% (pooled hazard ratio, 0.86; 95% CI, 0.80-0.93) lower risk during the subsequent entire follow-up through 2006 or 2007.\n\nCONCLUSIONS AND RELEVANCE:\nIncreasing red meat consumption over time is associated with an elevated subsequent risk of T2DM, and the association is partly mediated by body weight. Our results add further evidence that limiting red meat consumption over time confers benefits for T2DM prevention." + }, + "questions": [ + { + "id": "a5338517-92fa-4d35-b35f-3495cf16ecac", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1635, + "text": "increasing red meat intake of more than 0.50 servings per day" + }, + { + "answer_start": 2254, + "text": "Increasing red meat consumption over time" + } + ] + } + ] +} \ No newline at end of file diff --git a/e3498359-d8a5-4285-bee0-09d2f96fb44e.json b/e3498359-d8a5-4285-bee0-09d2f96fb44e.json new file mode 100644 index 0000000000000000000000000000000000000000..86e752283688690dbaed8c9c1d0afb58bcc8cbdb --- /dev/null +++ b/e3498359-d8a5-4285-bee0-09d2f96fb44e.json @@ -0,0 +1,34 @@ +{ + "id": "e3498359-d8a5-4285-bee0-09d2f96fb44e", + "disease": { + "id": "H00408", + "names": [ + "Type 1 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E10" + ], + "mesh": [ + "D003922" + ] + }, + "category": "Metabolic disease; Immune system disease; Endocrine disease" + }, + "article": { + "id": "15530631", + "text": "The incidence of childhood type 1 diabetes has risen over the past 50 years. We compared the frequency of HLA class II haplotypes in 194 patients diagnosed more than 50 years ago and 582 age-matched and sex-matched individuals diagnosed between 1985 and 2002. The proportion of high-risk susceptibility genotypes was increased in the earlier cohort (p=0.003), especially in those diagnosed at age 5 years or younger, which is consistent with the hypothesis that the rise of type 1 diabetes is due to a major environmental effect." + }, + "questions": [ + { + "id": "11d3db90-3380-413f-aae8-936cc1ca4fbf", + "text": "What are the risk factors of Type 1 diabetes mellitus?", + "answers": [ + { + "answer_start": 106, + "text": "HLA class II haplotypes" + } + ] + } + ] +} \ No newline at end of file diff --git a/e37fc4c2-46e8-41d6-bc38-5975bd2c4e29.json b/e37fc4c2-46e8-41d6-bc38-5975bd2c4e29.json new file mode 100644 index 0000000000000000000000000000000000000000..baa1c252217db68fe0328a8182e6e5a18a2afac0 --- /dev/null +++ b/e37fc4c2-46e8-41d6-bc38-5975bd2c4e29.json @@ -0,0 +1,46 @@ +{ + "id": "e37fc4c2-46e8-41d6-bc38-5975bd2c4e29", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "22983636", + "text": "AIMS/HYPOTHESIS:\nA diet rich in meat has been reported to contribute to the risk of type 2 diabetes. The present study aims to investigate the association between meat consumption and incident type 2 diabetes in the EPIC-InterAct study, a large prospective case-cohort study nested within the European Prospective Investigation into Cancer and Nutrition (EPIC) study.\n\nMETHODS:\nDuring 11.7 years of follow-up, 12,403 incident cases of type 2 diabetes were identified among 340,234 adults from eight European countries. A centre-stratified random subsample of 16,835 individuals was selected in order to perform a case-cohort design. Prentice-weighted Cox regression analyses were used to estimate HR and 95% CI for incident diabetes according to meat consumption.\n\nRESULTS:\nOverall, multivariate analyses showed significant positive associations with incident type 2 diabetes for increasing consumption of total meat (50 g increments: HR 1.08; 95% CI 1.05, 1.12), red meat (HR 1.08; 95% CI 1.03, 1.13) and processed meat (HR 1.12; 95% CI 1.05, 1.19), and a borderline positive association with meat iron intake. Effect modifications by sex and class of BMI were observed. In men, the results of the overall analyses were confirmed. In women, the association with total and red meat persisted, although attenuated, while an association with poultry consumption also emerged (HR 1.20; 95% CI 1.07, 1.34). These associations were not evident among obese participants.\n\nCONCLUSIONS/INTERPRETATION:\nThis prospective study confirms a positive association between high consumption of total and red meat and incident type 2 diabetes in a large cohort of European adults." + }, + "questions": [ + { + "id": "148869ba-2cbc-4aee-8188-1c0f665f4e91", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 880, + "text": "increasing consumption of total meat" + }, + { + "answer_start": 964, + "text": "red meat" + }, + { + "answer_start": 1006, + "text": "processed meat" + }, + { + "answer_start": 1557, + "text": "high consumption of total and red meat" + } + ] + } + ] +} \ No newline at end of file diff --git a/e3c5dd06-a30c-41b1-85b0-55e93e8199f1.json b/e3c5dd06-a30c-41b1-85b0-55e93e8199f1.json new file mode 100644 index 0000000000000000000000000000000000000000..bbd11bb69cad0950d759d1cad9a9ef497123c0b4 --- /dev/null +++ b/e3c5dd06-a30c-41b1-85b0-55e93e8199f1.json @@ -0,0 +1,35 @@ +{ + "id": "e3c5dd06-a30c-41b1-85b0-55e93e8199f1", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "26826364", + "text": "Alternaria alternata spores are considered a well-known biological contaminant and a very common potent aeroallergen source that is found in environmental samples. The most intense exposure to A. alternata allergens is likely to occur outdoors; however, Alternaria and other allergenic fungi can colonize in indoor environments and thereby increase the fungal aeroallergen exposure levels. A consequence of human exposure to fungal aeroallergens, sensitization to A. alternata, has been unequivocally associated with increased asthma severity. Among allergenic proteins described in this fungal specie, the major allergen, Alt a 1, has been reported as the main elicitor of airborne allergies in patients affected by a mold allergy and considered a marker of primary sensitization to A. alternata. Moreover, A. alternata sensitization seems to be a triggering factor in the development of poly-sensitization, most likely because of the capability of A. alternata to produce, in addition to Alt a 1, a broad and complex array of cross-reactive allergens that present homologs in several other allergenic sources. The study and understanding of A. alternata allergen information may be the key to explaining why sensitization to A. alternata is a risk factor for asthma and also why the severity of asthma is associated to this mold. Compared to other common environmental allergenic sources, such as pollens and dust mites, fungi are reported to be neglected and underestimated. The rise of the A. alternata allergy has enabled more research into the role of this fungal specie and its allergenic components in the induction of IgE-mediated respiratory diseases. Indeed, recent research on the identification and characterization of A. alternata allergens has allowed for the consideration of new perspectives in the categorization of allergenic molds, assessment of exposure and diagnosis of fungi-induced allergies." + }, + "questions": [ + { + "id": "223ec37f-7011-407b-942f-fac6c24d56d3", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1210, + "text": "sensitization to A. alternata" + } + ] + } + ] +} \ No newline at end of file diff --git a/e45d48a3-2b4c-41d7-bcc9-6bde8f0d4b9d.json b/e45d48a3-2b4c-41d7-bcc9-6bde8f0d4b9d.json new file mode 100644 index 0000000000000000000000000000000000000000..cc3194fa4215d17c9b54358032ae166c9602f350 --- /dev/null +++ b/e45d48a3-2b4c-41d7-bcc9-6bde8f0d4b9d.json @@ -0,0 +1,38 @@ +{ + "id": "e45d48a3-2b4c-41d7-bcc9-6bde8f0d4b9d", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "18714061", + "text": "CONTEXT:\nHigh chronic exposure to inorganic arsenic in drinking water has been related to diabetes development, but the effect of exposure to low to moderate levels of inorganic arsenic on diabetes risk is unknown. In contrast, arsenobetaine, an organic arsenic compound derived from seafood intake, is considered nontoxic.\n\nOBJECTIVE:\nTo investigate the association of arsenic exposure, as measured in urine, with the prevalence of type 2 diabetes in a representative sample of US adults.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nCross-sectional study in 788 adults aged 20 years or older who participated in the 2003-2004 National Health and Nutrition Examination Survey (NHANES) and had urine arsenic determinations.\n\nMAIN OUTCOME MEASURE:\nPrevalence of type 2 diabetes across intake of arsenic.\n\nRESULTS:\nThe median urine levels of total arsenic, dimethylarsinate, and arsenobetaine were 7.1, 3.0, and 0.9 mug/L, respectively. The prevalence of type 2 diabetes was 7.7%. After adjustment for diabetes risk factors and markers of seafood intake, participants with type 2 diabetes had a 26% higher level of total arsenic (95% confidence interval [CI], 2.0%-56.0%) and a nonsignificant 10% higher level of dimethylarsinate (95% CI, -8.0% to 33.0%) than participants without type 2 diabetes, and levels of arsenobetaine were similar to those of participants without type 2 diabetes. After similar adjustment, the odds ratios for type 2 diabetes comparing participants at the 80th vs the 20th percentiles were 3.58 for the level of total arsenic (95% CI, 1.18-10.83), 1.57 for dimethylarsinate (95% CI, 0.89-2.76), and 0.69 for arsenobetaine (95% CI, 0.33-1.48).\n\nCONCLUSIONS:\nAfter adjustment for biomarkers of seafood intake, total urine arsenic was associated with increased prevalence of type 2 diabetes. This finding supports the hypothesis that low levels of exposure to inorganic arsenic in drinking water, a widespread exposure worldwide, may play a role in diabetes prevalence. Prospective studies in populations exposed to a range of inorganic arsenic levels are needed to establish whether this association is causal." + }, + "questions": [ + { + "id": "9295735a-ecef-4b27-b615-c18e6aa9f63e", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1845, + "text": "low levels of exposure to inorganic arsenic in drinking water" + }, + { + "answer_start": 1517, + "text": "level of total arsenic" + } + ] + } + ] +} \ No newline at end of file diff --git a/e4d3a294-9541-4ce8-9dc3-5ff16399ab24.json b/e4d3a294-9541-4ce8-9dc3-5ff16399ab24.json new file mode 100644 index 0000000000000000000000000000000000000000..c16ea634694b7c4e86dc50fc21354a66f25f6be0 --- /dev/null +++ b/e4d3a294-9541-4ce8-9dc3-5ff16399ab24.json @@ -0,0 +1,59 @@ +{ + "id": "e4d3a294-9541-4ce8-9dc3-5ff16399ab24", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "30477003", + "text": "IMPORTANCE:\nTwo pathways have been hypothesized for the development of cutaneous melanoma: one typically affects the head and neck, a site with chronic sun damage, and the other affects the trunk, which is less exposed to the sun. However, the possible cause of limb melanomas is less studied under this hypothesis.\n\nOBJECTIVE:\nTo investigate the association between phenotypic characteristics, pattern of UV radiation exposure, and risk of melanoma on different body sites.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nThis study used data on 161 540 women with information on phenotypic characteristics and UV radiation exposure who were part of the Norwegian Women and Cancer study, a population-based prospective study established in 1991 with exposure information collected by questionnaires at baseline and every 4 to 6 years during follow-up through 2015. Data analysis was performed from October 2017 through May 2018.\n\nEXPOSURES:\nParticipants reported hair color, eye color, untanned skin color, number of small symmetric and large asymmetric nevi, and freckling, as well as histories of sunburns, sunbathing vacations, and indoor tanning in childhood, adolescence, and adulthood.\n\nMAIN OUTCOMES AND MEASURES:\nThe Norwegian Women and Cancer study was linked to the Cancer Registry of Norway for data on cancer diagnosis and date of death or emigration. Primary melanoma site was categorized as head and neck, trunk, upper limbs, and lower limbs.\n\nRESULTS:\nDuring follow-up of the 161 540 women in the study (mean age at study entry, 50 years [range, 34-70 years]; mean age at diagnosis, 60 years [range, 34-87 years]), 1374 incident cases of melanoma were diagnosed. Having large asymmetric nevi was a significant risk factor for all sites and was strongest for the lower limbs (relative risk [RR], 3.38; 95% CI, 2.62-4.38) and weakest for the upper limbs (RR, 1.96; 95% CI, 1.22-3.17; P = .02 for heterogeneity). Mean lifetime number of sunbathing vacations was significantly associated with risk of trunk melanomas (RR, 1.14; 95% CI, 1.07-1.22) and lower limb melanomas (RR, 1.12; 95% CI, 1.05-1.19) but not upper limb melanomas (RR, 0.98; 95% CI, 0.88-1.09) and head and neck melanomas (RR, 0.87; 95% CI, 0.73-1.04; P = .006 for heterogeneity). Indoor tanning was associated only with trunk melanomas (RR for the highest tertile, 1.49; 95% CI, 1.16-1.92) and lower limb melanomas (RR for the highest tertile, 1.33; 95% CI, 1.00-1.76; P = .002 for heterogeneity). Skin color, hair color, small symmetric nevi, and history of sunburns were associated with risk of melanoma on all sites.\n\nCONCLUSIONS AND RELEVANCE:\nThese results appear to support the hypothesis of divergent pathways to melanoma and that recreational sun exposure and indoor tanning are associated with melanoma on the lower limbs, the most common site of melanoma in women. These findings appear to have important preventive implications." + }, + "questions": [ + { + "id": "1b5158cb-1606-463d-bd28-4094281273ed", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 1667, + "text": "Having large asymmetric nevi" + }, + { + "answer_start": 1914, + "text": "Mean lifetime number of sunbathing vacations" + }, + { + "answer_start": 2248, + "text": "Indoor tanning" + }, + { + "answer_start": 2466, + "text": "Skin color" + }, + { + "answer_start": 2478, + "text": "hair color" + }, + { + "answer_start": 2706, + "text": "recreational sun exposure" + }, + { + "answer_start": 2736, + "text": "indoor tanning" + } + ] + } + ] +} \ No newline at end of file diff --git a/e558835e-d67d-42a9-bbeb-412adfe8fe56.json b/e558835e-d67d-42a9-bbeb-412adfe8fe56.json new file mode 100644 index 0000000000000000000000000000000000000000..543cedda7c5ff11bc09b3a4d82b5ae9423fa74d6 --- /dev/null +++ b/e558835e-d67d-42a9-bbeb-412adfe8fe56.json @@ -0,0 +1,39 @@ +{ + "id": "e558835e-d67d-42a9-bbeb-412adfe8fe56", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "10573048", + "text": "BACKGROUND:\nObesity and asthma are common disorders, and their prevalence rates continue to rise. Although individuals with asthma may gain weight as a result of activity limitations, the relationship between body mass index (BMI), which is calculated as weight in kilograms divided by the square of height in meters, and risk of developing asthma is not known.\n\nMETHODS:\nWe performed a prospective cohort study of female US registered nurses in the Nurses' Health Study II. In 1991, after excluding women who died with probable asthma or with incomplete data, there were 85911 participants, aged 26 to 46 years. The main outcome measure was self-report of physician-diagnosed asthma with recent use of an asthma medication.\n\nRESULTS:\nFrom 1991 to 1995, we identified 1596 incident cases of asthma. In a multivariate model controlling for 9 potential confounding factors (including age, race, smoking, physical activity, and energy intake), the relative risks of asthma for 6 increasing categories of BMI in 1991 were 0.9, 1.0 (reference), 1.1, 1.6, 1.7, and 2.7 (P for trend \u003c.001). Stronger associations were found using stricter definitions for asthma, and the finding was present in a variety of subgroups. In analyses controlling for the same variables, as well as BMI at age 18, women who gained weight after age 18 were at significantly increased risk of developing asthma during the 4-year follow-up period (P for trend \u003c.001).\n\nCONCLUSIONS:\nThe BMI has a strong, independent, and positive association with risk of adult-onset asthma. The increasing prevalence of obesity in developed nations may help explain concomitant increases in asthma prevalence." + }, + "questions": [ + { + "id": "c92ebd6a-f643-4303-b90a-8d7d405141f0", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1454, + "text": "BMI" + }, + { + "answer_start": 976, + "text": "increasing categories of BMI" + } + ] + } + ] +} \ No newline at end of file diff --git a/e57ca02f-f95e-4afa-a93b-ecb16a2659b0.json b/e57ca02f-f95e-4afa-a93b-ecb16a2659b0.json new file mode 100644 index 0000000000000000000000000000000000000000..5ccd6f22529f75d44d7c3bcbd101499d96ba2c22 --- /dev/null +++ b/e57ca02f-f95e-4afa-a93b-ecb16a2659b0.json @@ -0,0 +1,38 @@ +{ + "id": "e57ca02f-f95e-4afa-a93b-ecb16a2659b0", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "1973968", + "text": "To examine the hypothesis that sleep apnoea is a risk factor for ischaemic heart disease, overnight polysomnography was performed in 101 unselected male survivors of acute myocardial infarction (MI) aged less than 66 yr and in 53 male subjects of similar age without evidence of ischaemic heart disease. The apnoea index (AI, number of apnoea episodes per hour of sleep) was 6.9 (SEM 1.2) in the MI patients versus 1.4 (0.3) in the control subjects. After adjustment for age, body mass index, hypertension, smoking, and cholesterol level, multiple logistic regression analysis identified the top quartile of AI (greater than 5.3) as an independent predictor of MI patients. The relative risk for myocardial infarction between the highest and lowest quartiles of AI was 23.3 (95% confidence interval 3.9-139.9)." + }, + "questions": [ + { + "id": "fb0f2cbb-8b8a-490a-9a1d-090e4b4f2eee", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 592, + "text": "top quartile of AI" + }, + { + "answer_start": 304, + "text": "The apnoea index (AI, number of apnoea episodes per hour of sleep)" + } + ] + } + ] +} \ No newline at end of file diff --git a/e594ea27-ad85-4db1-a042-f40dbbe5a93b.json b/e594ea27-ad85-4db1-a042-f40dbbe5a93b.json new file mode 100644 index 0000000000000000000000000000000000000000..01ce97db9bbf05eaa5983a4ba50b55a9bbd09448 --- /dev/null +++ b/e594ea27-ad85-4db1-a042-f40dbbe5a93b.json @@ -0,0 +1,34 @@ +{ + "id": "e594ea27-ad85-4db1-a042-f40dbbe5a93b", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "12398822", + "text": "Aims To examine the relationship between history of myocardial infarction in first-degree relatives and the risk of developing coronary heart disease (myocardial infarction or coronary revascularization). Methods and Results A total of 9328 males and 10062 females, randomly selected residents of the Reykjavik area, aged 33-81 years, were examined in the period from 1967 to 1996 in a prospective cohort study. Cardiovascular risk assessment was based on characteristics at baseline. Information on history of myocardial infarction in first-degree relatives was obtained from a health questionnaire. Mean follow-up was 18 and 19 years for men and women, respectively. During follow-up 2700 men and 1070 women developed coronary heart disease. Compared with subjects without a family history, the hazard ratio of coronary heart disease was 1.75 (95% confidence interval, CI, 1.59-1.92) for men and 1.83 (95% CI, 1.60-2.11) for women, with one or more first-degree relatives with myocardial infarction. The risk factor profile was significantly worse in individuals with a positive family history. After allowance for these risk factors, the hazard ratio was still highly significant, 1.66 (CI, 1.51-1.82) and 1.64 (CI, 1.43-1.89) for men and women, respectively. Family history of myocardial infarction was attributed to 15.1% of all cases of coronary heart disease in men and 16.6% in women, independent of other known risk factors. Conclusion Family history of myocardial infarction increases the risk of developing coronary heart disease in both men and women and is largely independent of other classic risk factors. Approximately 15% of all myocardial infarctions can be attributed to familial factors that have not been measured in the study or remain to be elucidated." + }, + "questions": [ + { + "id": "e6157e91-5c98-4170-984c-2b7c67e7fd27", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1445, + "text": "Family history of myocardial infarction" + } + ] + } + ] +} \ No newline at end of file diff --git a/e5feb056-4f5e-4a36-a71f-3f80b0ab8579.json b/e5feb056-4f5e-4a36-a71f-3f80b0ab8579.json new file mode 100644 index 0000000000000000000000000000000000000000..152558ee447ee416c13b424b6ba9d994bfbea9ff --- /dev/null +++ b/e5feb056-4f5e-4a36-a71f-3f80b0ab8579.json @@ -0,0 +1,47 @@ +{ + "id": "e5feb056-4f5e-4a36-a71f-3f80b0ab8579", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "26239524", + "text": "OBJECTIVE:\nTo examine the association between symptoms of post-traumatic stress disorder (PTSD) and rheumatoid arthritis (RA) risk in a prospective cohort and to characterize the role of smoking in this relationship.\n\nMETHODS:\nA subset (n = 54,224) of the Nurses' Health Study II, a prospective cohort of female nurses, completed the Brief Trauma Questionnaire and a screen for PTSD symptoms. Participants were categorized based on trauma exposure and number of PTSD symptoms. Incident RA cases (n = 239) from 1989 to 2011 were identified. Cox proportional hazards models were used to calculate hazard ratios (HRs) and 95% confidence intervals (95% CIs) between PTSD symptoms and incident RA. To identify the impact of smoking, secondary and subgroup analyses were performed. In all analyses, PTSD and smoking were lagged 2 years before the development of RA.\n\nRESULTS:\nCompared to no history of trauma/PTSD symptoms, the HR for ≥4 PTSD symptoms and incident RA was 1.76 (95% CI 1.16-2.67) in models adjusted for age, race, and socioeconomic status. The risk for RA increased with an increasing number of PTSD symptoms (P = 0.01). When smoking was added to the model, the HR for RA remained elevated (HR 1.60 [95% CI 1.05-2.43]). In a subgroup analysis, excluding women who smoked before PTSD onset, results were unchanged (HR 1.68 [95% CI 1.04-2.70]).\n\nCONCLUSION:\nThis study suggests that women with high PTSD symptomatology have an elevated risk for RA, independent of smoking, adding to emerging evidence that stress is an important determinant of physical health." + }, + "questions": [ + { + "id": "b22d04ff-f27b-4f61-8e4c-2ec3529a2056", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 929, + "text": "≥4 PTSD symptoms" + }, + { + "answer_start": 1084, + "text": "increasing number of PTSD symptoms" + }, + { + "answer_start": 1402, + "text": "high PTSD symptomatology" + }, + { + "answer_start": 58, + "text": "post-traumatic stress disorder (PTSD)" + } + ] + } + ] +} \ No newline at end of file diff --git a/e63f6b50-8506-48bd-b74f-202f884f5e8b.json b/e63f6b50-8506-48bd-b74f-202f884f5e8b.json new file mode 100644 index 0000000000000000000000000000000000000000..0a5048af815905816092c415f5658862c3c77a45 --- /dev/null +++ b/e63f6b50-8506-48bd-b74f-202f884f5e8b.json @@ -0,0 +1,42 @@ +{ + "id": "e63f6b50-8506-48bd-b74f-202f884f5e8b", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "12594192", + "text": "STUDY OBJECTIVE:\nTo evaluate whether consumption of chlorinated drinking water is associated with bladder cancer.\n\nDESIGN:\nA bibliographic search was conducted and the authors selected studies evaluating individual consumption of chlorinated drinking water and bladder cancer. The authors extracted from each study risk estimates for intermediate and long term (\u003e40 years) consumption of chlorinated water, stratified by sex when possible, and performed meta-analysis for the two exposure levels. A meta-analysis was also performed of the dose-response regression slopes.\n\nSETTING:\nPopulations in Europe and North America.\n\nPARTICIPANTS:\nThose included in six case-control studies (6084 incident bladder cancer cases, 10,816 controls) and two cohort studies (124 incident bladder cancer cases) fulfilling the inclusion criteria.\n\nMAIN RESULTS:\nEver consumption of chlorinated drinking water was associated with an increased risk of bladder cancer in men (combined OR=1.4, 95%CI 1.1 to 1.9) and women (combined OR=1.2, 95%CI 0.7 to 1.8). The combined OR for mid-term exposure in both genders was 1.1 (95% CI 1.0 to 1.2) and for long term exposure was 1.4 (95%CI 1.2 to 1.7). The combined estimate of the slope for a linear increase in risk was 1.13 (95% CI 1.08 to 1.20) for 20 years and 1.27 (95% CI 1.15 to 1.43) for 40 years of exposure in both sexes.\n\nCONCLUSIONS:\nThis meta-analysis of the best available epidemiological evidence indicates that long term consumption of chlorinated drinking water is associated with bladder cancer, particularly in men. The observed relative risk is only moderately high, but the population attributable risk could be important as the vast majority of the population of industrialised countries is potentially exposed to chlorination byproducts for long time periods." + }, + "questions": [ + { + "id": "92699f6d-9326-4a89-9517-791d6702ae92", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 844, + "text": "Ever consumption of chlorinated drinking water" + }, + { + "answer_start": 1127, + "text": "long term exposure" + }, + { + "answer_start": 1449, + "text": "long term consumption of chlorinated drinking water" + } + ] + } + ] +} \ No newline at end of file diff --git a/e76fcd34-742a-436b-ad07-859a24f3fd14.json b/e76fcd34-742a-436b-ad07-859a24f3fd14.json new file mode 100644 index 0000000000000000000000000000000000000000..624ad1ef35e86c2420568fd52ab75b60e2c92abf --- /dev/null +++ b/e76fcd34-742a-436b-ad07-859a24f3fd14.json @@ -0,0 +1,39 @@ +{ + "id": "e76fcd34-742a-436b-ad07-859a24f3fd14", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "25354495", + "text": "Evidence of social determinants of disease and awareness of the impact of these factors on outcomes continues to increase. Social determinants include both socioeconomic and lifestyle factors. This review examines the interface between socioeconomic status (SES) and lifestyle and their effects on melanoma incidence and mortality. Lifestyle factors including occupation, occupational exposures, body mass index, marital status, smoking, recreational sun exposure and tanning were explored as they have a known relationship with melanoma. A remarkable association of SES with melanoma incidence and prognosis has been acknowledged worldwide. Melanoma incidence is increased in populations of higher SES, especially among the highly educated, while lower SES populations present with later-stage disease at time of diagnosis and display greater mortality. The aforementioned lifestyle factors are also related to SES, and have been shown internationally to affect melanoma incidence and mortality. This comprehensive systematic review suggests that lifestyle factors including occupation, occupational exposure, obesity, recreational sun exposure and tanning may explain the relationship between SES and melanoma." + }, + "questions": [ + { + "id": "5b2e4200-5816-47fb-b3ed-374fe8021b56", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 677, + "text": "populations of higher SES" + }, + { + "answer_start": 236, + "text": "socioeconomic status (SES)" + } + ] + } + ] +} \ No newline at end of file diff --git a/e95d7da8-92e3-4cfe-ad9c-f30b76e8eeaf.json b/e95d7da8-92e3-4cfe-ad9c-f30b76e8eeaf.json new file mode 100644 index 0000000000000000000000000000000000000000..27165ebd4da71943e87ee685435ec2c49370e198 --- /dev/null +++ b/e95d7da8-92e3-4cfe-ad9c-f30b76e8eeaf.json @@ -0,0 +1,38 @@ +{ + "id": "e95d7da8-92e3-4cfe-ad9c-f30b76e8eeaf", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "25422909", + "text": "BACKGROUND:\nAlcohol is a risk factor for cancer of the oral cavity, pharynx, oesophagus, colorectum, liver, larynx and female breast, whereas its impact on other cancers remains controversial.\n\nMETHODS:\nWe investigated the effect of alcohol on 23 cancer types through a meta-analytic approach. We used dose-response meta-regression models and investigated potential sources of heterogeneity.\n\nRESULTS:\nA total of 572 studies, including 486 538 cancer cases, were identified. Relative risks (RRs) for heavy drinkers compared with nondrinkers and occasional drinkers were 5.13 for oral and pharyngeal cancer, 4.95 for oesophageal squamous cell carcinoma, 1.44 for colorectal, 2.65 for laryngeal and 1.61 for breast cancer; for those neoplasms there was a clear dose-risk relationship. Heavy drinkers also had a significantly higher risk of cancer of the stomach (RR 1.21), liver (2.07), gallbladder (2.64), pancreas (1.19) and lung (1.15). There was indication of a positive association between alcohol consumption and risk of melanoma and prostate cancer. Alcohol consumption and risk of Hodgkin's and Non-Hodgkin's lymphomas were inversely associated.\n\nCONCLUSIONS:\nAlcohol increases risk of cancer of oral cavity and pharynx, oesophagus, colorectum, liver, larynx and female breast. There is accumulating evidence that alcohol drinking is associated with some other cancers such as pancreas and prostate cancer and melanoma." + }, + "questions": [ + { + "id": "680ecbdb-5ce7-47e9-bb8a-8adb6d557f17", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1166, + "text": "Alcohol" + }, + { + "answer_start": 500, + "text": "heavy drinkers" + } + ] + } + ] +} \ No newline at end of file diff --git a/e98cc536-9091-4d28-96fa-82c39cc42e1f.json b/e98cc536-9091-4d28-96fa-82c39cc42e1f.json new file mode 100644 index 0000000000000000000000000000000000000000..0dc8a92c17dd068c48d0e81686ae0b52949f25b8 --- /dev/null +++ b/e98cc536-9091-4d28-96fa-82c39cc42e1f.json @@ -0,0 +1,46 @@ +{ + "id": "e98cc536-9091-4d28-96fa-82c39cc42e1f", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "8565161", + "text": "BACKGROUND:\nFew epidemiological studies have investigated the relative importance of major coronary risk factors in the two sexes within the same study population. In particular, it is not clear whether smoking carries a similar risk of coronary heart disease in men and women.\n\nMETHODS AND RESULTS:\nThe associations between smoking, serum lipids, blood pressure, and myocardial infarction were examined in a population-based prospective study of 11,843 men and women aged 35 to 52 years at entry. During 12 years, 495 cases of first myocardial infarction among men and 103 cases among women were identified. Myocardial infarction incidence was 4.6 times higher among men. The incidence was increased sixfold in women and threefold in men who smoked at least 20 cigarettes per day compared with never-smokers, and the rate in female heavy smokers exceeded that of never-smoking men. Multivariate analysis identified current smoking as a stronger risk factor in women (relative risk, 3.3; 95% confidence interval [CI], 2.1 to 5.1) than in men (relative risk, 1.9; 95% CI, 1.6 to 2.3). Among those under 45 years old at entry, the smoking-related sex difference was more pronounced (in women: relative risk, 7.1; 95% CI, 2.6 to 19.1) (in men: relative risk, 2.3; 95% CI, 1.6 to 3.2). Serum total cholesterol, HDL cholesterol, and systolic blood pressure were also highly significant predictors in both sexes.\n\nCONCLUSIONS:\nSmoking was a stronger risk factor for myocardial infarction in middle-aged women than in men. Relative risks associated with serum lipids and blood pressure were similar despite large sex differences in myocardial infarction incidence rates." + }, + "questions": [ + { + "id": "92c59598-c083-47c0-9cd3-d4a1b91afd40", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 916, + "text": "current smoking" + }, + { + "answer_start": 1282, + "text": "Serum total cholesterol" + }, + { + "answer_start": 1328, + "text": "systolic blood pressure" + }, + { + "answer_start": 1307, + "text": "HDL cholesterol" + } + ] + } + ] +} \ No newline at end of file diff --git a/e9997db4-a155-4589-996a-f0d0813d3ec6.json b/e9997db4-a155-4589-996a-f0d0813d3ec6.json new file mode 100644 index 0000000000000000000000000000000000000000..b49eb58a9b8f22001d69ff0b2460a2124e6551ff --- /dev/null +++ b/e9997db4-a155-4589-996a-f0d0813d3ec6.json @@ -0,0 +1,34 @@ +{ + "id": "e9997db4-a155-4589-996a-f0d0813d3ec6", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "27074389", + "text": "BACKGROUND:\nIn light of the worldwide increase in childhood obesity, we examined the association between body-mass index (BMI) in late adolescence and death from cardiovascular causes in adulthood.\n\nMETHODS:\nWe grouped data on BMI, as measured from 1967 through 2010 in 2.3 million Israeli adolescents (mean age, 17.3±0.4 years), according to age- and sex-specific percentiles from the U.S. Centers for Disease Control and Prevention. Primary outcomes were the number of deaths attributed to coronary heart disease, stroke, sudden death from an unknown cause, or a combination of all three categories (total cardiovascular causes) by mid-2011. Cox proportional-hazards models were used.\n\nRESULTS:\nDuring 42,297,007 person-years of follow-up, 2918 of 32,127 deaths (9.1%) were from cardiovascular causes, including 1497 from coronary heart disease, 528 from stroke, and 893 from sudden death. On multivariable analysis, there was a graded increase in the risk of death from cardiovascular causes and all causes that started among participants in the group that was in the 50th to 74th percentiles of BMI (i.e., within the accepted normal range). Hazard ratios in the obese group (≥95th percentile for BMI), as compared with the reference group in the 5th to 24th percentiles, were 4.9 (95% confidence interval [CI], 3.9 to 6.1) for death from coronary heart disease, 2.6 (95% CI, 1.7 to 4.1) for death from stroke, 2.1 (95% CI, 1.5 to 2.9) for sudden death, and 3.5 (95% CI, 2.9 to 4.1) for death from total cardiovascular causes, after adjustment for sex, age, birth year, sociodemographic characteristics, and height. Hazard ratios for death from cardiovascular causes in the same percentile groups increased from 2.0 (95% CI, 1.1 to 3.9) during follow-up for 0 to 10 years to 4.1 (95% CI, 3.1 to 5.4) during follow-up for 30 to 40 years; during both periods, hazard ratios were consistently high for death from coronary heart disease. Findings persisted in extensive sensitivity analyses.\n\nCONCLUSIONS:\nA BMI in the 50th to 74th percentiles, within the accepted normal range, during adolescence was associated with increased cardiovascular and all-cause mortality during 40 years of follow-up. Overweight and obesity were strongly associated with increased cardiovascular mortality in adulthood. (Funded by the Environment and Health Fund.)." + }, + "questions": [ + { + "id": "e6e2e4e1-61d2-47f6-a0a0-d579b175effa", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 2005, + "text": "A BMI in the 50th to 74th percentiles, within the accepted normal range, during adolescence" + } + ] + } + ] +} \ No newline at end of file diff --git a/e9de4a04-5daa-43a7-99f7-f40efd10a1f7.json b/e9de4a04-5daa-43a7-99f7-f40efd10a1f7.json new file mode 100644 index 0000000000000000000000000000000000000000..65766ad86ba647492324fc3981c304ebb0455fb5 --- /dev/null +++ b/e9de4a04-5daa-43a7-99f7-f40efd10a1f7.json @@ -0,0 +1,43 @@ +{ + "id": "e9de4a04-5daa-43a7-99f7-f40efd10a1f7", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "10208188", + "text": "STUDY OBJECTIVES:\nTo examine the prevalence of asthma and hay fever, and the incidence and temporal relationships of asthma, hay fever, and chronic bronchitis among adult twins during a 15-year period.\n\nDESIGN:\nProspective cohort study.\n\nPARTICIPANTS:\nA population of 11,540 Finnish adult men and women, initially 18 to 45 years of age, who returned a health questionnaire in 1975, 1981, and 1990 as part of the Finnish Twin Cohort study.\n\nMETHODS:\nAge-standardized prevalences and cumulative incidences among individuals were calculated for asthma, hay fever, and chronic bronchitis. The incidence of asthma among subjects with and without hay fever or chronic bronchitis was analyzed in the entire cohort as well as in twin pairs discordant for incident asthma.\n\nRESULTS:\nThe prevalence of asthma increased slightly from 1975 (2.0% in men and 2.2% in women) to 1990 (2.9% in men and 3.1% in women). The prevalence of hay fever showed a larger increase in men and women (from 6.8% and 9.8% to 11.8% and 15.3%, respectively). Compared with figures for 1976 to 1981, no significant increase in asthma incidence occurred from 1982 to 1990, whereas the incidence of hay fever was lower during the latter period among men (incidence rate ratio, 0.7; 95% confidence interval, 0.6 to 0.9) as was the incidence of chronic bronchitis among women (incidence rate ratio, 0.7; 95% confidence interval, 0.6 to 0.9). Hay fever and chronic bronchitis were usually diagnosed before asthma. Both diseases increased the risk of asthma significantly on the basis of analyses of all individuals and of discordant twin pairs.\n\nCONCLUSIONS:\nThe pattern of increase in asthma and hay fever prevalence with time was similar, and hay fever was a strong predictor of asthma. These diseases showed no significant increase in incidence." + }, + "questions": [ + { + "id": "3de29c7b-f45f-4c81-9a6b-a87886950757", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1706, + "text": "hay fever" + }, + { + "answer_start": 1404, + "text": "Hay fever" + }, + { + "answer_start": 1418, + "text": "chronic bronchitis" + } + ] + } + ] +} \ No newline at end of file diff --git a/eac5a33a-bfb1-4204-a075-0eb562448cc1.json b/eac5a33a-bfb1-4204-a075-0eb562448cc1.json new file mode 100644 index 0000000000000000000000000000000000000000..5fa137e115a9a255be1fb1cd36e36ef8d2059c41 --- /dev/null +++ b/eac5a33a-bfb1-4204-a075-0eb562448cc1.json @@ -0,0 +1,38 @@ +{ + "id": "eac5a33a-bfb1-4204-a075-0eb562448cc1", + "disease": { + "id": "H00408", + "names": [ + "Type 1 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E10" + ], + "mesh": [ + "D003922" + ] + }, + "category": "Metabolic disease; Immune system disease; Endocrine disease" + }, + "article": { + "id": "11302899", + "text": "OBJECTIVE:\nTo assess the associations between birth weight or gestational age and risk of type 1 diabetes.\n\nDESIGN:\nPopulation based cohort study by record linkage of the medical birth registry and the National Childhood Diabetes Registry.\n\nSETTING:\nTwo national registries in Norway.\n\nPARTICIPANTS:\nAll live births in Norway between 1974 and 1998 (1 382 602 individuals) contributed a maximum of 15 years of observation, a total of 8 184 994 person years of observation in the period 1989 to 1998. 1824 children with type 1 diabetes were diagnosed between 1989 and 1998.\n\nMAIN OUTCOME MEASURES:\nEstimates of rate ratios with 95% confidence intervals for type 1 diabetes from Poisson regression analyses.\n\nRESULTS:\nThe incidence rate of type 1 diabetes increased almost linearly with birth weight. The rate ratio for children with birth weights 4500 g or more compared with those with birth weights less than 2000 g was 2.21 (95% confidence interval 1.24 to 3.94), test for trend P=0.0001. There was no significant association between gestational age and type 1 diabetes. The results persisted after adjustment for maternal diabetes and other potential confounders.\n\nCONCLUSION:\nThere is a relatively weak but significant association between birth weight and increased risk of type 1 diabetes consistent over a wide range of birth weights." + }, + "questions": [ + { + "id": "09153967-8e96-4c15-a31b-d372de50e637", + "text": "What are the risk factors of Type 1 diabetes mellitus?", + "answers": [ + { + "answer_start": 817, + "text": "children with birth weights 4500 g or" + }, + { + "answer_start": 1242, + "text": "birth weight and increased risk of type 1 diabetes consistent over a wide range of birth weights" + } + ] + } + ] +} \ No newline at end of file diff --git a/eaed8a7b-009d-4e0e-b84c-dea89eadfb1e.json b/eaed8a7b-009d-4e0e-b84c-dea89eadfb1e.json new file mode 100644 index 0000000000000000000000000000000000000000..bb9393372770be176997308714a11ad8700541df --- /dev/null +++ b/eaed8a7b-009d-4e0e-b84c-dea89eadfb1e.json @@ -0,0 +1,42 @@ +{ + "id": "eaed8a7b-009d-4e0e-b84c-dea89eadfb1e", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "16275870", + "text": "BACKGROUND:\nThe incidence of cardiovascular disease (CVD), coronary heart disease (CHD), and type 2 diabetes mellitus (T2DM) has not been well defined in persons with the metabolic syndrome (at least 3 of the following: abdominal adiposity, low HDL cholesterol, high triglycerides, hypertension, and impaired fasting glucose). The objective was to investigate risk for CVD, CHD, and T2DM according to metabolic syndrome traits.\n\nMETHODS AND RESULTS:\nThe study followed a cohort of 3323 middle-aged adults for the development of new CVD, CHD, and T2DM over an 8-year period. In persons without CVD or T2DM at baseline, the prevalence of the metabolic syndrome (\u003e or =3 of 5 traits) was 26.8% in men and 16.6% in women. There were 174 incident cases of CVD, 107 of CHD, and 178 of T2DM. In men, the metabolic syndrome age-adjusted relative risk (RR) and 95% CIs were RR=2.88 (95% CI 1.99 to 4.16) for CVD, RR=2.54 (95% CI 1.62 to 3.98) for CHD, and RR=6.92 (95% CI 4.47 to 10.81) for T2DM. Event rates and RRs were lower in women for CVD (RR=2.25, 95% CI 1.31 to 3.88) and CHD (RR=1.54, 95% CI 0.68 to 3.53), but they were similar for T2DM (RR=6.90, 95% CI 4.34 to 10.94). Population-attributable risk estimates associated with metabolic syndrome for CVD, CHD, and T2DM were 34%, 29%, and 62% in men and 16%, 8%, 47% in women.\n\nCONCLUSIONS:\nMetabolic syndrome is common and is associated with an increased risk for CVD and T2DM in both sexes. The metabolic syndrome accounts for up to one third of CVD in men and approximately half of new T2DM over 8 years of follow-up." + }, + "questions": [ + { + "id": "0ae4258f-af23-45f3-a6fd-14f066bae568", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1339, + "text": "Metabolic syndrome" + }, + { + "answer_start": 797, + "text": "metabolic syndrome" + }, + { + "answer_start": 1226, + "text": "metabolic syndrome" + } + ] + } + ] +} \ No newline at end of file diff --git a/eb67f833-c923-4c3b-963c-55cc4c1b4111.json b/eb67f833-c923-4c3b-963c-55cc4c1b4111.json new file mode 100644 index 0000000000000000000000000000000000000000..8e72b515bf4339437f585ca87521ead8a2cc251d --- /dev/null +++ b/eb67f833-c923-4c3b-963c-55cc4c1b4111.json @@ -0,0 +1,55 @@ +{ + "id": "eb67f833-c923-4c3b-963c-55cc4c1b4111", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "30760605", + "text": "OBJECTIVES:\nFarming has been associated with rheumatoid arthritis (RA). Some studies have evaluated the effects of pesticides, but other agricultural exposures may also affect immune response.\n\nMETHODS:\nWe investigated non-pesticide agricultural exposures in relation to RA in licensed pesticide applicators (n=27 175, mostly male farmers) and their spouses (n=22 231) in the Agricultural Health Study (AHS) cohort (1993-1997) who completed at least one follow-up survey through 2015. Incident RA cases (n=229 applicators and 249 spouses) were identified based on self-report confirmed by use of disease-modifying antirheumatic drugs or medical records. Hazard Ratios (HRs) and 95% Confidence Intervals (CIs) were estimated by Cox proportional hazard models adjusting for applicator status, state, smoking, education and specific pesticide use, allowing estimates to vary by median age when hazards assumptions were not met.\n\nRESULTS:\nOverall, RA was associated with regularly applying chemical fertilisers (HR=1.50; 95% CI 1.11 to 2.02), using non-gasoline solvents (HR=1.40; 95% CI 1.09 to 1.80), and painting (HR=1.26; 95% CI 1.00 to 1.59). In older applicators (\u003e62 years), RA was associated with driving combines (HR=2.46; 95% CI 1.05 to 5.78) and milking cows (HR=2.56; 95% CI 1.01 to 6.53). In younger participants (≤62 years), RA was inversely associated with raising animals as well as crops (HR=0.68; 95% CI 0.51 to 0.89 vs crops only). Associations with specific crops varied by age: some (eg, hay) were inversely associated with RA in younger participants, while others (eg, alfalfa) were associated with RA in older participants.\n\nCONCLUSION:\nThese findings suggest several agricultural tasks and exposures may contribute to development of RA." + }, + "questions": [ + { + "id": "3f3b257e-6495-437a-991d-f9c2b32a0677", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 967, + "text": "regularly applying chemical fertilisers" + }, + { + "answer_start": 1039, + "text": "using non-gasoline solvents" + }, + { + "answer_start": 1103, + "text": "painting" + }, + { + "answer_start": 1201, + "text": "driving combines" + }, + { + "answer_start": 1253, + "text": "milking cows" + }, + { + "answer_start": 1679, + "text": "several agricultural tasks" + } + ] + } + ] +} \ No newline at end of file diff --git a/eb6a8be6-c707-4089-a96e-4c4e01521d2a.json b/eb6a8be6-c707-4089-a96e-4c4e01521d2a.json new file mode 100644 index 0000000000000000000000000000000000000000..482d785fd612ad95023e14db2ca4159afd51584b --- /dev/null +++ b/eb6a8be6-c707-4089-a96e-4c4e01521d2a.json @@ -0,0 +1,51 @@ +{ + "id": "eb6a8be6-c707-4089-a96e-4c4e01521d2a", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "17206532", + "text": "OBJECTIVE:\nSun exposure is the main cause of melanoma in populations of European origin. No previous study has examined the effect of sun exposure on risk of multiple primary melanomas compared with people who have one melanoma.\n\nMETHODS:\nWe identified and enrolled 2,023 people with a first primary melanoma (controls) and 1,125 with multiple primary melanomas (cases) in seven centers in four countries, recorded their residential history to assign ambient UV and interviewed them about their sun exposure.\n\nRESULTS:\nRisk of multiple primary melanomas increased significantly (P\u003c0.05) to OR=2.10 for the highest exposure quarter of ambient UV irradiance at birth and 10 years of age, to OR=1.38 for lifetime recreational sun exposure, to OR=1.85 for beach and waterside activities, to OR=1.57 for vacations in a sunnier climate, to OR=1.50 for sunburns. Occupational sun exposure did not increase risk (OR=1.03 for highest exposure). Recreational exposure at any age increased risk and appeared to add to risk from ambient UV in early life.\n\nCONCLUSIONS:\nPeople who have had a melanoma can expect to reduce their risk of a further melanoma by reducing recreational sun exposure whatever their age. The same is probably true for a person who has never had a melanoma." + }, + "questions": [ + { + "id": "18d8b187-4897-4a79-bc18-f680438c63f9", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 606, + "text": "highest exposure quarter of ambient UV irradiance at birth and 10 years of age" + }, + { + "answer_start": 701, + "text": "lifetime recreational sun exposure" + }, + { + "answer_start": 752, + "text": "beach and waterside activities" + }, + { + "answer_start": 799, + "text": "vacations in a sunnier climate" + }, + { + "answer_start": 846, + "text": "sunburns" + } + ] + } + ] +} \ No newline at end of file diff --git a/ebb37095-fdfc-4c47-86cc-b0952cf7131b.json b/ebb37095-fdfc-4c47-86cc-b0952cf7131b.json new file mode 100644 index 0000000000000000000000000000000000000000..7cf22f733258e439b2757763fb3d6fad472ab62b --- /dev/null +++ b/ebb37095-fdfc-4c47-86cc-b0952cf7131b.json @@ -0,0 +1,42 @@ +{ + "id": "ebb37095-fdfc-4c47-86cc-b0952cf7131b", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "10588526", + "text": "AIMS:\nTo assess the impact of cigarette smoking on the incidence of Type 2 diabetes mellitus (DM) in middle-aged Japanese men.\n\nMETHODS:\nThe study enrolled 6250 men aged 35-60 years and free of diabetes, impaired fasting glucose and hypertension at entry. Type 2 DM was defined by a fasting plasma glucose level \u003e or =7.0 mmol/l or physician-diagnosed Type 2DM.\n\nRESULTS:\nFour hundred and fifty cases of Type 2 DM were confirmed during the 60904 person-years follow-up. After adjustment for multiple covariates, including age, body mass index, alcohol consumption, physical activity, parental history of diabetes and the level of fasting plasma glucose, total cholesterol, triglycerides, high-density lipoprotein cholesterol and haematocrit, the relative risk of Type 2 DM among current smokers compared with non-smokers was 1.47 (95% confidence interval (CI) 1.14-1.92). Men who smoked \u003e30 cigarettes/day had a multivariate-relative risk of 1.73 (95% CI 1.20-2.48) compared with non-smokers. The number of cigarettes smoked daily and the pack-year values were positively related to the development of Type 2 DM in a dose-dependent manner (P for trends = 0.0026 and 0.001, respectively).\n\nCONCLUSIONS:\nA cigarette smoking habit is an independent risk factor for Type 2 DM." + }, + "questions": [ + { + "id": "4ae4e8ce-1bd6-4773-8f28-58222176120d", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1202, + "text": "A cigarette smoking habit" + }, + { + "answer_start": 779, + "text": "current smokers" + }, + { + "answer_start": 993, + "text": "The number of cigarettes smoked daily and the pack-year values" + } + ] + } + ] +} \ No newline at end of file diff --git a/ebb55c0a-6ff2-4b65-bbd1-38fb6a0252ea.json b/ebb55c0a-6ff2-4b65-bbd1-38fb6a0252ea.json new file mode 100644 index 0000000000000000000000000000000000000000..dc3e04049fab137c3820e89835a28306f7d08217 --- /dev/null +++ b/ebb55c0a-6ff2-4b65-bbd1-38fb6a0252ea.json @@ -0,0 +1,42 @@ +{ + "id": "ebb55c0a-6ff2-4b65-bbd1-38fb6a0252ea", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "25336749", + "text": "OBJECTIVE:\nThe aims of this study were to investigate the association between smoking and incident type 2 diabetes, accounting for a large number of potential confounding factors, and to explore potential effect modifiers and intermediate factors.\n\nRESEARCH DESIGN AND METHODS:\nThe European Prospective Investigation into Cancer and Nutrition (EPIC)-InterAct is a prospective case-cohort study within eight European countries, including 12,403 cases of incident type 2 diabetes and a random subcohort of 16,835 individuals. After exclusion of individuals with missing data, the analyses included 10,327 cases and 13,863 subcohort individuals. Smoking status was used (never, former, current), with never smokers as the reference. Country-specific Prentice-weighted Cox regression models and random-effects meta-analysis were used to estimate hazard ratios (HRs) for type 2 diabetes.\n\nRESULTS:\nIn men, the HRs (95% CI) of type 2 diabetes were 1.40 (1.26, 1.55) for former smokers and 1.43 (1.27, 1.61) for current smokers, independent of age, education, center, physical activity, and alcohol, coffee, and meat consumption. In women, associations were weaker, with HRs (95% CI) of 1.18 (1.07, 1.30) and 1.13 (1.03, 1.25) for former and current smokers, respectively. There was some evidence of effect modification by BMI. The association tended to be slightly stronger in normal weight men compared with those with overall adiposity.\n\nCONCLUSIONS:\nFormer and current smoking was associated with a higher risk of incident type 2 diabetes compared with never smoking in men and women, independent of educational level, physical activity, alcohol consumption, and diet. Smoking may be regarded as a modifiable risk factor for type 2 diabetes, and smoking cessation should be encouraged for diabetes prevention." + }, + "questions": [ + { + "id": "6921a343-dfe8-4d9b-a1a2-d009a5642374", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 964, + "text": "former smokers" + }, + { + "answer_start": 1005, + "text": "current smokers" + }, + { + "answer_start": 1447, + "text": "Former and current smoking" + } + ] + } + ] +} \ No newline at end of file diff --git a/ec0e2704-9c9c-42d0-8460-bf3ef30825e8.json b/ec0e2704-9c9c-42d0-8460-bf3ef30825e8.json new file mode 100644 index 0000000000000000000000000000000000000000..749488185e4e5f9a95ad2dedf7c96a23f842b8dc --- /dev/null +++ b/ec0e2704-9c9c-42d0-8460-bf3ef30825e8.json @@ -0,0 +1,56 @@ +{ + "id": "ec0e2704-9c9c-42d0-8460-bf3ef30825e8", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "33171069", + "text": "The Global Burden of Disease program identified smoking and ambient and household air pollution as the main drivers of death and disability from chronic obstructive pulmonary disease (COPD). To estimate the attributable risk of chronic airflow obstruction (CAO), a quantifiable characteristic of COPD, due to several risk factors. The Burden of Obstructive Lung Disease study is a cross-sectional study of adults, aged ≥40, in a globally distributed sample of 41 urban and rural sites. Based on data from 28,459 participants, we estimated the prevalence of CAO, defined as a postbronchodilator FEV-to-FVC ratio less than the lower limit of normal, and the relative risks associated with different risk factors. Local relative risks were estimated using a Bayesian hierarchical model borrowing information from across sites. From these relative risks and the prevalence of risk factors, we estimated local population attributable risks. The mean prevalence of CAO was 11.2% in men and 8.6% in women. The mean population attributable risk for smoking was 5.1% in men and 2.2% in women. The next most influential risk factors were poor education levels, working in a dusty job for ≥10 years, low body mass index, and a history of tuberculosis. The risk of CAO attributable to the different risk factors varied across sites. Although smoking remains the most important risk factor for CAO, in some areas, poor education, low body mass index, and passive smoking are of greater importance. Dusty occupations and tuberculosis are important risk factors at some sites." + }, + "questions": [ + { + "id": "daecd16f-9522-46f2-9698-095d68cf8ef2", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 1330, + "text": "smoking" + }, + { + "answer_start": 1485, + "text": "Dusty occupations" + }, + { + "answer_start": 1128, + "text": "poor education levels" + }, + { + "answer_start": 1151, + "text": "working in a dusty job for ≥10 years" + }, + { + "answer_start": 1189, + "text": "low body mass index" + }, + { + "answer_start": 1214, + "text": "a history of tuberculosis" + } + ] + } + ] +} \ No newline at end of file diff --git a/ec11b756-af5e-43ef-80bf-5ac01ee413d8.json b/ec11b756-af5e-43ef-80bf-5ac01ee413d8.json new file mode 100644 index 0000000000000000000000000000000000000000..36e03f3425377cffde25a3f2b2cb21742abf6e1f --- /dev/null +++ b/ec11b756-af5e-43ef-80bf-5ac01ee413d8.json @@ -0,0 +1,40 @@ +{ + "id": "ec11b756-af5e-43ef-80bf-5ac01ee413d8", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "7881652", + "text": "We have performed a 4-yr prospective survey of the association of allergen skin test positivity, total serum immunoglobulin E (IgE), and bronchial responsiveness to methacholine, with longitudinal decline in FEV1, in subjects over 65 yr of age. In 1987, 324 subjects completed a respiratory questionnaire, and underwent measurement of FEV1 and FVC, methacholine challenge, skin prick testing (to Dermatophagoides pteronyssinus, cat fur, mixed grasses, and Aspergillus fumigatus) and estimation of total serum IgE. After an interval of 4 yr, 212 subjects were reexamined. The mean annual decline in FEV1 was significantly higher in males than in females, but was not significantly influenced by smoking habits defined at the start of the study. The relation of atopy (skin test reaction to allergen \u003e or = 3 mm greater than saline control), increased bronchial responsiveness (PD20FEV1 \u003c or = 6.4 mumoles methacholine) and serum IgE \u003e 80 IU/ml, to annual decline in FEV1 was examined for each risk factor individually with adjustment for age, sex, height, and initial FEV1, by multiple linear regression. Both atopy and bronchial responsiveness were significantly associated with accelerated decline in FEV1. Elevated IgE was correlated with faster FEV1 decline in subjects who were current smokers at the start of the study. In a multiple regression model examining the mutually adjusted associations of all relevant variables with annual decline in FEV1, male sex was the most important predictor (B = 38.6 ml/yr, 95% Cl = 4.3, 72.9). Increased bronchial responsiveness also tended to be associated with accelerated decline in FEV1. In further analyses incorporating the same variables, but restricted to specific smoking categories, age was the only significant factor in the never-smokers, whereas both atopy (B = 44.5 ml/yr, 95% Cl = 3.8, 85.3) and increased bronchial responsiveness (B = 43.5 ml/yr, 95% Cl = 4.6, 82.3) were significant predictors of accelerated FEV1 decline in former and current smokers combined.(ABSTRACT TRUNCATED AT 250 WORDS)" + }, + "questions": [ + { + "id": "805d53dd-d34d-46ec-827b-9f6392303cf7", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 1853, + "text": "increased bronchial responsiveness" + }, + { + "answer_start": 1806, + "text": "atopy" + } + ] + } + ] +} \ No newline at end of file diff --git a/ec7beefd-ee43-4b91-bece-5003964ecd62.json b/ec7beefd-ee43-4b91-bece-5003964ecd62.json new file mode 100644 index 0000000000000000000000000000000000000000..2745e049bcc67302d37141a54700de24bffb1fe4 --- /dev/null +++ b/ec7beefd-ee43-4b91-bece-5003964ecd62.json @@ -0,0 +1,38 @@ +{ + "id": "ec7beefd-ee43-4b91-bece-5003964ecd62", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "11369742", + "text": "BACKGROUND:\nNarrative reviews have concluded that there is a small association between coffee consumption and an increased risk of urinary tract cancer, possibly due to confounding by smoking. No association for tea consumption has been indicated. This systematic review attempts to summarize and quantify these associations both unadjusted and adjusted for age, smoking and sex.\n\nMETHOD:\nThirty-four case-control and three follow-up studies were included in this systematic review. Summary odds ratios (OR) were calculated by meta-regression analyses.\n\nRESULTS:\nThe unadjusted summary OR indicated a small increased risk of urinary tract cancer for current coffee consumers versus non-drinkers. The adjusted summary OR were: 1.26 (95% CI : 1.09-1.46) for studies with only men, 1.08 (95% CI : 0.79-1.46) for studies with only women and 1.18 (95% CI : 1.01-1.38) for studies with men and women combined. Neither unadjusted nor adjusted summary OR provided evidence for a positive association between tea consumption and urinary tract cancer. Even though studies differed in methodology, the results were rather consistent. We did not perform dose-response analyses for coffee and tea consumption due to sparse data.\n\nCONCLUSIONS:\nIn accordance with earlier reviews, we found that coffee consumption increases the risk of urinary tract cancer by approximately 20%. The consumption of tea seems not to be related to an increased risk of urinary tract cancer." + }, + "questions": [ + { + "id": "0ff4debb-4437-492e-9fc0-e34d66111342", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 650, + "text": "current coffee consumers" + }, + { + "answer_start": 1280, + "text": "coffee consumption" + } + ] + } + ] +} \ No newline at end of file diff --git a/ecc600e9-d8b2-4b75-a8b7-deecb01c746e.json b/ecc600e9-d8b2-4b75-a8b7-deecb01c746e.json new file mode 100644 index 0000000000000000000000000000000000000000..37f24671519998c6daf2ea328e5f8533656dff83 --- /dev/null +++ b/ecc600e9-d8b2-4b75-a8b7-deecb01c746e.json @@ -0,0 +1,42 @@ +{ + "id": "ecc600e9-d8b2-4b75-a8b7-deecb01c746e", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "11827496", + "text": "BACKGROUND:\nThe role of diet in the development of type 2 diabetes mellitus remains unsettled.\n\nOBJECTIVE:\nTo examine the association between major dietary patterns and risk for type 2 diabetes mellitus.\n\nDESIGN:\nProspective cohort study.\n\nSETTING:\nUnited States.\n\nPARTICIPANTS:\n42 504 male health professionals, 40 to 75 years of age, without diagnosed diabetes, cardiovascular disease, or cancer at baseline.\n\nMEASUREMENTS:\nUsing factor analysis based on data from food-frequency questionnaires, we identified and validated two major dietary patterns that we labeled \"prudent\" (characterized by higher consumption of vegetables, fruit, fish, poultry and whole grains) and \"western\" (characterized by higher consumption of red meat, processed meat, French fries, high-fat dairy products, refined grains, and sweets and desserts). Relative risks and 95% CIs were adjusted for potential confounders, including body mass index (BMI), physical activity, and cigarette smoking.\n\nRESULTS:\nDuring 12 years of follow-up (466 508 person-years), we documented 1321 cases of type 2 diabetes. The prudent dietary pattern score was associated with a modestly lower risk for type 2 diabetes (relative risk for extreme quintiles, 0.84 [CI, 0.70 to 1.00]). In contrast, the western dietary pattern score was associated with an increased risk for type 2 diabetes (relative risk, 1.59 [CI, 1.32 to 1.93]; P \u003c 0.001 for trend). A high score for the western dietary pattern combined with low physical activity (relative risk comparing extreme quintiles of dietary pattern score and physical activity, 1.96 [CI, 1.35 to 2.84]) or obesity (relative risk for BMI \u003e or = 30 kg/m2 vs. \u003c25 kg/m2, 11.2 [CI, 8.07 to 15.6]) was associated with a particularly high risk for type 2 diabetes.\n\nCONCLUSION:\nOur findings suggest that a western dietary pattern is associated with a substantially increased risk for type 2 diabetes in men." + }, + "questions": [ + { + "id": "5c0895a4-b352-464c-ae62-f5f0ccf8472b", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1258, + "text": " western dietary pattern" + }, + { + "answer_start": 1431, + "text": "western dietary pattern combined with low physical activity" + }, + { + "answer_start": 1803, + "text": " western dietary pattern" + } + ] + } + ] +} \ No newline at end of file diff --git a/ed083b02-f992-4e79-b4dc-83a3b7f8126f.json b/ed083b02-f992-4e79-b4dc-83a3b7f8126f.json new file mode 100644 index 0000000000000000000000000000000000000000..edefd4c7311fe9ff2dc25e2eed2fa010500d462e --- /dev/null +++ b/ed083b02-f992-4e79-b4dc-83a3b7f8126f.json @@ -0,0 +1,59 @@ +{ + "id": "ed083b02-f992-4e79-b4dc-83a3b7f8126f", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "30238644", + "text": "Background Asthma prevalence in African children is high. Factors driving the prevalence or disease severity are poorly understood. This study aims to investigate environmental factors associated with asthma and severity in African children. Methods Population based cross-sectional study of children aged 13-14 years from 10 African centers who participated in ISAAC III. Self-reported environmental exposures included engaging in physical exercise, television watching, various biomass and ETS exposure, consumption of paracetamol, large family sizes and having pets in the home. Univariable and multivariable analyses were done adjusting for center variations. Prevalences, odds ratio and 95% confidence intervals (CI) were calculated. Results There were 258 267 children recruited among the 13-14-year-old participants. Of these, 28,391 respondents from 232 schools completed both the written questionnaire (WQ) and environmental questionnaire (EQ). The prevalence of asthma and severe asthma were 12.8% (CI 12.4-13.2), and 8.7% (CI 8.4-8.0) respectively. Factors strongly associated with asthma were maternal smoking (OR = 1.41; 95%CI: 1.23-1.64), open fire heating (OR = 1.28; 95%CI: 1.08-1.51) electric heating (OR = 1.13; 95%CI: 1.01-1.28), physical exercise (OR = 1.29; 95%CI: 1.11-1.50), monthly paracetamol use (OR 1.23; 95%CI 1.13-1.33), having an elder sibling (OR = 0.87; 95%CI 0.77-0.98). Factors associated with severe asthma were maternal smoking (OR = 1.61; 95%CI: 1.38-1.89), cat pet (OR = 1.14; 95%CI: 1.04-1.25), frequent physical exercise (OR = 1.42; 95%CI: 1.23-1.64) and monthly paracetamol use (OR = 1.20; 95%CI 1.07, 1.34). Conclusion Several environmental exposures were associated with asthma and severe disease." + }, + "questions": [ + { + "id": "6486066f-fc21-4e82-9842-6890761d4738", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1105, + "text": "maternal smoking" + }, + { + "answer_start": 1153, + "text": "open fire heating" + }, + { + "answer_start": 1201, + "text": "electric heating" + }, + { + "answer_start": 1249, + "text": "physical exercise" + }, + { + "answer_start": 1298, + "text": "monthly paracetamol use" + }, + { + "answer_start": 1495, + "text": "cat pet" + }, + { + "answer_start": 1595, + "text": "monthly paracetamol use" + } + ] + } + ] +} \ No newline at end of file diff --git a/ed7dda6c-7e9e-46e2-9045-896b46044599.json b/ed7dda6c-7e9e-46e2-9045-896b46044599.json new file mode 100644 index 0000000000000000000000000000000000000000..5d5ba35457ae339a53e9cd737db9034b187a3992 --- /dev/null +++ b/ed7dda6c-7e9e-46e2-9045-896b46044599.json @@ -0,0 +1,42 @@ +{ + "id": "ed7dda6c-7e9e-46e2-9045-896b46044599", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "16110031", + "text": "PURPOSE:\nSince chronic inflammation contributes to tumorigenesis, we hypothesized that the risk and clinical outcome of bladder cancer (BC) might be modulated by genetic variations in inflammation genes.\n\nMETHODS:\nUsing the TaqMan method, we genotyped single nucleotide polymorphisms in interleukin (IL) -6 (-174 G--\u003eC), IL-8 (-251 T--\u003eA), tumor necrosis factor-alpha (TNF-alpha; -308 G--\u003eA), and peroxisome proliferator-activated receptor gamma (PPARG; Pro12Ala), and determined their associations with BC initiation and clinical outcome.\n\nRESULTS:\nWe found that the IL-6 variant genotype (C/C) was associated with an increased BC risk (OR, 1.77; 95% CI, 1.25 to 2.51). There were joint effects between the variant IL-6 genotypes and smoking status, and between the variant genotypes of IL-6 and other genes. To assess effect on recurrence, we grouped non-muscle-invasive BC patients according to intravesical Bacillus Calmette-Guerin (BCG) treatment status: no BCG, induction BCG (iBCG), and maintenance BCG (mBCG). In the Cox proportional hazards model, the variant IL-6 genotype was associated with an increased recurrence risk (hazard ratio [HR], 4.60; 95% CI, 1.24 to 17.09) in patients receiving mBCG. The variant PPARG genotype was associated with a reduced recurrence risk (HR, 0.41; 95% CI, 0.20 to 0.86) among untreated patients. In patients with non-muscle-invasive BC, the variant IL-6 genotype was associated with an increased progression risk (HR, 1.88; 95% CI, 0.80 to 4.11). In patients with invasive BC, variant IL-6 was associated with improved 5-year overall and disease-specific survival (HR, 0.43; 95% CI, 0.19 to 0.94 and HR, 0.39; 95% CI, 0.15 to 1.00, respectively).\n\nCONCLUSION:\nInflammation gene polymorphisms are associated with modified BC risk, treatment response, and survival." + }, + "questions": [ + { + "id": "2b365fae-db8b-4dc3-b44f-ee0c61a94f23", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 1705, + "text": "Inflammation gene polymorphisms" + }, + { + "answer_start": 568, + "text": "IL-6 variant genotype (C/C)" + }, + { + "answer_start": 1061, + "text": "variant IL-6 genotype" + } + ] + } + ] +} \ No newline at end of file diff --git a/ed98733e-eb07-45ed-bbe5-c12baef5f1b0.json b/ed98733e-eb07-45ed-bbe5-c12baef5f1b0.json new file mode 100644 index 0000000000000000000000000000000000000000..9f1ddead76ca961c2c13193e521892c22fbbaf6a --- /dev/null +++ b/ed98733e-eb07-45ed-bbe5-c12baef5f1b0.json @@ -0,0 +1,41 @@ +{ + "id": "ed98733e-eb07-45ed-bbe5-c12baef5f1b0", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "11522737", + "text": "BACKGROUND \u0026 AIMS:\nResults concerning an association between cholecystectomy and right-sided colon cancer are inconsistent. Little is known about the relation between cholecystectomy and small bowel cancer. Therefore, we evaluated cholecystectomy and risk of bowel cancer.\n\nMETHODS:\nCholecystectomized patients, identified through the Swedish Inpatient Register, from 1965 through 1997, were followed up for subsequent cancer. The standardized incidence ratio (SIR) estimated relative risk.\n\nRESULTS:\nIn total, 278,460 cholecystectomized patients, contributing 3,519,682 person-years, were followed up for a maximum of 33 years after surgery. Cholecystectomized patients had an increased risk of proximal intestinal adenocarcinoma, which gradually declined with increasing distance from the common bile duct. The risk was significantly increased for adenocarcinoma (SIR, 1.77; 95% confidence interval [CI], 1.37-2.24) and carcinoids of the small bowel (SIR, 1.71; 95% CI, 1.39-2.08), and right-sided colon cancer (SIR, 1.16; 95% CI, 1.08-1.24). No association was found with more distal bowel cancer. The gradient was further pronounced when surgery of the common bile duct was included. The associations remained increased up to 33 years after cholecystectomy. No differences between sexes were found.\n\nCONCLUSIONS:\nCholecystectomy increases the risk of intestinal cancer, a risk that declines with increasing distance from the common bile duct. Changes in the intestinal exposure to bile might be the underlying biological mechanism." + }, + "questions": [ + { + "id": "0140afa6-637d-4517-a70b-33882aff7089", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1317, + "text": "Cholecystectomy" + }, + { + "answer_start": 643, + "text": "Cholecystectomized patients" + } + ] + } + ] +} \ No newline at end of file diff --git a/eda5b94a-698e-4293-869b-eccfd566e960.json b/eda5b94a-698e-4293-869b-eccfd566e960.json new file mode 100644 index 0000000000000000000000000000000000000000..7215a2e98780a342f58ced63efcc623a364436d4 --- /dev/null +++ b/eda5b94a-698e-4293-869b-eccfd566e960.json @@ -0,0 +1,39 @@ +{ + "id": "eda5b94a-698e-4293-869b-eccfd566e960", + "disease": { + "id": "H00056", + "names": [ + "Alzheimer disease", + "Dementia due to Alzheimer disease" + ], + "dbLinks": { + "icd10": [ + "G30" + ], + "mesh": [ + "D000544" + ] + }, + "category": "Neurodegenerative disease" + }, + "article": { + "id": "24928124", + "text": "OBJECTIVE:\nTo identify factors influencing age at symptom onset and disease course in autosomal dominant Alzheimer disease (ADAD), and develop evidence-based criteria for predicting symptom onset in ADAD.\n\nMETHODS:\nWe have collected individual-level data on ages at symptom onset and death from 387 ADAD pedigrees, compiled from 137 peer-reviewed publications, the Dominantly Inherited Alzheimer Network (DIAN) database, and 2 large kindreds of Colombian (PSEN1 E280A) and Volga German (PSEN2 N141I) ancestry. Our combined dataset includes 3,275 individuals, of whom 1,307 were affected by ADAD with known age at symptom onset. We assessed the relative contributions of several factors in influencing age at onset, including parental age at onset, age at onset by mutation type and family, and APOE genotype and sex. We additionally performed survival analysis using data on symptom onset collected from 183 ADAD mutation carriers followed longitudinally in the DIAN Study.\n\nRESULTS:\nWe report summary statistics on age at onset and disease course for 174 ADAD mutations, and discover strong and highly significant (p \u003c 10(-16), r2 \u003e 0.38) correlations between individual age at symptom onset and predicted values based on parental age at onset and mean ages at onset by mutation type and family, which persist after controlling for APOE genotype and sex.\n\nCONCLUSIONS:\nSignificant proportions of the observed variance in age at symptom onset in ADAD can be explained by family history and mutation type, providing empirical support for use of these data to estimate onset in clinical research." + }, + "questions": [ + { + "id": "c1a0f314-43dd-4109-aade-9d7c73086004", + "text": "What are the risk factors of Alzheimer disease?", + "answers": [ + { + "answer_start": 1471, + "text": "family history" + }, + { + "answer_start": 1490, + "text": "mutation type" + } + ] + } + ] +} \ No newline at end of file diff --git a/ee19b6e0-d5a0-4004-9b1b-9e4570adfc53.json b/ee19b6e0-d5a0-4004-9b1b-9e4570adfc53.json new file mode 100644 index 0000000000000000000000000000000000000000..15ea0c17adbbeaa0a8fb9c99a2551697210bd9dc --- /dev/null +++ b/ee19b6e0-d5a0-4004-9b1b-9e4570adfc53.json @@ -0,0 +1,38 @@ +{ + "id": "ee19b6e0-d5a0-4004-9b1b-9e4570adfc53", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "20048267", + "text": "BACKGROUND:\nCigarette smoking is an established predictor of incident type 2 diabetes mellitus, but the effects of smoking cessation on diabetes risk are unknown.\n\nOBJECTIVE:\nTo test the hypothesis that smoking cessation increases diabetes risk in the short term, possibly owing to cessation-related weight gain.\n\nDESIGN:\nProspective cohort study.\n\nSETTING:\nThe ARIC (Atherosclerosis Risk in Communities) Study.\n\nPATIENTS:\n10,892 middle-aged adults who initially did not have diabetes in 1987 to 1989.\n\nMEASUREMENTS:\nSmoking was assessed by interview at baseline and at subsequent follow-up. Incident diabetes was ascertained by fasting glucose assays through 1998 and self-report of physician diagnosis or use of diabetes medications through 2004.\n\nRESULTS:\nDuring 9 years of follow-up, 1254 adults developed type 2 diabetes. Compared with adults who never smoked, the adjusted hazard ratio of incident diabetes in the highest tertile of pack-years was 1.42 (95% CI, 1.20 to 1.67). In the first 3 years of follow-up, 380 adults quit smoking. After adjustment for age, race, sex, education, adiposity, physical activity, lipid levels, blood pressure, and ARIC Study center, compared with adults who never smoked, the hazard ratios of diabetes among former smokers, new quitters, and continuing smokers were 1.22 (CI, 0.99 to 1.50), 1.73 (CI, 1.19 to 2.53), and 1.31 (CI, 1.04 to 1.65), respectively. Further adjustment for weight change and leukocyte count attenuated these risks substantially. In an analysis of long-term risk after quitting, the highest risk occurred in the first 3 years (hazard ratio, 1.91 [CI, 1.19 to 3.05]), then gradually decreased to 0 at 12 years.\n\nLIMITATION:\nResidual confounding is possible even with meticulous adjustment for established diabetes risk factors.\n\nCONCLUSION:\nCigarette smoking predicts incident type 2 diabetes, but smoking cessation leads to higher short-term risk. For smokers at risk for diabetes, smoking cessation should be coupled with strategies for diabetes prevention and early detection." + }, + "questions": [ + { + "id": "51d8842b-ef81-4f21-9453-031ba0060c2e", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1265, + "text": "new quitters" + }, + { + "answer_start": 1283, + "text": "continuing smokers" + } + ] + } + ] +} \ No newline at end of file diff --git a/ee8dc679-514d-4a22-b1e3-16a91259f37b.json b/ee8dc679-514d-4a22-b1e3-16a91259f37b.json new file mode 100644 index 0000000000000000000000000000000000000000..0a359bfbad91a72af72888c16ee330050bae68a2 --- /dev/null +++ b/ee8dc679-514d-4a22-b1e3-16a91259f37b.json @@ -0,0 +1,47 @@ +{ + "id": "ee8dc679-514d-4a22-b1e3-16a91259f37b", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "14980988", + "text": "BACKGROUND:\nFemale reproductive hormones appear to influence asthma, although data are conflicting, and may modulate development of chronic obstructive pulmonary disease (COPD). Therefore, in a prospective cohort study, we evaluated whether postmenopausal hormone use was associated with an increased rate of newly diagnosed asthma and, separately, newly diagnosed COPD.\n\nMETHODS:\nPostmenopausal hormone use was assessed by questionnaire biennially from 1976 onward. New physician diagnoses of asthma or COPD were reported on questionnaires from 1988 to 1996 and confirmed in 1998 using supplementary questionnaires. Grades of diagnostic certainty were established from reports of medication use and pulmonary function using validated definitions.\n\nRESULTS:\nDuring 546259 person-years of follow-up, current use of estrogen alone was associated with an increased rate of asthma (multivariate rate ratio, 2.29; 95% confidence interval [CI], 1.59-3.29) compared with those who never used hormones. Current users of estrogen plus progestin had a similarly increased rate of newly diagnosed asthma. Rate ratios increased with certainty of diagnosis of asthma. In contrast, rates of newly diagnosed COPD were the same among hormone users and nonusers (multivariate rate ratio, 1.05; 95% CI, 0.80-1.37).\n\nCONCLUSIONS:\nPostmenopausal hormone use was associated with an increased rate of newly diagnosed asthma but not newly diagnosed COPD. Female reproductive hormones may contribute to the onset of asthma among adult women, but do not appear to hasten the development of COPD." + }, + "questions": [ + { + "id": "cd3ff48a-5de4-4420-ae77-d5c9bbc34964", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 799, + "text": "current use of estrogen alone" + }, + { + "answer_start": 995, + "text": "Current users of estrogen plus progestin" + }, + { + "answer_start": 1311, + "text": "Postmenopausal hormone use" + }, + { + "answer_start": 1432, + "text": "Female reproductive hormones" + } + ] + } + ] +} \ No newline at end of file diff --git a/ef03b76a-eb39-43d8-bc7e-e1edf442b2d5.json b/ef03b76a-eb39-43d8-bc7e-e1edf442b2d5.json new file mode 100644 index 0000000000000000000000000000000000000000..249a069eb03deee0963f086ddb5c6269a0919966 --- /dev/null +++ b/ef03b76a-eb39-43d8-bc7e-e1edf442b2d5.json @@ -0,0 +1,47 @@ +{ + "id": "ef03b76a-eb39-43d8-bc7e-e1edf442b2d5", + "disease": { + "id": "H01633", + "names": [ + "High blood pressure", + "Hypertension" + ], + "dbLinks": { + "icd10": [ + "I10" + ], + "mesh": [ + "D006973" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "18362257", + "text": "BACKGROUND:\nParental hypertension is used to classify hypertension risk in young adults, but the long-term association of parental hypertension with blood pressure (BP) change and risk of hypertension over the adult life span has not been well studied.\n\nMETHODS:\nWe examined the association of parental hypertension with BP change and hypertension risk from young adulthood through the ninth decade of life in a longitudinal cohort of 1160 male former medical students with 54 years of follow-up.\n\nRESULTS:\nIn mixed-effects models using 29 867 BP measurements, mean systolic and diastolic BP readings were significantly higher at baseline among participants with parental hypertension. The rate of annual increase was slightly higher for systolic (0.03 mm Hg, P= .04), but not diastolic, BP in those with parental hypertension. After adjustment for baseline systolic and diastolic BP and time-dependent covariates--body mass index, alcohol consumption, coffee drinking, physical activity, and cigarette smoking--the hazard ratio (95% confidence interval [CI]) of hypertension development was 1.5 (1.2-2.0) for men with maternal hypertension only, 1.8 (1.4-2.4) for men with paternal hypertension only, and 2.4 (1.8-3.2) for men with hypertension in both parents compared with men whose parents never developed hypertension. Early-onset (at age \u003cor=55 years) hypertension in both parents imparted a 6.2-fold higher adjusted risk (95% CI, 3.6-10.7) for the development of hypertension throughout adult life and a 20.0-fold higher adjusted risk (95% CI, 8.4-47.9) at the age of 35 years.\n\nCONCLUSION:\nHypertension in both mothers and fathers has a strong independent association with elevated BP levels and incident hypertension over the course of adult life." + }, + "questions": [ + { + "id": "0bf00917-bd86-406c-8ca5-151b62b577fa", + "text": "What are the risk factors for Hypertension?", + "answers": [ + { + "answer_start": 1110, + "text": "men with maternal hypertension only" + }, + { + "answer_start": 1165, + "text": "men with paternal hypertension only" + }, + { + "answer_start": 1224, + "text": "men with hypertension in both parents" + }, + { + "answer_start": 1324, + "text": "Early-onset (at age \u003cor=55 years) hypertension in both parents" + } + ] + } + ] +} \ No newline at end of file diff --git a/ef432eee-4d7c-456c-aeea-32108fea5ac8.json b/ef432eee-4d7c-456c-aeea-32108fea5ac8.json new file mode 100644 index 0000000000000000000000000000000000000000..03ea0b30d9c5437989d1d2da74776319ef3dc458 --- /dev/null +++ b/ef432eee-4d7c-456c-aeea-32108fea5ac8.json @@ -0,0 +1,45 @@ +{ + "id": "ef432eee-4d7c-456c-aeea-32108fea5ac8", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "23569324", + "text": "PURPOSE:\nSite-specific risk of colorectal cancer (CRC) among survivors of endometrial cancer (EC) is not known. The objective of the present study was to assess the risk of CRC (overall and subsite specific) among EC survivors.\n\nMETHODS:\nA historical cohort study was performed by linking the Manitoba Cancer Registry and the Manitoba Health administrative databases. Each subject diagnosed with EC as her first cancer between 1987 and 2008 was age matched with up to five women with no history of invasive cancer on the index date (date of EC diagnosis). All subjects were followed up to the date of diagnosis of CRC or another cancer, death, migration, or study end point (December 31, 2009). Competing-risk proportional hazards models were used to compare the CRC incidence rates with adjustment for age, history of lower gastrointestinal endoscopy, and socioeconomic status. There were three mutually exclusive (and competing) outcomes: CRC, another primary cancer, and death.\n\nRESULTS:\nA total of 3,115 women with EC and 15,084 without EC were followed up for a total of 145,502 person-years. Women diagnosed with EC at age ≤ 50 years had an increased risk of being diagnosed with CRC (all CRC: hazard ratio [HR] = 4.41; 95% CI, 1.47 to 13.26; right-sided CRC: HR = 7.48; 95% CI, 1.29 to 43.28). There was no increased risk of all CRC among women 51 to 65 years of age or those older than 65 years at the time of EC diagnosis. However, women 51 to 65 years of age at EC diagnosis had an increased risk of right-sided CRC (HR = 2.30; 95% CI, 1.05 to 5.01).\n\nCONCLUSION:\nThis study suggests young women (age ≤ 50 years) with EC are at increased risk of CRC; risk of right-sided CRC is also increased in women 51 to 65 years old at EC diagnosis." + }, + "questions": [ + { + "id": "38cd5b1f-ae6e-410a-b49f-f86714be6cc6", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1098, + "text": "Women diagnosed with EC at age ≤ 50 years" + }, + { + "answer_start": 1594, + "text": "young women (age ≤ 50 years) with EC" + }, + { + "answer_start": 74, + "text": "endometrial cancer (EC)" + } + ] + } + ] +} \ No newline at end of file diff --git a/ef48197d-40f0-45f7-8d94-52d4c5a37fc7.json b/ef48197d-40f0-45f7-8d94-52d4c5a37fc7.json new file mode 100644 index 0000000000000000000000000000000000000000..4ef91b9bfe117dfd9ff8f263a650e22ba111407d --- /dev/null +++ b/ef48197d-40f0-45f7-8d94-52d4c5a37fc7.json @@ -0,0 +1,43 @@ +{ + "id": "ef48197d-40f0-45f7-8d94-52d4c5a37fc7", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "15593211", + "text": "OBJECTIVE:\nTo investigate the association of red meat and other specific dietary components in predicting the development of inflammatory polyarthritis.\n\nMETHODS:\nThis nested case-control study was conducted within a prospective population-based study of cancer incidence (European Prospective Investigation of Cancer in Norfolk [EPIC-Norfolk]). EPIC-Norfolk recruited 25,630 subjects ages 45-75 years between 1993 and 1997. Dietary intake was assessed at baseline using a 7-day food diary, and the information was analyzed using dietary analysis software. Patients with new cases of inflammatory polyarthritis were identified by linkage with the Norfolk Arthritis Register, a primary care-based inception study of inflammatory polyarthritis, and were matched for age and sex to 2 controls from EPIC-Norfolk. The risk for development of inflammatory polyarthritis was compared between subjects in the highest and lowest tertiles of dietary intake using conditional logistic regression and was expressed as odds ratios (ORs) with 95% confidence intervals (95% CIs).\n\nRESULTS:\nBetween 1993 and 2002, 88 new patients with inflammatory polyarthritis were identified and matched with 176 controls. Among patients, the level of red meat intake was higher (P = 0.04) and that of vitamin C was lower (P = 0.03) compared with intake among controls, but no difference in total energy intake was observed. Patients were more likely to be smokers. After adjusting for total energy intake, smoking, and other possible dietary confounders, subjects with the highest level of consumption of red meat (OR 1.9, 95% CI 0.9-4.0), meat and meat products combined (OR 2.3, 95% CI 1.1-4.9), and total protein (OR 2.9, 95% CI 1.1-7.5) were at an increased risk for inflammatory polyarthritis.\n\nCONCLUSION:\nA high level of red meat consumption may represent a novel risk factor for inflammatory arthritis or may act as a marker for a group of persons with an increased risk from other lifestyle causes." + }, + "questions": [ + { + "id": "0e89af3c-c4cd-412b-baff-96a052d4b5be", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 1611, + "text": "meat and meat products combined" + }, + { + "answer_start": 1673, + "text": "total protein" + }, + { + "answer_start": 1785, + "text": "high level of red meat consumption" + } + ] + } + ] +} \ No newline at end of file diff --git a/f03895d6-0020-4d56-90b6-6c0a962a933a.json b/f03895d6-0020-4d56-90b6-6c0a962a933a.json new file mode 100644 index 0000000000000000000000000000000000000000..67894640ff4d393f701de8ab482c023d6126f7c9 --- /dev/null +++ b/f03895d6-0020-4d56-90b6-6c0a962a933a.json @@ -0,0 +1,34 @@ +{ + "id": "f03895d6-0020-4d56-90b6-6c0a962a933a", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "11157711", + "text": "BACKGROUND:\nP-selectin, a cell-surface adhesion molecule involved in leukocyte rolling and attachment, has been hypothesized to play a role in the initiation of atherosclerosis. However, little clinical data are available evaluating the role of soluble P-selectin in determining vascular risk.\n\nMETHODS AND RESULTS:\nIn a large-scale prospective study of apparently healthy women, we measured baseline plasma concentration of soluble P-selectin among 115 participants who subsequently developed cardiovascular events and among 230 age- and smoking-matched participants who remained free of disease during 3.5 years of follow-up. Overall, mean levels of soluble P-selectin were significantly higher at baseline among women who subsequently experienced cardiovascular events compared with those who did not (83.2 versus 69.3 ng/mL; P:=0.003). The risk of future cardiovascular events increased with increasing quartiles of soluble P-selectin (P:=0.02), such that women in the highest quartile at study entry had an age- and smoking-matched relative risk 2.2 times higher than those in the lowest quartile (95% confidence interval, 1.2 to 4.2; P:=0.01). This effect was independent of traditional risk factors. For each quartile increase in soluble P-selectin, the risk of future cardiovascular events increased 28% (P:=0.03) after additional adjustment for obesity, hypertension, hyperlipidemia, diabetes, and exercise frequency. The highest risks were observed among women with the very highest levels of P-selectin (\u003e137.3 ng/mL, the 95th percentile cut point of the control distribution).\n\nCONCLUSIONS:\nSoluble P-selectin levels are elevated among apparently healthy women at risk for future vascular events." + }, + "questions": [ + { + "id": "65e26ffa-df1f-406c-8bad-01429fe7b3bf", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1603, + "text": "Soluble P-selectin levels" + } + ] + } + ] +} \ No newline at end of file diff --git a/f0759161-3c74-47c9-841c-55dd18dae656.json b/f0759161-3c74-47c9-841c-55dd18dae656.json new file mode 100644 index 0000000000000000000000000000000000000000..52ddac98d8e88dae10e06afdae0a786c0a6ec491 --- /dev/null +++ b/f0759161-3c74-47c9-841c-55dd18dae656.json @@ -0,0 +1,43 @@ +{ + "id": "f0759161-3c74-47c9-841c-55dd18dae656", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "25890172", + "text": "INTRODUCTION:\nThe evidence from published studies on the association between obesity and rheumatoid arthritis has been contradictory. To clarify the association between obesity and rheumatoid arthritis, we conducted a systematic review and dose-response meta-analysis to assess the relationship between body mass index and rheumatoid arthritis risk.\n\nMETHODS:\nA systematic literature search of PubMed and Embase (up to 12 July 2014) was performed to identify all eligible published reports. The pooled relative risk results with corresponding 95% confidence intervals of rheumatoid arthritis development were estimated using a random-effects model.\n\nRESULTS:\nEleven eligible related citations fulfilled the inclusion criteria and were included in the study. Compared with individuals with a body mass index under 30, obese individuals showed an association with a significantly increased risk of rheumatoid arthritis (relative risk = 1.25, 95% confidence interval: 1.07 to 1.45, P heterogeneity \u003c0.01, I(2) = 63%). Compared to normal weight subjects, the pooled relative risks for rheumatoid arthritis were 1.31 (1.12 to 1.53) and 1.15 (1.03 to 1.29) for the categories of obese and overweight, respectively. In the dose-response analysis, there was evidence of a nonlinear association (P nonlinear = 0.005) and the estimated summary relative risk for a 5-unit increment was 1.03 (95% confidence interval: 1.01 to 1.05, P heterogeneity = 0.001, I(2) = 70.0%).\n\nCONCLUSIONS:\nAn increase in body mass index can contribute to a higher risk for rheumatoid arthritis development. However, the finding also highlights the need for research on the association between body mass index and rheumatoid arthritis risk with adjustment for more confounding factors." + }, + "questions": [ + { + "id": "f2337d0d-aa60-400e-8cab-cece241d99e8", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 1173, + "text": "obese" + }, + { + "answer_start": 1183, + "text": "overweight" + }, + { + "answer_start": 1474, + "text": "An increase in body mass index" + } + ] + } + ] +} \ No newline at end of file diff --git a/f0c1575a-fe1a-49ff-a9e2-8243b1af7a4f.json b/f0c1575a-fe1a-49ff-a9e2-8243b1af7a4f.json new file mode 100644 index 0000000000000000000000000000000000000000..118f8ecb0026c3cd42bb1bf0958b4078a7fab0e1 --- /dev/null +++ b/f0c1575a-fe1a-49ff-a9e2-8243b1af7a4f.json @@ -0,0 +1,35 @@ +{ + "id": "f0c1575a-fe1a-49ff-a9e2-8243b1af7a4f", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "11799364", + "text": "BACKGROUND:\nIt has been suggested that the rise in prevalence of allergic disease in westernized countries is due in part to a decrease in exposure to infections and an increase in the use of antibiotics early in life.\n\nOBJECTIVE:\nThe purpose of this investigation was to quantify the relationships between (1) exposure to personal infections, infections in siblings, and use of antibiotics in early life and (2) the incidence of allergic disease.\n\nMETHODS:\nUsing the West Midlands section of the UK General Practice Research Database, we established a historical birth cohort of children (N = 29,238). For each child, we identified all personal infections and infections in siblings and determined the use of antibiotics in early life; we also noted incident diagnoses of asthma, eczema, and hay fever. The data were analyzed through use of Cox regression.\n\nRESULTS:\nThere was no clear protective effect of exposure to either personal infections or infections in siblings with respect to the incidence of allergic disease. Antibiotic exposure was associated with an increased risk of developing allergic disease in a dose-related manner: having 4 or more courses of antibiotics in the first year of life was associated with an increased incidence of asthma (hazard ratio [HR], 3.13; 95% CI, 2.75-3.57), eczema (HR, 1.48; 95% CI, 1.31-1.68), and hay fever (HR, 2.12; 95% CI, 1.68-2.66). However, adjusting for consulting behavior reduced these effects (adjusted HR [95% CI]: asthma, 1.99 [1.72-2.31]; eczema, 1.01 [0.88-1.17]; hay fever, 1.14 [0.88-1.47]).\n\nCONCLUSIONS:\nWe found no evidence that exposure to infections reduced the incidence of allergic disease, and infections did not explain the previous findings of a strong birth order effect in this cohort. The use of antibiotics might be associated with early diagnoses of allergic disease." + }, + "questions": [ + { + "id": "111d1e66-2b7e-4147-948c-6ab3fabebe91", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1139, + "text": "having 4 or more courses of antibiotics in the first year of life" + } + ] + } + ] +} \ No newline at end of file diff --git a/f0c3737a-353b-4707-89cd-289326d7aff9.json b/f0c3737a-353b-4707-89cd-289326d7aff9.json new file mode 100644 index 0000000000000000000000000000000000000000..63e8626addce438a8fb1790b796a12a398b2e15d --- /dev/null +++ b/f0c3737a-353b-4707-89cd-289326d7aff9.json @@ -0,0 +1,35 @@ +{ + "id": "f0c3737a-353b-4707-89cd-289326d7aff9", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "29438161", + "text": "There is accumulating evidence that the vitamin D pathway may play a role in melanoma. The aim of this study was to investigate the association between 25-hydroxyvitamin D [25(OH)D] serum levels and the risk of cutaneous melanoma. A case-control study with 137 incident cases of melanoma (serum samples collected at the time of diagnosis) and 99 healthy controls (serum samples collected between October and April) was carried out and evaluated in the framework of an evidence synthesis of clinical epidemiological studies on the topic to facilitate comparisons and summarize the scientific evidence produced so far. There was a statistically significant difference in the median levels of serum vitamin D between melanoma patients and healthy controls (18.0 vs. 27.8 ng/ml, P\u003c0.001). Among melanoma patients, 66.2%, compared with 15.2% of healthy controls, had vitamin D deficiency (≤20 ng/ml), whereas vitamin D sufficiency (≥30 ng/ml) was observed in only 7.4% of melanoma patients and in 37.4% of the healthy controls (P\u003c0.001). A multivariate model including age, sex, and BMI showed a statistically significant inverse association between melanoma and vitamin D sufficiency versus deficiency (odds ratio=0.04; 95% confidence interval: 0.02-0.10, P\u003c0.001). Also, vitamin D insufficiency versus deficiency was significantly inversely associated with melanoma (odds ratio=0.13; 95% confidence interval: 0.06-0.27, P\u003c0.001). These results suggest that both deficient and insufficient serum levels of vitamin D are associated with melanoma and that a trend seems to be present with a reduced risk of melanoma when vitamin D approaches normal values." + }, + "questions": [ + { + "id": "08c939d2-feb8-4b6f-9642-98586775badc", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 862, + "text": "vitamin D deficiency (≤20 ng/ml)" + } + ] + } + ] +} \ No newline at end of file diff --git a/f0d4f236-0a25-4af9-a214-cc05c8449ca8.json b/f0d4f236-0a25-4af9-a214-cc05c8449ca8.json new file mode 100644 index 0000000000000000000000000000000000000000..4b62251e7b2cc9566a9ea68d4627c4ba58683bb4 --- /dev/null +++ b/f0d4f236-0a25-4af9-a214-cc05c8449ca8.json @@ -0,0 +1,50 @@ +{ + "id": "f0d4f236-0a25-4af9-a214-cc05c8449ca8", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "15252848", + "text": "The evidence for anthropometric factors influencing breast cancer risk is accumulating, but uncertainties remain concerning the role of fat distribution and potential effect modifiers. We used data from 73,542 premenopausal and 103,344 postmenopausal women from 9 European countries, taking part in the EPIC study. RRs from Cox regression models were calculated, using measured height, weight, BMI and waist and hip circumferences; categorized by cohort-wide quintiles; and expressed as continuous variables, adjusted for study center, age and other risk factors. During 4.7 years of follow-up, 1,879 incident invasive breast cancers were identified. In postmenopausal women, current HRT modified the body size-breast cancer association. Among nonusers, weight, BMI and hip circumference were positively associated with breast cancer risk (all ptrend \u003c or = 0.002); obese women (BMI \u003e 30) had a 31% excess risk compared to women with BMI \u003c 25. Among HRT users, body measures were inversely but nonsignificantly associated with breast cancer. Excess breast cancer risk with HRT was particularly evident among lean women. Pooled RRs per height increment of 5 cm were 1.05 (95% CI 1.00-1.16) in premenopausal and 1.10 (95% CI 1.05-1.16) in postmenopausal women. Among premenopausal women, hip circumference was the only other measure significantly related to breast cancer (ptrend = 0.03), after accounting for BMI. In postmenopausal women not taking exogenous hormones, general obesity is a significant predictor of breast cancer, while abdominal fat assessed as waist-hip ratio or waist circumference was not related to excess risk when adjusted for BMI. Among premenopausal women, weight and BMI showed nonsignificant inverse associations with breast cancer." + }, + "questions": [ + { + "id": "7188d7e3-fb87-4790-a501-7f45a2830edb", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1413, + "text": "In postmenopausal women not taking exogenous hormones, general obesity" + }, + { + "answer_start": 1259, + "text": "Among premenopausal women, hip circumference" + }, + { + "answer_start": 754, + "text": "weight" + }, + { + "answer_start": 762, + "text": "BMI" + }, + { + "answer_start": 770, + "text": "hip circumference" + } + ] + } + ] +} \ No newline at end of file diff --git a/f0eb7fe0-e48e-4ba4-bb4c-ed8eff1cff06.json b/f0eb7fe0-e48e-4ba4-bb4c-ed8eff1cff06.json new file mode 100644 index 0000000000000000000000000000000000000000..b555d9ab332c86c826753ed976e2fd851d09ca64 --- /dev/null +++ b/f0eb7fe0-e48e-4ba4-bb4c-ed8eff1cff06.json @@ -0,0 +1,51 @@ +{ + "id": "f0eb7fe0-e48e-4ba4-bb4c-ed8eff1cff06", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "25104173", + "text": "BACKGROUND:\nPosttraumatic stress disorder (PTSD) is associated with endocrine and immune abnormalities that could increase risk for autoimmune disorders. However, little is known about the risk for autoimmune disorders among individuals with PTSD.\n\nMETHODS:\nWe conducted a retrospective cohort study of 666,269 Iraq and Afghanistan veterans under age 55 who were enrolled in the Department of Veterans Affairs health care system between October 7, 2001, and March 31, 2011. Generalized linear models were used to examine if PTSD, other psychiatric disorders, and military sexual trauma exposure increased risk for autoimmune disorders, including thyroiditis, inflammatory bowel disease, rheumatoid arthritis, multiple sclerosis, and lupus erythematosus, adjusting for age, gender, race, and primary care visits.\n\nRESULTS:\nPTSD was diagnosed in 203,766 veterans (30.6%), and psychiatric disorders other than PTSD were diagnosed in an additional 129,704 veterans (19.5%). Veterans diagnosed with PTSD had significantly higher adjusted relative risk (ARR) for diagnosis with any of the autoimmune disorders alone or in combination compared with veterans with no psychiatric diagnoses (ARR = 2.00; 95% confidence interval, 1.91-2.09) and compared with veterans diagnosed with psychiatric disorders other than PTSD (ARR = 1.51; 95% confidence interval, 1.43-1.59; p \u003c .001). The magnitude of the PTSD-related increase in risk for autoimmune disorders was similar in women and men, and military sexual trauma exposure was independently associated with increased risk in both women and men.\n\nCONCLUSIONS:\nTrauma exposure and PTSD may increase risk for autoimmune disorders. Altered immune function, lifestyle factors, or shared etiology may underlie this association." + }, + "questions": [ + { + "id": "f171a92c-edde-4cd2-ab02-47e830099c52", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 1598, + "text": "Trauma exposure" + }, + { + "answer_start": 1618, + "text": "PTSD" + }, + { + "answer_start": 12, + "text": "Posttraumatic stress disorder (PTSD)" + }, + { + "answer_start": 970, + "text": "Veterans diagnosed with PTSD" + }, + { + "answer_start": 1480, + "text": "military sexual trauma exposure" + } + ] + } + ] +} \ No newline at end of file diff --git a/f229f933-df11-4a04-a237-25497cc20185.json b/f229f933-df11-4a04-a237-25497cc20185.json new file mode 100644 index 0000000000000000000000000000000000000000..7259d7b39f9fb4d3c096608c40f4a63573e12a6c --- /dev/null +++ b/f229f933-df11-4a04-a237-25497cc20185.json @@ -0,0 +1,39 @@ +{ + "id": "f229f933-df11-4a04-a237-25497cc20185", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "15957164", + "text": "The incidence of most epithelial cancers rises with a power of age. However, second breast cancers have a high constant incidence independent of age. The skin is one of the few other sites allowing examination of age incidence curves of second neoplasms of the same organ. We considered the risk of second primary cutaneous malignant melanoma (CMM) in a population-based series of 3,439 first CMM registered and followed-up between 1974 and 2003 in the Swiss Cantons of Vaud and Neuchâtel (about 786,000 inhabitants). A total of 43 cases of second CMM were observed vs. 9.3 expected, corresponding to a standardized incidence ratio (SIR) of 4.6. The SIR was 8.5 under age 50, 5.7 at age 50-59 and 3.5 at age 60 or over. At 20 years, the cumulative risk of second CMM was 5%. Age-specific incidence rates of second primary CMM did not vary across age groups 30-39 through 80+, ranging between 1 and 2.5 per 1,000 person-years. Thus, the risk of CMM is substantially increased in subjects diagnosed with a CMM, and the relative risk is greater at younger age and declines with advancing age. The high constant incidence curve of second CMM is compatible with the occurrence of a single mutational event in a population of susceptible individuals." + }, + "questions": [ + { + "id": "c458221e-f4c0-4825-ab04-a721689263af", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 978, + "text": "subjects diagnosed with a CMM" + }, + { + "answer_start": 314, + "text": "cutaneous malignant melanoma (CMM)" + } + ] + } + ] +} \ No newline at end of file diff --git a/f2865486-8ccf-4768-a43b-06bd0ecf180c.json b/f2865486-8ccf-4768-a43b-06bd0ecf180c.json new file mode 100644 index 0000000000000000000000000000000000000000..59c51ae7c1ba18f8387e3602fadb97b4c7e0fdec --- /dev/null +++ b/f2865486-8ccf-4768-a43b-06bd0ecf180c.json @@ -0,0 +1,34 @@ +{ + "id": "f2865486-8ccf-4768-a43b-06bd0ecf180c", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "15249351", + "text": "BACKGROUND:\nEpidemiological studies have reported that patients with type 2 diabetes mellitus (DM) have increased mortality and morbidity from cardiovascular diseases, independent of other risk factors. However, most of these studies have been performed in selected patient groups. The purpose of the present study was prospectively to assess the impact of type 2 DM on cardiovascular morbidity and mortality in an unselected population.\n\nMETHODS:\nA total of 13,105 subjects from the Copenhagen City Heart Study were followed up prospectively for 20 years. Adjusted relative risks of first, incident, admission for, or death from ischemic heart disease, acute myocardial infarction, or stroke, as well as total mortality in persons with type 2 DM compared with healthy controls, were estimated.\n\nRESULTS:\nThe relative risk of first, incident, and admission for myocardial infarction was increased 1.5- to 4.5-fold in women and 1.5- to 2-fold in men, with a significant difference between sexes. The relative risk of first, incident, and admission for stroke was increased 2- to 6.5-fold in women and 1.5- to 2-fold in men, with a significant difference between sexes. In both women and men the relative risk of death was increased 1.5 to 2 times.\n\nCONCLUSIONS:\nIn persons with type 2 DM, the risk of having an incident myocardial infarction or stroke is increased 2- to 3-fold and the risk of death is increased 2-fold, independent of other known risk factors for cardiovascular diseases." + }, + "questions": [ + { + "id": "ee147c77-3fd6-4e4f-b61d-bab36acb7b5b", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1264, + "text": "persons with type 2 DM" + } + ] + } + ] +} \ No newline at end of file diff --git a/f3292969-cf82-415f-adfe-964a4dce1574.json b/f3292969-cf82-415f-adfe-964a4dce1574.json new file mode 100644 index 0000000000000000000000000000000000000000..f33632b5f7e39bc5bf2784458cc809c9bca24492 --- /dev/null +++ b/f3292969-cf82-415f-adfe-964a4dce1574.json @@ -0,0 +1,38 @@ +{ + "id": "f3292969-cf82-415f-adfe-964a4dce1574", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "20920699", + "text": "PURPOSE:\nTo evaluate the impact of serum uric acid levels on the future risk of developing type 2 diabetes independent of other factors.\n\nMETHODS:\nWe used prospective data from the Framingham Heart Study original (n=4883) and offspring (n=4292) cohorts to examine the association between serum uric acid levels and the incidence of diabetes. We used Cox proportional hazards models to estimate the relative risk of incident diabetes adjusting for age, sex, physical activity, alcohol consumption, smoking, hypertension, body mass index, and blood levels of glucose, cholesterol, creatinine, and triglycerides.\n\nRESULTS:\nWe identified 641 incident cases of diabetes in the original cohort and 497 cases in the offspring cohort. The incidence rates of diabetes per 1000 person-years for serum uric acid levels \u003c5.0, 5.0-5.9, 6.0-6.9, 7.0-7.9 and ≥8.0 mg/dL were 3.3, 6.1, 8.7, 11.5, and 15.9, respectively, in the original cohort; and 2.9, 5.0, 6.6, 8.7, and 10.9, respectively, in the offspring cohort (P-values for trends \u003c.001). Multivariable relative risks per mg/dL increase in serum uric acid levels were 1.20 (95% confidence interval; 1.11-1.28) for the original cohort and 1.15 (95% confidence interval; 1.06-1.23) for the offspring cohort.\n\nCONCLUSIONS:\nThese prospective data from 2 generations of the Framingham Heart Study provide evidence that individuals with higher serum uric acid; including younger adults, are at a higher future risk of type 2 diabetes independent of other known risk factors. These data expand on cross-sectional associations between hyperuricemia and the metabolic syndrome, and extend the link to the future risk of type 2 diabetes." + }, + "questions": [ + { + "id": "3cd4328a-f4e0-4fa5-b9e0-2faef8530dae", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1059, + "text": "per mg/dL increase in serum uric acid levels" + }, + { + "answer_start": 1372, + "text": "higher serum uric acid" + } + ] + } + ] +} \ No newline at end of file diff --git a/f380e6d2-2bfd-4163-ba63-b08910852bb8.json b/f380e6d2-2bfd-4163-ba63-b08910852bb8.json new file mode 100644 index 0000000000000000000000000000000000000000..b82977aa5e440cdd76816c979faea3229898af1d --- /dev/null +++ b/f380e6d2-2bfd-4163-ba63-b08910852bb8.json @@ -0,0 +1,34 @@ +{ + "id": "f380e6d2-2bfd-4163-ba63-b08910852bb8", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "26756460", + "text": "BACKGROUND:\nEstimates of risk for radiation-induced breast cancer from mammography screening have not considered variation in dose exposure or diagnostic work-up after abnormal screening results.\n\nOBJECTIVE:\nTo estimate distributions of radiation-induced breast cancer incidence and mortality from digital mammography screening while considering exposure from screening and diagnostic mammography and dose variation among women.\n\nDESIGN:\n2 simulation-modeling approaches.\n\nSETTING:\nU.S. population.\n\nPATIENTS:\nWomen aged 40 to 74 years.\n\nINTERVENTION:\nAnnual or biennial digital mammography screening from age 40, 45, or 50 years until age 74 years.\n\nMEASUREMENTS:\nLifetime breast cancer deaths averted (benefits) and radiation-induced breast cancer incidence and mortality (harms) per 100,000 women screened.\n\nRESULTS:\nAnnual screening of 100,000 women aged 40 to 74 years was projected to induce 125 breast cancer cases (95% CI, 88 to 178) leading to 16 deaths (CI, 11 to 23), relative to 968 breast cancer deaths averted by early detection from screening. Women exposed at the 95th percentile were projected to develop 246 cases of radiation-induced breast cancer leading to 32 deaths per 100,000 women. Women with large breasts requiring extra views for complete examination (8% of population) were projected to have greater radiation-induced breast cancer risk (266 cancer cases and 35 deaths per 100,000 women) than other women (113 cancer cases and 15 deaths per 100,000 women). Biennial screening starting at age 50 years reduced risk for radiation-induced cancer 5-fold.\n\nLIMITATION:\nLife-years lost from radiation-induced breast cancer could not be estimated.\n\nCONCLUSION:\nRadiation-induced breast cancer incidence and mortality from digital mammography screening are affected by dose variability from screening, resultant diagnostic work-up, initiation age, and screening frequency. Women with large breasts may have a greater risk for radiation-induced breast cancer.\n\nPRIMARY FUNDING SOURCE:\nAgency for Healthcare Research and Quality, U.S. Preventive Services Task Force, National Cancer Institute." + }, + "questions": [ + { + "id": "5e512f1e-6529-48c9-94c2-fe8575faba4f", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1207, + "text": "Women with large breasts" + } + ] + } + ] +} \ No newline at end of file diff --git a/f3d79024-715d-4acb-a86f-789379eadff3.json b/f3d79024-715d-4acb-a86f-789379eadff3.json new file mode 100644 index 0000000000000000000000000000000000000000..39ec71040d2a00f1577aa733ebac1aa2f140d2da --- /dev/null +++ b/f3d79024-715d-4acb-a86f-789379eadff3.json @@ -0,0 +1,34 @@ +{ + "id": "f3d79024-715d-4acb-a86f-789379eadff3", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "20368650", + "text": "BACKGROUND:\nWomen treated with therapeutic chest radiation may develop breast cancer.\n\nPURPOSE:\nTo summarize breast cancer risk and breast cancer surveillance in women after chest radiation for pediatric or young adult cancer.\n\nDATA SOURCES:\nStudies from MEDLINE, EMBASE, the Cochrane Library, and CINAHL (1966 to December 2008).\n\nSTUDY SELECTION:\nArticles were selected to answer any of 3 questions: What is the incidence and excess risk for breast cancer in women after chest radiation for pediatric or young adult cancer? For these women, are the clinical characteristics of breast cancer and the outcomes after therapy different from those of women with sporadic breast cancer in the general population? What are the potential benefits and harms associated with breast cancer surveillance among women exposed to chest radiation?\n\nDATA EXTRACTION:\nThree investigators independently extracted data and assessed study quality.\n\nDATA SYNTHESIS:\nStandardized incidence ratios ranged from 13.3 to 55.5; cumulative incidence of breast cancer by age 40 to 45 years ranged from 13% to 20%. Risk for breast cancer increased linearly with chest radiation dose. Available limited evidence suggests that the characteristics of breast cancer in these women and the outcomes after diagnosis are similar to those of women in the general population; mammography can detect breast cancer, although sensitivity is limited.\n\nLIMITATION:\nThe quality of evidence for key questions 2 and 3 is limited by substantial study heterogeneity, variation in study design, and small sample size.\n\nCONCLUSION:\nWomen treated with chest radiation have a substantially elevated risk for breast cancer at a young age, which does not seem to plateau. In this high-risk population, there seems to be a benefit associated with early detection. Further research is required to better define the harms and benefits of lifelong surveillance." + }, + "questions": [ + { + "id": "9c341275-bd60-4edd-b20b-711126124df9", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 1132, + "text": "chest radiation dose" + } + ] + } + ] +} \ No newline at end of file diff --git a/f3f1e426-72e3-49dc-8ed6-6d3b0d0d902c.json b/f3f1e426-72e3-49dc-8ed6-6d3b0d0d902c.json new file mode 100644 index 0000000000000000000000000000000000000000..2da14a623ed1368fe6a8a2707d6be3f35bb63399 --- /dev/null +++ b/f3f1e426-72e3-49dc-8ed6-6d3b0d0d902c.json @@ -0,0 +1,47 @@ +{ + "id": "f3f1e426-72e3-49dc-8ed6-6d3b0d0d902c", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "20086181", + "text": "Epidemiologic research has shown convincingly that certain phenotypic attributes are associated with increased relative risks of melanoma. Although such findings have intrinsic utility, there have been few attempts to translate such knowledge into estimates of disease burden suitable for framing public health policy. We aimed to estimate the population attributable fraction (PAF) for melanoma associated with melanocytic nevi using relative risk estimates derived from a systematic review and meta-analysis. We identified eligible studies using citation databases, followed by manual review of retrieved references. Of 49 studies identified, 25 and 23, respectively, were included in meta-analyses of atypical and common nevi. For people with \u003e or =1 atypical nevi, the summary relative risk was 3.63 (95% confidence interval, 2.85-4.62), with a PAF of 0.25. The relative risk increased by 1.017 (95% confidence interval, 1.014-1.020) for each common nevus; however, significant heterogeneity in risk estimates was observed. We estimated that 42% of melanomas were attributable to having \u003e or =25 common nevi (PAF 25-49 nevi = 0.15; PAF \u003e or =50 nevi = 0.27), whereas PAFs for low nevus counts were modest (PAF 0-10 nevi = 0.04; PAF 11-24 nevi = 0.07). We modeled PAF under scenarios of varying nevus prevalence; the highest melanoma burden was always among those with high nevus counts (PAF range of 0.31-0.62 for \u003e or =25 common nevi). Patients with \u003e or =25 common nevi and/or \u003e or =1 atypical nevi are a high-risk group, which might be targeted for identification, screening, and education. This work is the necessary first step in designing targeted preventive strategies for melanoma, which must now be overlaid with information about cost and utility." + }, + "questions": [ + { + "id": "af249681-55b1-4bf7-8645-415544ef442c", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 734, + "text": "people with \u003e or =1 atypical nevi" + }, + { + "answer_start": 1084, + "text": "having \u003e or =25 common nevi" + }, + { + "answer_start": 1361, + "text": "those with high nevus counts" + }, + { + "answer_start": 1441, + "text": "Patients with \u003e or =25 common nevi and/or \u003e or =1 atypical nevi" + } + ] + } + ] +} \ No newline at end of file diff --git a/f4da9dcd-87af-42ce-a70a-f18e3dc7f65e.json b/f4da9dcd-87af-42ce-a70a-f18e3dc7f65e.json new file mode 100644 index 0000000000000000000000000000000000000000..00645269b8151cbffd3da47e91457083906b5719 --- /dev/null +++ b/f4da9dcd-87af-42ce-a70a-f18e3dc7f65e.json @@ -0,0 +1,38 @@ +{ + "id": "f4da9dcd-87af-42ce-a70a-f18e3dc7f65e", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "9365784", + "text": "In order to assess the effect of the HLA region on familiality of coeliac disease (CD), we carried out a study on 121 CD index cases and 325 first degree relatives. The transmission disequilibrium test confirmed the importance of the HLA-DR3 haplotype in CD susceptibility. However, the different distortion found in affected children inheriting maternal or paternal DR3 alleles suggested that the sex of the parent might influence the risk conferred by this haplotype. The increase in risk to siblings of affected individuals relative to the risk in the general population (lambda s) and the contribution of the HLA genes to this clustering (lambda sHLA) have also been estimated. Non-overlapping data from the literature have been collected and combined with our sample to extend such analysis. Then, the percentage contribution of the HLA region to the development of CD among siblings was 36.2%. This result confirms that the HLA genotypes are an important genetic background to CD development but shows that additional susceptibility factors remain to be identified." + }, + "questions": [ + { + "id": "96982379-7df1-45b9-8fe4-e171a236300c", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 234, + "text": "HLA-DR3 haplotype" + }, + { + "answer_start": 494, + "text": "siblings of affected individuals" + } + ] + } + ] +} \ No newline at end of file diff --git a/f5d9f560-0d60-49ae-a00e-4690fe7bae2d.json b/f5d9f560-0d60-49ae-a00e-4690fe7bae2d.json new file mode 100644 index 0000000000000000000000000000000000000000..77ffeeed75c5fc8e54983d348e0847ab4a368688 --- /dev/null +++ b/f5d9f560-0d60-49ae-a00e-4690fe7bae2d.json @@ -0,0 +1,43 @@ +{ + "id": "f5d9f560-0d60-49ae-a00e-4690fe7bae2d", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "11080708", + "text": "BACKGROUND:\nEvents occurring during fetal life may affect the development of the immune and respiratory systems and increase the risk of asthma and allergic diseases.\n\nOBJECTIVES:\nWe sought to elaborate the relations between the occurrence of pregnancy complications and other pregnancy-related conditions and the risk of bronchial obstruction during the first 2 years of life and the occurrence of asthma and allergic rhinitis by the age of 4 years. Pregnancy complications were considered both as predictors of the health outcomes and as possible effects caused by other prenatal factors.\n\nMETHODS:\nA population-based, 4-year, cohort study was carried out involving 2531 children born in Oslo, Norway. We collected information on maternally related (hyperemesis, hypertension, and preeclampsia) and uterus-related complications in pregnancy (antepartum hemorrhage, preterm contractions, insufficient placenta, and restricted growth of the uterus) and the child's health and environmental exposures at birth and at 6, 12, 18, and 24 months and 4 years of age. The outcomes of interest were bronchial obstruction during the first 2 years and asthma and allergic rhinitis at the age of 4 years.\n\nRESULTS:\nIn a logistic regression analysis adjusting for potential confounders, uterus-related, but not other pregnancy-related, complications increased the risk of bronchial obstruction (odds ratio [OR], 2.1; 95% confidence interval [CI], 1.3-3.4), asthma (OR, 3.0; 95% CI, 1.8-5.4), and allergic rhinitis (OR, 2.9; 95% CI, 1.6-5.2). These relations were similar in children of atopic and nonatopic parents.\n\nCONCLUSIONS:\nUterus-related complications in pregnancy increase the risk of having asthma and allergic rhinitis in childhood." + }, + "questions": [ + { + "id": "4854f50f-bd09-43eb-b9a0-2d8948205655", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1275, + "text": "uterus-related, but not other pregnancy-related, complications" + }, + { + "answer_start": 1618, + "text": "Uterus-related complications in pregnancy" + }, + { + "answer_start": 801, + "text": "uterus-related complications in pregnancy (antepartum hemorrhage, preterm contractions, insufficient placenta, and restricted growth of the uterus)" + } + ] + } + ] +} \ No newline at end of file diff --git a/f60e1d6d-07df-4fb2-82c1-f261616cad15.json b/f60e1d6d-07df-4fb2-82c1-f261616cad15.json new file mode 100644 index 0000000000000000000000000000000000000000..a69e41a437e833fc1aa748a89af12aee80e7a2dd --- /dev/null +++ b/f60e1d6d-07df-4fb2-82c1-f261616cad15.json @@ -0,0 +1,43 @@ +{ + "id": "f60e1d6d-07df-4fb2-82c1-f261616cad15", + "disease": { + "id": "H00630", + "names": [ + "Rheumatoid arthritis" + ], + "dbLinks": { + "icd10": [ + "M05" + ], + "mesh": [ + "D001172" + ] + }, + "category": "Immune system disease", + "description": "Rheumatoid arthritis (RA) is a common autoimmune disease that primarily manifests as chronic inflammatory arthropathy. Persistent synovitis leads to cartilage destruction, bone erosions and periarticular decalcification, subsequently resulting in impaired joint function. It is more common between the ages of 35 and 50 years, affecting three times more women than men. Susceptibility to RA is genetically determined with multiple genes contributing. Inheritance of HLA DRB1 alleles encoding a distinctive five-amino-acid sequence known as the \"shared epitope\" (SE) is the best characterized genetic risk factor. The mechanism by which the SE alleles contribute to the development of RA is not very clear. It has been postulated that the presence of these conserved sequences in the antigen-binding groove alters the way antigenic peptides are bound to and presented to T-cell lymphocytes. This, in turn, may trigger abnormal immune responses and lead to RA." + }, + "article": { + "id": "30124939", + "text": "OBJECTIVES:\nTo investigate the link between smoking status, including childhood and adult passive exposure, and the risk of incident RA.\n\nMETHODS:\nThe French E3N cohort includes 98 995 female volunteers prospectively followed since 1990. Self-administered questionnaires sent every 2-3 years collected medical events, general, lifestyle and environmental characteristics. RA diagnoses were collected in three successive questionnaires and confirmed if women received reimbursement for an RA-specific medication. The risk of incident RA was estimated using an age-adjusted Cox model that considers smoking status as a time-dependent variable.\n\nRESULTS:\nAmong 71 248 women, 371 incident RA cases were confirmed. Ever-smokers not exposed to passive smoking had an increased risk of RA [1.38 (95% CI 1.10, 1.74)]. In never-smokers, passive smoking exposure during childhood was associated with a borderline increased risk of RA in the same range as active smoking in adults, with an hazard ratio (HR) of 1.43 (95% CI 0.97, 2.11). Ever-smokers who also had childhood passive smoking exposure had a higher risk of RA than smokers not exposed during childhood [HR 1.67 (95% CI 1.17, 2.39)], but without a significant difference (P = 0.30). RA began earlier in smokers exposed to childhood passive smoking.\n\nCONCLUSION:\nThis study confirms that active smoking is associated with an increased risk of RA. It suggests for the first time that passive exposure to tobacco during childhood might also increase the risk of RA in future light smokers and probably non-smokers. Our results highlight the importance of avoiding any tobacco environment in children, especially in those with a family history of RA." + }, + "questions": [ + { + "id": "083ce49e-fb3b-4758-ac6f-89243a39e127", + "text": "What are the risk factors of Rheumatoid arthritis?", + "answers": [ + { + "answer_start": 1026, + "text": "Ever-smokers who also had childhood passive smoking exposure" + }, + { + "answer_start": 1337, + "text": "active smoking" + }, + { + "answer_start": 710, + "text": "Ever-smokers not exposed to passive smoking" + } + ] + } + ] +} \ No newline at end of file diff --git a/f7609781-00e4-4cd7-b723-dfcdce48dc31.json b/f7609781-00e4-4cd7-b723-dfcdce48dc31.json new file mode 100644 index 0000000000000000000000000000000000000000..bd49098e114536b6ba2e22e7870c7f72ad519df5 --- /dev/null +++ b/f7609781-00e4-4cd7-b723-dfcdce48dc31.json @@ -0,0 +1,55 @@ +{ + "id": "f7609781-00e4-4cd7-b723-dfcdce48dc31", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "9335442", + "text": "To assess the association between the incidence of cutaneous melanoma; intermittent, occupational and total sun exposure; and history of sunburn at different ages, we conducted a systematic review using results of all published case-control studies which have assessed incident melanoma, sun exposure and sunburn. Twenty-nine studies contributed data on sun exposure and 21 on sunburn. Overall, there was a significant positive association (odds ratio [OR] = 1.71) for intermittent exposure, a significantly reduced risk for heavy occupational exposure (OR = 0.86) and a small, marginally significant excess risk for total exposure (OR = 1.18). There was a significantly increased risk with sunburn at all ages or in adult life (OR = 1.91) and similarly elevated relative risks for sunburn in adolescence (OR = 1.73) and in childhood (OR = 1.95). There was significant heterogeneity with all of these estimates except that of all ages or adult sunburn. These results show the specificity of the positive association between melanoma risk and intermittent sun exposure, in contrast to a reduced risk with high levels of occupational exposure. The association with sunburn also is likely to reflect intermittent exposure; the results do not suggest any strong relationship to age at sunburn. These associations are similar to those reported for basal cell skin cancer but different from those reported for squamous cell cancer. The mechanisms by which intermittent exposure increases risk, while other patterns of exposure do not, remain to be elucidated." + }, + "questions": [ + { + "id": "76b82487-876a-4cb6-920f-ca420ccc3846", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 469, + "text": "intermittent exposure" + }, + { + "answer_start": 617, + "text": "total exposure" + }, + { + "answer_start": 691, + "text": "sunburn at all ages or in adult life" + }, + { + "answer_start": 782, + "text": "sunburn in adolescence" + }, + { + "answer_start": 824, + "text": "childhood" + }, + { + "answer_start": 1042, + "text": "intermittent sun exposure" + } + ] + } + ] +} \ No newline at end of file diff --git a/f7bcfd09-c800-4596-9fad-b1dea20b1b03.json b/f7bcfd09-c800-4596-9fad-b1dea20b1b03.json new file mode 100644 index 0000000000000000000000000000000000000000..5827a72c3acba4c77a96bc5e0e8939de46bbe761 --- /dev/null +++ b/f7bcfd09-c800-4596-9fad-b1dea20b1b03.json @@ -0,0 +1,37 @@ +{ + "id": "f7bcfd09-c800-4596-9fad-b1dea20b1b03", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "26036212", + "text": "BACKGROUND:\nThe preponderance of observational studies describe an association between the use of estrogen alone and a lower incidence of colorectal cancer. In contrast, no difference in the incidence of colorectal cancer was seen in the Women's Health Initiative (WHI) randomized, placebo-controlled trial with estrogen alone after a mean intervention of 7.1 years and cumulative follow-up of 13.2 years. This study extends these findings by providing detailed analyses of the effects of estrogen alone on the histology, grade, and stage of colorectal cancer, relevant subgroups, and deaths from and after colorectal cancer.\n\nMETHODS:\nThe WHI study was a randomized, double-blind, placebo-controlled trial involving 10,739 postmenopausal women with prior hysterectomy. Participants were assigned to conjugated equine estrogen at 0.625 mg/d (n = 5279) or a matching placebo (n = 5409). Rates of colorectal cancer diagnoses and deaths from and after colorectal cancer were assessed throughout the study.\n\nRESULTS:\nColorectal cancer rates in the estrogen-alone and placebo groups were comparable: 0.14% and 0.12% per year, respectively (hazard ratio [HR], 1.13; 95% confidence interval [CI], 0.83-1.58; P = .43). Bowel screening examinations were comparable between the 2 groups throughout the study. The grade, stage, and location of colorectal cancer did not differ between the randomization groups. There were more colorectal cancer deaths in the estrogen-alone group (34 [0.05%] vs 24 [0.03%]; HR, 1.46, 95% CI, 0.86-2.46; P = .16), but the difference was not statistically significant. The colorectal cancer incidence was higher for participants with a history of colon polyp removal in the estrogen-alone group (0.23% vs 0.02%; HR, 13.47; nominal 95% CI, 1.76-103.0; P \u003c .001).\n\nCONCLUSIONS:\nThe use of estrogen alone in postmenopausal women with prior hysterectomy does not influence the incidence of colorectal cancer or deaths from or after colorectal cancer. A possibly higher risk of colorectal cancer in women with prior colon polyp removal who use estrogen alone requires confirmation." + }, + "questions": [ + { + "id": "9fa33aee-bd5b-4921-8a7c-939d725cd236", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 2014, + "text": "women with prior colon polyp removal who use estrogen alone" + } + ] + } + ] +} \ No newline at end of file diff --git a/f7d787b3-c918-475b-921f-c936c9083921.json b/f7d787b3-c918-475b-921f-c936c9083921.json new file mode 100644 index 0000000000000000000000000000000000000000..0a3f7a44b6c905e99d8d91f6ecc4688beac6f3e5 --- /dev/null +++ b/f7d787b3-c918-475b-921f-c936c9083921.json @@ -0,0 +1,45 @@ +{ + "id": "f7d787b3-c918-475b-921f-c936c9083921", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "7707417", + "text": "BACKGROUND:\nMethylation of DNA, which may have a role in the regulation of gene expression, depends on dietary folate and methionine. Because aberrant DNA methylation may contribute to the initiation or progression of colon cancer, we hypothesized that deficient intakes of folate or methionine and high consumption of alcohol, an antagonist of methyl-group metabolism, increase risk of colon neoplasia. Previously, a high-alcohol and low-methionine--low-folate (methyl-deficient) diet was shown to be related to a higher risk of colon adenomas, precursors of cancer.\n\nPURPOSE:\nOur goal was to determine if ingestion of a high-alcohol, methyl-deficient diet is related directly to risk of colon cancer.\n\nMETHODS:\nWe assessed dietary intake for a 1-year period for a cohort of 47,931 U.S. male health professionals, 40-75 years old and free of diagnosed cancer in 1986. We assessed diet by using a validated, semiquantitative food-frequency questionnaire. During 6 years of follow-up, we documented 205 new cases of colon cancer in this cohort.\n\nRESULTS:\nCurrent alcohol intake was directly related to risk of colon cancer (multivariate relative risk [RR] = 2.07; 95% confidence interval [CI] = 1.29-3.32, for \u003e 2 drinks versus \u003c or = 0.25 drink daily; P trend = .005), and past drinkers were also at higher risk (RR = 1.95; 95% CI = 1.22-3.10). Individually, folate and methionine intakes were weakly inversely associated with risk of colon cancer. An adverse effect of a high-alcohol, low-methyl diet was not observed among regular users of aspirin, who have previously been shown to be at lower risk for colon cancer. Combinations of high alcohol and low methionine and folate intakes yielded striking associations for total colon cancer (RR = 3.30 [95% CI = 1.58-6.88] comparing high-methyl diets with low-methyl diets among nonusers of aspirin) and for cancers of the distal colon (RR = 7.44; 95% CI = 1.72-32.1). Among men with high intakes of folate or methionine, alcohol levels of \u003e 2 drinks daily were not associated with risk of colon cancer. The increased risk of colon cancer associated with alcohol and methyl-deficient diets was not confounded by smoking; intakes of fat, red meat, and fiber; level of physical activity; multivitamin or aspirin use; and body mass index.\n\nCONCLUSIONS:\nThese findings support the hypothesis that substantial consumption of alcohol, when combined with inadequate intakes of folate and methionine, may increase risk of colon cancer and confirm similar findings in adenomas.\n\nIMPLICATIONS:\nThese data provide further support of recommendations to avoid excess alcohol consumption and to increase dietary folate to lower the risk of colon cancer." + }, + "questions": [ + { + "id": "fe74e3a3-1cb7-4fb1-b2b5-e4b463820e93", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1054, + "text": "Current alcohol intake" + }, + { + "answer_start": 1620, + "text": "Combinations of high alcohol and low methionine and folate intakes" + }, + { + "answer_start": 2342, + "text": "substantial consumption of alcohol, when combined with inadequate intakes of folate and methionine" + } + ] + } + ] +} \ No newline at end of file diff --git a/f837f44d-da86-412c-b49e-19a4b938c43b.json b/f837f44d-da86-412c-b49e-19a4b938c43b.json new file mode 100644 index 0000000000000000000000000000000000000000..de43f623b000bfd05e2ca09d9ee591634868ffc1 --- /dev/null +++ b/f837f44d-da86-412c-b49e-19a4b938c43b.json @@ -0,0 +1,35 @@ +{ + "id": "f837f44d-da86-412c-b49e-19a4b938c43b", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "15706003", + "text": "The prevalence of asthma has increased worldwide. The reasons for this rise remain unclear. Various studies have reported an association between acetaminophen, a widely used analgesic, and diagnosed asthma. In a prospective cohort study, the rate of newly diagnosed asthma was 63% higher among frequent acetaminophen users than nonusers in multivariate analyses. Studies of patients with asthma suggest that acetaminophen challenge can precipitate a decline in FEV(1) \u003e 15% among sensitive individuals. Plausible mechanisms to explain this association include depletion of pulmonary glutathione and oxidative stress. This article reviews the existing literature and evaluates the epidemiologic and pathophysiologic evidence underlying a possible link between acetaminophen and asthma." + }, + "questions": [ + { + "id": "35d848f5-d8e2-4772-bc2a-f8cd370370e4", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 294, + "text": "frequent acetaminophen users" + } + ] + } + ] +} \ No newline at end of file diff --git a/f911df9a-f409-4b29-a7cf-f13e8a3af085.json b/f911df9a-f409-4b29-a7cf-f13e8a3af085.json new file mode 100644 index 0000000000000000000000000000000000000000..7e049f309ae0d22683aca199e50af82a67f4414d --- /dev/null +++ b/f911df9a-f409-4b29-a7cf-f13e8a3af085.json @@ -0,0 +1,36 @@ +{ + "id": "f911df9a-f409-4b29-a7cf-f13e8a3af085", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "17071833", + "text": "BACKGROUND:\nSmokers are more prone to develop chronic obstructive pulmonary disease (COPD) than non-smokers, but this finding comes from studies spanning 10 years or less. The aim of this study was to determine the 25 year absolute risk of developing COPD in men and women from the general population.\n\nMETHODS:\nAs part of the Copenhagen City Heart Study, 8045 men and women aged 30-60 years with normal lung function at baseline were followed for 25 years. Lung function measurements were collected and mortality from COPD during the 25 year observation period was analysed.\n\nRESULTS:\nThe percentage of men with normal lung function ranged from 96% of never smokers to 59% of continuous smokers; for women the proportions were 91% and 69%, respectively. The 25 year incidence of moderate and severe COPD was 20.7% and 3.6%, respectively, with no apparent difference between men and women. Smoking cessation, especially early in the follow up period, decreased the risk of developing COPD substantially compared with continuous smoking. During the follow up period there were 2912 deaths, 109 of which were from COPD. 92% of the COPD deaths occurred in subjects who were current smokers at the beginning of the follow up period.\n\nCONCLUSION:\nThe absolute risk of developing COPD among continuous smokers is at least 25%, which is larger than was previously estimated." + }, + "questions": [ + { + "id": "b270c90b-042c-458c-bd22-b95feda3d757", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 1285, + "text": "continuous smokers" + } + ] + } + ] +} \ No newline at end of file diff --git a/f94a9f13-128f-48d1-847e-18362bbbf467.json b/f94a9f13-128f-48d1-847e-18362bbbf467.json new file mode 100644 index 0000000000000000000000000000000000000000..7719d7c90a07b80c3d8e202477ee2fc15f9a77b7 --- /dev/null +++ b/f94a9f13-128f-48d1-847e-18362bbbf467.json @@ -0,0 +1,42 @@ +{ + "id": "f94a9f13-128f-48d1-847e-18362bbbf467", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "11560847", + "text": "BACKGROUND:\nVascular cell adhesion molecule (VCAM)-1, intercellular adhesion molecule (ICAM)-1, and E-selectin mediate adhesion and transmigration of leukocytes to the vascular endothelial wall and may promote plaque growth and instability. In a prospective study, we evaluated the effect of soluble adhesion molecules on the risk of future cardiovascular events among patients with angiographically documented coronary artery disease (CAD). Methods and Results- -We obtained baseline samples from a prospective cohort of 1246 patients with CAD. Besides various markers of inflammation, soluble VCAM-1 (sVCAM-1), sICAM-1, and sE-selectin were determined. Follow-up information on cardiovascular events was obtained (mean, 2.7; maximum, 4.1 years). Independently higher levels of sVCAM-1 (1932 versus 1128 ng/mL; P\u003c0.0001), sICAM-1 (353 versus 287 ng/mL; P=0.015), and sE-selectin (81 versus 63 ng/mL; P=0.003) were observed in patients with future death from cardiovascular causes. In a multivariate model, fatal risk was 2.1-fold (1.1 to 4.0) higher in patients within the top quartile of baseline sVCAM-1 concentrations compared with lower quartiles. This association was present independent of general inflammatory response as reflected by low or high C-reactive protein (hs-CRP) levels. In a model that simultaneously controlled for all inflammatory and soluble adhesion markers determined, only sVCAM-1 remained independently significant for future fatal cardiovascular events, with a 2.8-fold increase in risk (P=0.003).\n\nCONCLUSIONS:\nSoluble adhesion molecules sVCAM-1, sICAM-1, and sE-selectin were significantly related to future death from cardiovascular causes among patients with documented CAD. Especially sVCAM-1 added to the predictive value of classic risk factors and hs-CRP in determining the risk of future cardiovascular death." + }, + "questions": [ + { + "id": "7c4fde88-8c3b-4b65-bab6-2ae974e16fc4", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 1568, + "text": "sVCAM-1" + }, + { + "answer_start": 1577, + "text": "sICAM-1" + }, + { + "answer_start": 1590, + "text": "sE-selectin" + } + ] + } + ] +} \ No newline at end of file diff --git a/f94f976d-2f77-40ae-856f-5e8fcc2a6e68.json b/f94f976d-2f77-40ae-856f-5e8fcc2a6e68.json new file mode 100644 index 0000000000000000000000000000000000000000..aeb7c0e7ead4e0e5b34ebdb09068ccd78b79b32e --- /dev/null +++ b/f94f976d-2f77-40ae-856f-5e8fcc2a6e68.json @@ -0,0 +1,58 @@ +{ + "id": "f94f976d-2f77-40ae-856f-5e8fcc2a6e68", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "14750529", + "text": "OBJECTIVES:\nWe examined which occupations and industries are currently at high risk for bladder cancer in men.\n\nMETHODS:\nWe combined data from 11 case-control studies conducted between 1976-1996 in six European countries. The study comprised 3346 incident cases and 6840 controls, aged 30-79 years. Lifetime occupational and smoking histories were examined using common coding.\n\nRESULTS:\nOdds ratios for eight a priori defined high-risk occupations were low, and with the exception of metal workers and machinists (OR = 1.16, 95% CI = 1.02-1.32), were not statistically significant. Higher risks were observed for specific categories of painters, metal, textile and electrical workers, for miners, transport operators, excavating-machine operators, and also for non-industrial workers such as concierges and janitors. Industries entailing a high risk included salt mining, manufacture of carpets, paints, plastics and industrial chemicals. An increased risk was found for exposure to PAHs (OR for highest exposure tertile = 1.23, 95% CI = 1.07-1.4). The risk attributable to occupation ranged from 4.2 to 7.4%, with an estimated 4.3% for exposure to PAHs.\n\nCONCLUSIONS:\nMetal workers, machinists, transport equipment operators and miners are among the major occupations contributing to occupational bladder cancer in men in Western Europe. In this population one in 10 to one in 20 cancers of the bladder can be attributed to occupation." + }, + "questions": [ + { + "id": "91201bb6-b6ae-4740-a1ed-5666b51f9895", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 485, + "text": "metal workers" + }, + { + "answer_start": 503, + "text": "machinists" + }, + { + "answer_start": 860, + "text": "salt mining" + }, + { + "answer_start": 1170, + "text": "Metal workers" + }, + { + "answer_start": 1185, + "text": "machinists" + }, + { + "answer_start": 1197, + "text": "transport equipment operators" + }, + { + "answer_start": 1231, + "text": "miners" + } + ] + } + ] +} \ No newline at end of file diff --git a/f99ff2f1-bd6b-45c2-81a2-2d3fb39acd65.json b/f99ff2f1-bd6b-45c2-81a2-2d3fb39acd65.json new file mode 100644 index 0000000000000000000000000000000000000000..e13e6771a22b7f2cd53c4d7f63663440c49fa886 --- /dev/null +++ b/f99ff2f1-bd6b-45c2-81a2-2d3fb39acd65.json @@ -0,0 +1,54 @@ +{ + "id": "f99ff2f1-bd6b-45c2-81a2-2d3fb39acd65", + "disease": { + "id": "H01730", + "names": [ + "Myocardial infarction" + ], + "dbLinks": { + "icd10": [ + "I21" + ], + "mesh": [ + "D009203" + ] + }, + "category": "Cardiovascular disease" + }, + "article": { + "id": "18212285", + "text": "BACKGROUND:\nSeparate multivariable risk algorithms are commonly used to assess risk of specific atherosclerotic cardiovascular disease (CVD) events, ie, coronary heart disease, cerebrovascular disease, peripheral vascular disease, and heart failure. The present report presents a single multivariable risk function that predicts risk of developing all CVD and of its constituents.\n\nMETHODS AND RESULTS:\nWe used Cox proportional-hazards regression to evaluate the risk of developing a first CVD event in 8491 Framingham study participants (mean age, 49 years; 4522 women) who attended a routine examination between 30 and 74 years of age and were free of CVD. Sex-specific multivariable risk functions (\"general CVD\" algorithms) were derived that incorporated age, total and high-density lipoprotein cholesterol, systolic blood pressure, treatment for hypertension, smoking, and diabetes status. We assessed the performance of the general CVD algorithms for predicting individual CVD events (coronary heart disease, stroke, peripheral artery disease, or heart failure). Over 12 years of follow-up, 1174 participants (456 women) developed a first CVD event. All traditional risk factors evaluated predicted CVD risk (multivariable-adjusted P\u003c0.0001). The general CVD algorithm demonstrated good discrimination (C statistic, 0.763 [men] and 0.793 [women]) and calibration. Simple adjustments to the general CVD risk algorithms allowed estimation of the risks of each CVD component. Two simple risk scores are presented, 1 based on all traditional risk factors and the other based on non-laboratory-based predictors.\n\nCONCLUSIONS:\nA sex-specific multivariable risk factor algorithm can be conveniently used to assess general CVD risk and risk of individual CVD events (coronary, cerebrovascular, and peripheral arterial disease and heart failure). The estimated absolute CVD event rates can be used to quantify risk and to guide preventive care." + }, + "questions": [ + { + "id": "2b32674c-de23-4694-828b-b58ae51449b5", + "text": "What are the risk factors of Myocardial infarction?", + "answers": [ + { + "answer_start": 759, + "text": "age" + }, + { + "answer_start": 764, + "text": "total and high-density lipoprotein cholesterol" + }, + { + "answer_start": 812, + "text": "systolic blood pressure" + }, + { + "answer_start": 837, + "text": "treatment for hypertension" + }, + { + "answer_start": 865, + "text": "smoking" + }, + { + "answer_start": 878, + "text": "diabetes status" + } + ] + } + ] +} \ No newline at end of file diff --git a/f9f36d50-bbd4-494d-9da4-5c4476fab45f.json b/f9f36d50-bbd4-494d-9da4-5c4476fab45f.json new file mode 100644 index 0000000000000000000000000000000000000000..71717bbae4dac6cfeaed5b8ed6dec2746eab82bd --- /dev/null +++ b/f9f36d50-bbd4-494d-9da4-5c4476fab45f.json @@ -0,0 +1,38 @@ +{ + "id": "f9f36d50-bbd4-494d-9da4-5c4476fab45f", + "disease": { + "id": "H00031", + "names": [ + "Breast cancer" + ], + "dbLinks": { + "icd10": [ + "C50" + ], + "mesh": [ + "D001943" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "19002173", + "text": "In the 1950s, the Mayak nuclear weapons facility in Russia discharged liquid radioactive wastes into the Techa River causing exposure of riverside residents to protracted low-to-moderate doses of radiation. Almost 10,000 women received estimated doses to the stomach of up to 0.47 Gray (Gy) (mean dose=0.04 Gy) from external gamma-exposure and (137)Cs incorporation. We have been following this population for cancer incidence and mortality and as in the general Russian population, we found a significant temporal trend of breast cancer incidence. A significant linear radiation dose-response relationship was observed (P=0.01) with an estimated excess relative risk per Gray (ERR/Gy) of 5.00 (95% confidence interval (CI), 0.80, 12.76). We estimated that approximately 12% of the 109 observed cases could be attributed to radiation." + }, + "questions": [ + { + "id": "dc475374-7fbc-485f-81be-2399ec7029d9", + "text": "What are the risk factors of Breast Cancer?", + "answers": [ + { + "answer_start": 570, + "text": "radiation dose-response" + }, + { + "answer_start": 672, + "text": "Gray (ERR/Gy) of 5.00" + } + ] + } + ] +} \ No newline at end of file diff --git a/fa0fccef-06d3-4923-a258-bc035403d3fb.json b/fa0fccef-06d3-4923-a258-bc035403d3fb.json new file mode 100644 index 0000000000000000000000000000000000000000..8f55857b327fa5c1da0617ac2076fa1ecf04c79d --- /dev/null +++ b/fa0fccef-06d3-4923-a258-bc035403d3fb.json @@ -0,0 +1,42 @@ +{ + "id": "fa0fccef-06d3-4923-a258-bc035403d3fb", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "16186287", + "text": "OBJECTIVE:\nThe objective of this study was to determine the association between smoking and incident diabetes among U.S. adults.\n\nRESEARCH DESIGN AND METHODS:\nThe Insulin Resistance Atherosclerosis Study (IRAS) was a prospective study of the associations of insulin sensitivity and cardiovascular risk factors. We examined the relationship between smoking status categories (never, former, and current) and incident 5-year type 2 diabetes among 906 participants free of diabetes at baseline. We also considered the effect of pack-year categories (never, former \u003c20 pack-years, former \u003e or = 20 pack-years, current \u003c20 pack-years, and current \u003e or = 20 pack-years) upon diabetes incidence.\n\nRESULTS:\nOf current smokers, 96 (25%) developed diabetes at 5 years, compared with 60 (14%) never smokers. After multivariable adjustment, current smokers exhibited increased incidence of diabetes compared with never smokers (odds ratio [OR] 2.66, P = 0.001). Similar results were found among current smokers with \u003e or = 20 pack-years with normal glucose tolerance (5.66, P = 0.001).\n\nCONCLUSIONS:\nSmoking shares a robust association with incident diabetes, supporting the current Surgeon General's warnings against cigarette smoking." + }, + "questions": [ + { + "id": "106849ef-7c2e-482f-891d-e065997fb12b", + "text": "what are the risk factors of type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1088, + "text": "Smoking" + }, + { + "answer_start": 829, + "text": "current smokers" + }, + { + "answer_start": 983, + "text": "current smokers with \u003e or = 20 pack-years with normal glucose tolerance" + } + ] + } + ] +} \ No newline at end of file diff --git a/fa21eb47-85c4-4d79-84d8-f899586a9db7.json b/fa21eb47-85c4-4d79-84d8-f899586a9db7.json new file mode 100644 index 0000000000000000000000000000000000000000..87b4e5a2436e531e71bdfbd424fba90bd8739a89 --- /dev/null +++ b/fa21eb47-85c4-4d79-84d8-f899586a9db7.json @@ -0,0 +1,51 @@ +{ + "id": "fa21eb47-85c4-4d79-84d8-f899586a9db7", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "17928596", + "text": "BACKGROUND:\nPathological features of the airway in young children with severe recurrent wheeze suggest an association between bacterial colonization and the initiating events of early asthma. We conducted a study to investigate a possible association between bacterial colonization of the hypopharynx in asymptomatic neonates and later development of recurrent wheeze, asthma, and allergy during the first 5 years of life.\n\nMETHODS:\nThe subjects were children from the Copenhagen Prospective Study on Asthma in Childhood birth cohort who were born to mothers with asthma. Aspirates from the hypopharyngeal region of asymptomatic 1-month-old infants were cultured for Streptococcus pneumoniae, Haemophilus influenzae, Moraxella catarrhalis, and Staphylococcus aureus. Wheeze was monitored prospectively on diary cards during the first 5 years of life. Blood eosinophil count and total IgE and specific IgE were measured at 4 years of age. Lung function was measured and asthma was diagnosed at 5 years of age.\n\nRESULTS:\nHypopharyngeal samples were cultured from 321 neonates at 1 month of age. Twenty-one percent of the infants were colonized with S. pneumoniae, M. catarrhalis, H. influenzae, or a combination of these organisms; colonization with one or more of these organisms, but not colonization with S. aureus, was significantly associated with persistent wheeze (hazard ratio, 2.40; 95% confidence interval [CI], 1.45 to 3.99), acute severe exacerbation of wheeze (hazard ratio, 2.99; 95% CI, 1.66 to 5.39), and hospitalization for wheeze (hazard ratio, 3.85; 95% CI, 1.90 to 7.79). Blood eosinophil counts and total IgE at 4 years of age were significantly increased in children colonized neonatally with S. pneumoniae, M. catarrhalis, H. influenzae, or a combination of these organisms, but specific IgE was not significantly affected. The prevalence of asthma and the reversibility of airway resistance after beta2-agonist administration at 5 years of age were significantly increased in the children colonized neonatally with these organisms as compared with the children without such colonization (33% vs. 10% and 23% vs. 18%, respectively).\n\nCONCLUSIONS:\nNeonates colonized in the hypopharyngeal region with S. pneumoniae, H. influenzae, or M. catarrhalis, or with a combination of these organisms, are at increased risk for recurrent wheeze and asthma early in life." + }, + "questions": [ + { + "id": "5e2bd662-a7b3-4ffd-97e8-82eee953ed49", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 667, + "text": "Streptococcus pneumoniae" + }, + { + "answer_start": 693, + "text": "Haemophilus influenzae" + }, + { + "answer_start": 717, + "text": "Moraxella catarrhalis" + }, + { + "answer_start": 744, + "text": "Staphylococcus aureus" + }, + { + "answer_start": 2168, + "text": "Neonates colonized in the hypopharyngeal region with S. pneumoniae, H. influenzae, or M. catarrhalis, or with a combination of these organisms" + } + ] + } + ] +} \ No newline at end of file diff --git a/fa796acd-f875-4947-a159-a3ffaa48a691.json b/fa796acd-f875-4947-a159-a3ffaa48a691.json new file mode 100644 index 0000000000000000000000000000000000000000..452078d818cb6a0595bf4752545de394c0bcb29c --- /dev/null +++ b/fa796acd-f875-4947-a159-a3ffaa48a691.json @@ -0,0 +1,38 @@ +{ + "id": "fa796acd-f875-4947-a159-a3ffaa48a691", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "9430264", + "text": "We conducted a population-based case-control study of bladder cancer in Iowa in 1986-1989 to evaluate the risk posed by tapwater containing chlorination byproducts. We combined information about residential history, drinking water source, beverage intake, and other factors with historical data from water utilities and measured contaminant levels to create indices of past exposure to chlorination byproducts. The study comprised 1,123 cases and 1,983 controls who had data relating to at least 70% of their lifetime drinking water source. After we adjusted for potential confounders, we calculated odds ratios for duration of chlorinated surface water of 1.0 (referent), 1.0, 1.1, 1.2, and 1.5 for 0, 1-19, 20-39, 40-59, and \u003e or =60 years of use. We also found associations with total and average lifetime byproduct intake, as represented by trihalomethane estimates. Positive findings were restricted to men and to ever-smokers. Among men, odds ratios were 1.0 (referent), 1.1, 1.3, 1.5, and 1.9, and among ever-smokers, 1.0, 1.1, 1.3, 1.8, and 2.2, after adjustment for intensity and timing of smoking. Among nonsmoking men and women, regardless of smoking habit, there was no association. Among men, smoking and exposure to chlorinated surface water mutually enhanced the risk of bladder cancer. The overall association of bladder cancer risk with duration of chlorinated surface water use that we found is consistent with the findings of other investigations, but the differences in risk between men and women, and between smokers and nonsmokers, have not been widely observed." + }, + "questions": [ + { + "id": "8abb9f50-ac58-44ab-a574-c18531fc9da7", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 1195, + "text": "Among men, smoking and exposure to chlorinated surface water" + }, + { + "answer_start": 1353, + "text": " duration of chlorinated surface water" + } + ] + } + ] +} \ No newline at end of file diff --git a/face8e42-12e4-412e-94da-3997a192ce16.json b/face8e42-12e4-412e-94da-3997a192ce16.json new file mode 100644 index 0000000000000000000000000000000000000000..f07c3aeb760d8cbb09b3543c0c76a6a485a44684 --- /dev/null +++ b/face8e42-12e4-412e-94da-3997a192ce16.json @@ -0,0 +1,37 @@ +{ + "id": "face8e42-12e4-412e-94da-3997a192ce16", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "30740587", + "text": "BACKGROUND:\nColorectal cancer (CRC) diagnosed before age 50 years, or young-onset CRC, is increasing globally with undefined etiology. A sedentary lifestyle is an emerging risk factor for CRC after age 50 years, but its role in young-onset CRC is unknown.\n\nMETHODS:\nWe prospectively evaluated sedentary behaviors, primarily time watching television (TV), and risk of young-onset CRC among 89 278 women in the Nurses' Health Study II ages 25-42 years at recruitment (1991-2011). We used Cox proportional hazards modelling to estimate relative risks (RR) and 95% confidence intervals (CIs). Statistical tests were two-sided.\n\nRESULTS:\nWe documented 118 young-onset CRCs over 1 262 540 person-years. Sedentary TV viewing time was statistically significantly associated with increased risk of young-onset CRC, after adjusting for putative risk factors, including obesity and physical activity. Compared 7 hours, women with 7.1-14 hours per week of TV time had a multivariable relative risk (RR) of 1.12 (95% confidence interval [CI] = 0.72 to 1.75), further increased for greater than14 hours per week (RR = 1.69, 95% CI = 1.07 to 2.67, = .03). This association was observed among participants without a CRC family history and was more pronounced for rectal cancer (RR for \u003e14 vs \u003c7 hours per week 2.44, 95% CI = 1.03 to 5.78, = .04). Overweight or obese participants may be more susceptible.\n\nCONCLUSION:\nIndependent of exercise and obesity, prolonged sedentary TV viewing time, a surrogate for a more inactive lifestyle, was associated with increased risk of young-onset CRC, particularly of the rectum. These findings provide further evidence on the importance of maintaining an active lifestyle." + }, + "questions": [ + { + "id": "6bf1840d-ea73-4f04-a577-c0a14a0fc56a", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1439, + "text": "prolonged sedentary TV viewing time" + } + ] + } + ] +} \ No newline at end of file diff --git a/fb03a436-c1e7-4bd3-96e1-e6d026fe3155.json b/fb03a436-c1e7-4bd3-96e1-e6d026fe3155.json new file mode 100644 index 0000000000000000000000000000000000000000..a6ea0381b32d04f9fa7862135cfd4a64d65a27df --- /dev/null +++ b/fb03a436-c1e7-4bd3-96e1-e6d026fe3155.json @@ -0,0 +1,34 @@ +{ + "id": "fb03a436-c1e7-4bd3-96e1-e6d026fe3155", + "disease": { + "id": "H00022", + "names": [ + "Bladder cancer" + ], + "dbLinks": { + "icd10": [ + "C67" + ], + "mesh": [ + "D001749" + ] + }, + "category": "Cancer" + }, + "article": { + "id": "7581498", + "text": "Bladder cancer provides the most definitive example for an association between environmental agents and cancer. However, in the absence of industrial occupational exposure, the primary carcinogen is rarely identified, and the mechanisms involved in cancer formation are poorly understood. The environmental procarcinogen hypothesis of tumour pathogenesis proposes that many carcinogens require metabolic activation by drug metabolizing enzymes to form the proximate carcinogen. A balance of exposure to the carcinogen, the activity of the enzymes involved in either formation of proximate carcinogen, or production of non-toxic metabolites, will determine tumour risk. We have used mephenytoin, debrisoquine and dapsone as selective probes for the phenotypic measures of activity of CYP2C19, CYP2D6, and CYP3A4, respectively. Within subject reproducibility of phenotypic measures, and the lack of cross-inhibition when the three drugs are given in a concurrent cocktail, have been confirmed. We have applied the cocktail drug approach in two, non-overlapping series of cases with bladder cancer and matched controls. In both series, patients with aggressive bladder cancer (GIII histopathology) had a history of excess alcohol intake, an under-representation of poor metabolizers of debrisoquine, a significant mean reduction in dapsone recovery ratio, but no difference in mephenytoin phenotype. Collectively, these observations involving multiple routes of drug metabolism support the procarcinogen environmental hypothesis for bladder cancer and suggest that measurement of activity of selected individual drug metabolizing enzymes involved in the pathogenesis of this tumour can be used to identify subjects at high risk of developing bladder cancer." + }, + "questions": [ + { + "id": "f762d9cd-d041-449a-9487-cd6aa005d544", + "text": "What are the risk factors of Bladder cancer?", + "answers": [ + { + "answer_start": 1201, + "text": "history of excess alcohol intake" + } + ] + } + ] +} \ No newline at end of file diff --git a/fb9c3ad4-ab7c-456e-abac-85c8a05b21f9.json b/fb9c3ad4-ab7c-456e-abac-85c8a05b21f9.json new file mode 100644 index 0000000000000000000000000000000000000000..b0408bc24c45a25f68a1f3d488c88fd8a9f1a7b2 --- /dev/null +++ b/fb9c3ad4-ab7c-456e-abac-85c8a05b21f9.json @@ -0,0 +1,34 @@ +{ + "id": "fb9c3ad4-ab7c-456e-abac-85c8a05b21f9", + "disease": { + "id": "H00408", + "names": [ + "Type 1 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E10" + ], + "mesh": [ + "D003922" + ] + }, + "category": "Metabolic disease; Immune system disease; Endocrine disease" + }, + "article": { + "id": "12880126", + "text": "The effect of a number of host and environmental factors on the onset of type 1 diabetes mellitus (DM1) in a group of Lebanese children and young adults was studied. Results showed that DM1 in a group of 253 patients presented no gender preference and that the age of onset was similar in both genders. The overall body mass index reflected good metabolic control. HbA1c had a mean value of 8.98%, suggesting poor glucose control. Family history of DM1 and type 2 diabetes mellitus as well as consanguinity in patients' families were not different from those reported in the literature. Finally, onset of DM1 showed seasonal variation, peaking during winter months. DM1 showed a higher prevalence of onset among children born first and a decreased incidence as birth order increased. This study provides valuable data for the diagnosis, control and prevention of DM1 in children." + }, + "questions": [ + { + "id": "fa915752-dd58-4334-be2f-48545a1d2596", + "text": "What are the risk factors of Type 1 diabetes mellitus?", + "answers": [ + { + "answer_start": 712, + "text": "children born first" + } + ] + } + ] +} \ No newline at end of file diff --git a/fd491ec8-66a1-4cb3-9562-a584c89944ef.json b/fd491ec8-66a1-4cb3-9562-a584c89944ef.json new file mode 100644 index 0000000000000000000000000000000000000000..aa6028ad769d7908a9683f6331e5129c76772063 --- /dev/null +++ b/fd491ec8-66a1-4cb3-9562-a584c89944ef.json @@ -0,0 +1,49 @@ +{ + "id": "fd491ec8-66a1-4cb3-9562-a584c89944ef", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "34467395", + "text": "BACKGROUND:\nAntibiotics use may increase colorectal cancer (CRC) risk by altering the gut microbiota, with suggestive evidence reported. Our study aims to investigate antibiotics use in relation to subsequent CRC risk.\n\nMETHODS:\nThis is a nationwide, population-based study with a matched case-control design (first primary CRC cases and 5 matched, cancer-free controls). Complete-population data, extracted from Swedish national registers for the period 2005-2016, were used to calculate odds ratios and 95% confidence intervals.\n\nRESULTS:\nWe included 40 545 CRC cases and 202 720 controls. Using the full dataset, we found a positive association between more frequent antibiotics use and CRC, excluding antibiotics prescribed within 2 years of diagnosis attenuated results toward the null. In site-specific analyses, excluding the 2-year washout, the positive association was confined to the proximal colon (adjusted odds ratio for very high use vs no use = 1.17, 95% confidence interval = 1.05 to 1.31). For rectal cancer, an inverse association, which appears to be driven by women, was observed. Quinolones and sulfonamides and/or trimethoprims were positively associated with proximal colon cancer, whereas a more general inverse association, across antibiotics classes, was observed for rectal cancer. We found no association between methenamine hippurate, a urinary tract antiseptic not affecting the gut microbiota, and CRC risk.\n\nCONCLUSIONS:\nThis register-based study covering the entire population of Sweden found a robust association between antibiotics use and higher risk of proximal colon cancer and an inverse association with rectal cancer in women. This study strengthens the evidence from previous investigations and adds important insight into site-specific colorectal carcinogenesis." + }, + "questions": [ + { + "id": "5a01d733-7261-4885-8cf2-d82e55407ec5", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1101, + "text": "Quinolones" + }, + { + "answer_start": 1116, + "text": "sulfonamides" + }, + { + "answer_start": 1136, + "text": "trimethoprims" + }, + { + "answer_start": 1555, + "text": "antibiotics use" + } + ] + } + ] +} \ No newline at end of file diff --git a/fdcdb9d7-2e81-49e2-919c-bb1307226f97.json b/fdcdb9d7-2e81-49e2-919c-bb1307226f97.json new file mode 100644 index 0000000000000000000000000000000000000000..cd0a6b6021b4f5c38fccc412dda8cf75ca925490 --- /dev/null +++ b/fdcdb9d7-2e81-49e2-919c-bb1307226f97.json @@ -0,0 +1,46 @@ +{ + "id": "fdcdb9d7-2e81-49e2-919c-bb1307226f97", + "disease": { + "id": "H02123", + "names": [ + "Celiac disease" + ], + "dbLinks": { + "icd10": [ + "K90.0" + ], + "mesh": [ + "D002446" + ] + }, + "category": "Digestive system disease" + }, + "article": { + "id": "24988556", + "text": "BACKGROUND:\nThe presence of HLA haplotype DR3-DQ2 or DR4-DQ8 is associated with an increased risk of celiac disease. In addition, nearly all children with celiac disease have serum antibodies against tissue transglutaminase (tTG).\n\nMETHODS:\nWe studied 6403 children with HLA haplotype DR3-DQ2 or DR4-DQ8 prospectively from birth in the United States, Finland, Germany, and Sweden. The primary end point was the development of celiac disease autoimmunity, which was defined as the presence of tTG antibodies on two consecutive tests at least 3 months apart. The secondary end point was the development of celiac disease, which was defined for the purpose of this study as either a diagnosis on biopsy or persistently high levels of tTG antibodies.\n\nRESULTS:\nThe median follow-up was 60 months (interquartile range, 46 to 77). Celiac disease autoimmunity developed in 786 children (12%). Of the 350 children who underwent biopsy, 291 had confirmed celiac disease; an additional 21 children who did not undergo biopsy had persistently high levels of tTG antibodies. The risks of celiac disease autoimmunity and celiac disease by the age of 5 years were 11% and 3%, respectively, among children with a single DR3-DQ2 haplotype, and 26% and 11%, respectively, among those with two copies (DR3-DQ2 homozygosity). In the adjusted model, the hazard ratios for celiac disease autoimmunity were 2.09 (95% confidence interval [CI], 1.70 to 2.56) among heterozygotes and 5.70 (95% CI, 4.66 to 6.97) among homozygotes, as compared with children who had the lowest-risk genotypes (DR4-DQ8 heterozygotes or homozygotes). Residence in Sweden was also independently associated with an increased risk of celiac disease autoimmunity (hazard ratio, 1.90; 95% CI, 1.61 to 2.25).\n\nCONCLUSIONS:\nChildren with the HLA haplotype DR3-DQ2, especially homozygotes, were found to be at high risk for celiac disease autoimmunity and celiac disease early in childhood. The higher risk in Sweden than in other countries highlights the importance of studying environmental factors associated with celiac disease. (Funded by the National Institute of Diabetes and Digestive and Kidney Diseases and others.)." + }, + "questions": [ + { + "id": "37ea72dd-dc9e-4198-a01f-43186ed5925d", + "text": "What are the risk factors of Celiac disease?", + "answers": [ + { + "answer_start": 1790, + "text": "HLA haplotype DR3-DQ2, especially homozygotes" + }, + { + "answer_start": 1606, + "text": "Residence in Sweden" + }, + { + "answer_start": 1198, + "text": "single DR3-DQ2 haplotype" + }, + { + "answer_start": 1272, + "text": "two copies (DR3-DQ2 homozygosity)" + } + ] + } + ] +} \ No newline at end of file diff --git a/fe11c52a-5872-4f5e-bd69-d651c2c4d735.json b/fe11c52a-5872-4f5e-bd69-d651c2c4d735.json new file mode 100644 index 0000000000000000000000000000000000000000..00ff15fdfb8354083f7e39d2d8896d07553431a7 --- /dev/null +++ b/fe11c52a-5872-4f5e-bd69-d651c2c4d735.json @@ -0,0 +1,41 @@ +{ + "id": "fe11c52a-5872-4f5e-bd69-d651c2c4d735", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "24316595", + "text": "We tested the hypothesis that an altered community of gut microbes is associated with risk of colorectal cancer (CRC) in a study of 47 CRC case subjects and 94 control subjects. 16S rRNA genes in fecal bacterial DNA were amplified by universal primers, sequenced by 454 FLX technology, and aligned for taxonomic classification to microbial genomes using the QIIME pipeline. Taxonomic differences were confirmed with quantitative polymerase chain reaction and adjusted for false discovery rate. All statistical tests were two-sided. From 794217 16S rRNA gene sequences, we found that CRC case subjects had decreased overall microbial community diversity (P = .02). In taxonomy-based analyses, lower relative abundance of Clostridia (68.6% vs 77.8%) and increased carriage of Fusobacterium (multivariable odds ratio [OR] = 4.11; 95% confidence interval [CI] = 1.62 to 10.47) and Porphyromonas (OR = 5.17; 95% CI = 1.75 to 15.25) were found in case subjects compared with control subjects. Because of the potentially modifiable nature of the gut bacteria, our findings may have implications for CRC prevention." + }, + "questions": [ + { + "id": "6075ca19-43d3-4f07-a5bd-55ada396d4d7", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 692, + "text": "lower relative abundance of Clostridia" + }, + { + "answer_start": 752, + "text": "increased carriage of Fusobacterium" + } + ] + } + ] +} \ No newline at end of file diff --git a/fe8b53d5-851e-4ba7-b139-cf27b9fef415.json b/fe8b53d5-851e-4ba7-b139-cf27b9fef415.json new file mode 100644 index 0000000000000000000000000000000000000000..50c720b5d8e4840a6459120b6b81af0ba9f97862 --- /dev/null +++ b/fe8b53d5-851e-4ba7-b139-cf27b9fef415.json @@ -0,0 +1,45 @@ +{ + "id": "fe8b53d5-851e-4ba7-b139-cf27b9fef415", + "disease": { + "id": "M2023_04_26_16_38_52", + "names": [ + "Migraine" + ], + "dbLinks": { + "icd10": [ + "G43" + ], + "icd11": [ + "8A80" + ], + "mesh": [ + "C10.228.140.546.399.750" + ] + }, + "description": "Migraine is a chronic neurological disorder characterized by recurrent episodes of unilateral, pulsatile headaches associated with autonomic symptoms such as nausea, vomiting, photophobia, and phonophobia. The pathophysiology of migraine is multifactorial and involves complex interactions between genetic, environmental, and neurochemical factors that modulate cerebral vascular tone and nociception. Migraine attacks can be triggered by a variety of factors, including stress, hormonal changes, sleep disturbances, and certain foods or medications. Treatment options for migraine include pharmacotherapy for acute attacks, preventive medications for frequent or severe headaches, and lifestyle modifications to avoid triggers. In refractory cases, interventional therapies such as nerve blocks or neuromodulation techniques may be considered." + }, + "article": { + "id": "7737864", + "text": "We studied the inheritance of migraine and concomitant symptoms among 2690 monozygotic (1524 female and 1166 male) pairs and 5497 dizygotic (2951 female and 2546 male) twin pairs. Our material consists of a population-based questionnaire study among Finnish twins in 1981. The definition of migraine is based on a questionnaire method. Concordance was assessed using probandwise concordance rates and tetrachoric correlations for monozygotic (MZ) and dizygotic (DZ) twin pairs. For estimating the contribution of genetic factors to the susceptibility of migraine, a polygenic multifactorial model was used. Structural equation models were applied for estimating variance components and to compare different genetic models. Nearly one-half (40% to 50%) of the liability to migraine is attributable to genetic factors. In all structural analyses, the model with both additive genetic and unshared environmental component had the best goodness-of-fit value. The genetic component varied between 34% to 51% in different migraine types. There were no remarkable differences between sexes except in the effects due to dominance, where the proportion was 26% for men and 14% for women. Concomitant symptoms among subjects within pairs concordant for headache had genetic effects varying from 56% (subjects with unilaterality) and 56% (subjects with visual symptoms) to 45% (persons with nausea and vomiting). The two threshold model of headache points to the continuum model of headache, and the thresholds represent different levels of severity of the pain. Our results emphasize a multifactorial and higher than previously reported genetic pattern in the etiology of migraine. Also unshared environmental factors play an important role." + }, + "questions": [ + { + "id": "d2e23c75-ca9b-4ff5-ae74-86e9855f8ee2", + "text": "what are the risk factors of Migraine?", + "answers": [ + { + "answer_start": 800, + "text": "genetic factors" + }, + { + "answer_start": 955, + "text": "The genetic component" + }, + { + "answer_start": 1627, + "text": "genetic pattern" + } + ] + } + ] +} \ No newline at end of file diff --git a/fea9fc79-a650-4add-bdea-881d28e01e0b.json b/fea9fc79-a650-4add-bdea-881d28e01e0b.json new file mode 100644 index 0000000000000000000000000000000000000000..f2e711412ed5d92bbaa3b93d939200ddfe78d070 --- /dev/null +++ b/fea9fc79-a650-4add-bdea-881d28e01e0b.json @@ -0,0 +1,39 @@ +{ + "id": "fea9fc79-a650-4add-bdea-881d28e01e0b", + "disease": { + "id": "H00038", + "names": [ + "Melanoma" + ], + "dbLinks": { + "icd10": [ + "C43" + ], + "mesh": [ + "D008545" + ] + }, + "category": "Cancer", + "description": "Melanoma is a form of skin cancer that has a poor prognosis and which is on the rise in Western populations. Melanoma arises from the malignant transformation of pigment-producing cells, melanocytes. The only known environmental risk factor is exposure to ultraviolet (UV) light and in people with fair skin the risk is greatly increased. Melanoma pathogenesis is also driven by genetic factors. Oncogenic NRAS mutations activate both effector pathways Raf-MEK-ERK and PI3K-Akt. The Raf-MEK-ERK pathway may also be activated via mutations in the BRAF gene. The PI3K-Akt pathway may be activated through loss or mutation of the inhibitory tumor suppressor gene PTEN. These mutations arise early during melanoma pathogenesis and are preserved throughout tumor progression. Melanoma development has been shown to be strongly associated with inactivation of the p16INK4a/cyclin dependent kinases 4 and 6/retinoblastoma protein (p16INK4a/CDK4,6/pRb) and p14ARF/human double minute 2/p53 (p14ARF/HMD2/p53) tumor suppressor pathways. MITF and TP53 are implicated in further melanoma progression." + }, + "article": { + "id": "24710960", + "text": "IMPORTANCE:\nThe RAS/RAF/mitogen-activated protein kinase and extracellular signal-regulated kinase (ERK) kinase/ERK cascade plays a crucial role in melanoma cell proliferation and survival. Sildenafil citrate (Viagra) is a phosphodiesterase (PDE) 5A inhibitor commonly used for erectile dysfunction. Recent studies have shown that BRAF activation down-regulates PDE5A levels, and low PDE5A expression by BRAF activation or sildenafil use increases the invasiveness of melanoma cells, which raises the possible adverse effect of sildenafil use on melanoma risk.\n\nOBJECTIVE:\nTo evaluate the association between sildenafil use and risk of incident melanoma among men in the United States.\n\nDESIGN, SETTING, AND PARTICIPANTS:\nOur study is a prospective cohort study. In 2000, participants in the Health Professionals' Follow-up Study were questioned regarding sildenafil use for erectile dysfunction. Participants who reported cancers at baseline were excluded. A total of 25,848 men remained in the analysis.\n\nMAIN OUTCOMES AND MEASURES:\nThe incidence of skin cancers, including melanoma, squamous cell carcinoma (SCC), and basal cell carcinoma (BCC), was obtained in the self-reported questionnaires biennially. The diagnosis of melanoma and SCC was pathologically confirmed.\n\nRESULTS:\nWe identified 142 melanoma, 580 SCC, and 3030 BCC cases during follow-up (2000-2010). Recent sildenafil use at baseline was significantly associated with an increased risk of subsequent melanoma with a multivariate-adjusted hazard ratio (HR) of 1.84 (95% CI, 1.04-3.22). In contrast, we did not observe an increase in risk of SCC (HR, 0.84; 95% CI, 0.59-1.20) or BCC (1.08; 0.93-1.25) associated with sildenafil use. Moreover, erectile function itself was not associated with an altered risk of melanoma. Ever use of sildenafil was also associated with a higher risk of melanoma (HR, 1.92; 95% CI, 1.14-3.22). A secondary analysis excluding those reporting major chronic diseases at baseline did not appreciably change the findings; the HR of melanoma was 2.24 (95% CI, 1.05-4.78) for sildenafil use at baseline and 2.77 (1.32-5.85) for ever use.\n\nCONCLUSIONS AND RELEVANCE:\nSildenafil use may be associated with an increased risk of developing melanoma. Although this study is insufficient to alter clinical recommendations, we support a need for continued investigation of this association." + }, + "questions": [ + { + "id": "0cbee860-f519-460e-8114-0ff6a30d8844", + "text": "What are the risk factors of Melanoma?", + "answers": [ + { + "answer_start": 1789, + "text": "Ever use of sildenafil" + }, + { + "answer_start": 2159, + "text": "Sildenafil use" + } + ] + } + ] +} \ No newline at end of file diff --git a/ff2b0ce4-5a59-4756-9de2-bb05590a5379.json b/ff2b0ce4-5a59-4756-9de2-bb05590a5379.json new file mode 100644 index 0000000000000000000000000000000000000000..b4cf812452973fdfd38fc2c06f13fa4af8a7f124 --- /dev/null +++ b/ff2b0ce4-5a59-4756-9de2-bb05590a5379.json @@ -0,0 +1,38 @@ +{ + "id": "ff2b0ce4-5a59-4756-9de2-bb05590a5379", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "21673296", + "text": "CONTEXT:\nProlonged television (TV) viewing is the most prevalent and pervasive sedentary behavior in industrialized countries and has been associated with morbidity and mortality. However, a systematic and quantitative assessment of published studies is not available.\n\nOBJECTIVE:\nTo perform a meta-analysis of all prospective cohort studies to determine the association between TV viewing and risk of type 2 diabetes, fatal or nonfatal cardiovascular disease, and all-cause mortality.\n\nDATA SOURCES AND STUDY SELECTION:\nRelevant studies were identified by searches of the MEDLINE database from 1970 to March 2011 and the EMBASE database from 1974 to March 2011 without restrictions and by reviewing reference lists from retrieved articles. Cohort studies that reported relative risk estimates with 95% confidence intervals (CIs) for the associations of interest were included.\n\nDATA EXTRACTION:\nData were extracted independently by each author and summary estimates of association were obtained using a random-effects model.\n\nDATA SYNTHESIS:\nOf the 8 studies included, 4 reported results on type 2 diabetes (175,938 individuals; 6428 incident cases during 1.1 million person-years of follow-up), 4 reported on fatal or nonfatal cardiovascular disease (34,253 individuals; 1052 incident cases), and 3 reported on all-cause mortality (26,509 individuals; 1879 deaths during 202,353 person-years of follow-up). The pooled relative risks per 2 hours of TV viewing per day were 1.20 (95% CI, 1.14-1.27) for type 2 diabetes, 1.15 (95% CI, 1.06-1.23) for fatal or nonfatal cardiovascular disease, and 1.13 (95% CI, 1.07-1.18) for all-cause mortality. While the associations between time spent viewing TV and risk of type 2 diabetes and cardiovascular disease were linear, the risk of all-cause mortality appeared to increase with TV viewing duration of greater than 3 hours per day. The estimated absolute risk differences per every 2 hours of TV viewing per day were 176 cases of type 2 diabetes per 100,000 individuals per year, 38 cases of fatal cardiovascular disease per 100,000 individuals per year, and 104 deaths for all-cause mortality per 100,000 individuals per year.\n\nCONCLUSION:\nProlonged TV viewing was associated with increased risk of type 2 diabetes, cardiovascular disease, and all-cause mortality." + }, + "questions": [ + { + "id": "f7c03a5a-dd0e-4b42-adca-712134d9a5cc", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 2186, + "text": "Prolonged TV viewing" + }, + { + "answer_start": 1439, + "text": "2 hours of TV viewing per day" + } + ] + } + ] +} \ No newline at end of file diff --git a/ff873bd5-cb2c-42a7-8165-0a1f506af268.json b/ff873bd5-cb2c-42a7-8165-0a1f506af268.json new file mode 100644 index 0000000000000000000000000000000000000000..ea011237195b9575555a396e4e12930b75bfeebc --- /dev/null +++ b/ff873bd5-cb2c-42a7-8165-0a1f506af268.json @@ -0,0 +1,42 @@ +{ + "id": "ff873bd5-cb2c-42a7-8165-0a1f506af268", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "11874924", + "text": "OBJECTIVE:\nTo examine dietary fat and meat intake in relation to risk of type 2 diabetes.\n\nRESEARCH DESIGN AND METHODS:\nWe prospectively followed 42,504 male participants of the Health Professionals Follow-Up Study who were aged 40-75 years and free of diagnosed diabetes, cardiovascular disease, and cancer in 1986. Diet was assessed by a validated food frequency questionnaire and updated in 1990 and 1994. During 12 years of follow-up, we ascertained 1,321 incident cases of type 2 diabetes.\n\nRESULTS:\nIntakes of total fat (multivariate RR for extreme quintiles 1.27, CI 1.04-1.55, P for trend=0.02) and saturated fat (1.34, 1.09-1.66, P for trend=0.01) were associated with a higher risk of type 2 diabetes. However, these associations disappeared after additional adjustment for BMI (total fat RR 0.97, CI 0.79-1.18; saturated fat 0.97, 0.79-1.20). Intakes of oleic acid, trans-fat, long-chain n-3 fat, and alpha-linolenic acid were not associated with diabetes risk after multivariate adjustment. Linoleic acid was associated with a lower risk of type 2 diabetes in men \u003c65 years of age (RR 0.74, CI 0.60-0.92, P for trend=0.01) and in men with a BMI \u003c25 kg/m(2) (0.53, 0.33-0.85, P for trend=0.006) but not in older and obese men. Frequent consumption of processed meat was associated with a higher risk for type 2 diabetes (RR 1.46, CI 1.14-1.86 for \u003e or = 5/week vs. \u003c1/month, P for trend \u003c0.0001).\n\nCONCLUSIONS:\nTotal and saturated fat intake were associated with a higher risk of type 2 diabetes, but these associations were not independent of BMI. Frequent consumption of processed meats may increase risk of type 2 diabetes." + }, + "questions": [ + { + "id": "6bcad287-93d2-4a9d-b931-14350a44b11d", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 505, + "text": "Intakes of total fat" + }, + { + "answer_start": 607, + "text": "saturated fat" + }, + { + "answer_start": 1422, + "text": "Total and saturated fat intake" + } + ] + } + ] +} \ No newline at end of file diff --git a/ff8acf28-2b08-4f71-bb3b-e55a16cfa2b0.json b/ff8acf28-2b08-4f71-bb3b-e55a16cfa2b0.json new file mode 100644 index 0000000000000000000000000000000000000000..b842598fcdc1608bd7345bdce48ce40176c5138b --- /dev/null +++ b/ff8acf28-2b08-4f71-bb3b-e55a16cfa2b0.json @@ -0,0 +1,35 @@ +{ + "id": "ff8acf28-2b08-4f71-bb3b-e55a16cfa2b0", + "disease": { + "id": "H00079", + "names": [ + "Asthma" + ], + "dbLinks": { + "icd10": [ + "J45" + ], + "mesh": [ + "D001249" + ] + }, + "category": "Immune system disease", + "description": "Asthma is a complex syndrome with many clinical phenotypes in both adults and children. Its major characteristics include a variable degree of airflow obstruction, bronchial hyperresponsiveness, and airway inflammation. Inhaled allergens encounter antigen presenting cells (APC) that line the airway. Upon recognition of the antigen and activation by APC, naive T cells differentiate into TH2 cells. Activated TH2 stimulate the formation of IgE by B cells. IgE molecules bind to IgE receptors located on mast cells. The crosslinking of mast-cell-bound IgE by allergens leads to the release of biologically active mediators (histamine, leukotrienes) by means of degranulation and, so, to the immediate symptoms of allergy. Mast cells also release chemotactic factors that contribute to the recruitment of inflammatory cells, particularly eosinophils, whose proliferation and differentiation from bone marrow progenitors is promoted by IL-5. The activation of eosinophils leads to release of toxic granules and oxygen free radicals that lead to tissue damage and promote the development of chronic inflammation." + }, + "article": { + "id": "17575100", + "text": "RATIONALE:\nAlthough it is widely assumed that the incidence of childhood respiratory allergies to common aeroallergens is directly related to allergen exposure in early life, few longitudinal studies have investigated this issue, and available data are scarce and mainly limited to high-risk groups.\n\nOBJECTIVES:\nTo assess, in a prospective manner and in a general population, the role of early life exposures to Der p1 and Fel d1 on the inception of sensitization and asthma.\n\nMETHODS:\nPregnant women and their children were recruited for the Asthma Multicentre Infant Cohort Study. Overall, 1,611 newborns were initially enrolled in three cohorts in the United Kingdom and Spain. Der p1 and Fel d1 allergens were measured in household dust samples at 3 months of age for 1,474 (91.5%) participants, and skin prick tests were performed at 6 years of age on 1,182 (80.2%) participants. Wheeze and diagnosed asthma were reported in yearly questionnaires.\n\nMEASUREMENTS AND MAIN RESULTS:\nExposure to Der p1 early in life was not related to a positive specific prick test or to asthma or persistent wheeze at 6 years of age. Fel d1 showed an association with all these outcomes (third vs. first tertile; odds ratio, 4.43 for positive specific prick test and 2.6 for diagnosed asthma).\n\nCONCLUSIONS:\nDose-response relationships between allergen exposure and sensitization or asthma may be allergen specific and nonlinear; a minimum threshold level is needed to induce sensitization, but no dose-response relationship exists above this level. The effect of a particular allergen seems to be similar on atopy and asthma inception." + }, + "questions": [ + { + "id": "910e9c7a-0794-4a1d-9743-7acaa3025ecb", + "text": "What are the risk factors of Asthma?", + "answers": [ + { + "answer_start": 1122, + "text": "Fel d1" + } + ] + } + ] +} \ No newline at end of file diff --git a/ffcc0790-1ea0-4700-b5a4-0a2041329e0c.json b/ffcc0790-1ea0-4700-b5a4-0a2041329e0c.json new file mode 100644 index 0000000000000000000000000000000000000000..64a6dbd9bf05ab9c59a12dad483fc2f001825203 --- /dev/null +++ b/ffcc0790-1ea0-4700-b5a4-0a2041329e0c.json @@ -0,0 +1,37 @@ +{ + "id": "ffcc0790-1ea0-4700-b5a4-0a2041329e0c", + "disease": { + "id": "H00020", + "names": [ + "Colorectal cancer" + ], + "dbLinks": { + "icd10": [ + "C18", + "C19", + "C20" + ], + "mesh": [ + "D015179" + ] + }, + "category": "Cancer", + "description": "Colorectal cancer (CRC) is the second largest cause of cancer-related deaths in Western countries. CRC arises from the colorectal epithelium as a result of the accumulation of genetic alterations in defined oncogenes and tumour suppressor genes (TSG). Two major mechanisms of genomic instability have been identified in sporadic CRC progression. The first, known as chromosomal instability (CIN), results from a series of genetic changes that involve the activation of oncogenes such as K-ras and inactivation of TSG such as p53, DCC/Smad4, and APC. The second, known as microsatellite instability (MSI), results from inactivation of the DNA mismatch repair genes MLH1 and/or MSH2 by hypermethylation of their promoter, and secondary mutation of genes with coding microsatellites, such as transforming growth factor receptor II (TGF-RII) and BAX. Hereditary syndromes have germline mutations in specific genes (mutation in the tumour suppressor gene APC on chromosome 5q in FAP, mutated DNA mismatch repair genes in HNPCC)." + }, + "article": { + "id": "20661287", + "text": "BACKGROUND:\nPatients with multiple serrated polyps are at an increased risk for developing colorectal cancer (CRC). Recent reports have linked cigarette smoking with the subset of CRC that develops from serrated polyps. The aim of this work therefore was to investigate the association between smoking and the risk of CRC in high-risk genetics clinic patients presenting with multiple serrated polyps.\n\nMETHODS AND FINDINGS:\nWe identified 151 Caucasian individuals with multiple serrated polyps including at least 5 outside the rectum, and classified patients into non-smokers, current or former smokers at the time of initial diagnosis of polyposis. Cases were individuals with multiple serrated polyps who presented with CRC. Controls were individuals with multiple serrated polyps and no CRC. Multivariate logistic regression was performed to estimate associations between smoking and CRC with adjustment for age at first presentation, sex and co-existing traditional adenomas, a feature that has been consistently linked with CRC risk in patients with multiple serrated polyps. CRC was present in 56 (37%) individuals at presentation. Patients with at least one adenoma were 4 times more likely to present with CRC compared with patients without adenomas (OR = 4.09; 95%CI 1.27 to 13.14; P = 0.02). For females, the odds of CRC decreased by 90% in current smokers as compared to never smokers (OR = 0.10; 95%CI 0.02 to 0.47; P = 0.004) after adjusting for age and adenomas. For males, there was no relationship between current smoking and CRC. There was no statistical evidence of an association between former smoking and CRC for both sexes.\n\nCONCLUSION:\nA decreased odds for CRC was identified in females with multiple serrated polyps who currently smoke, independent of age and the presence of a traditional adenoma. Investigations into the biological basis for these observations could lead to non-smoking-related therapies being developed to decrease the risk of CRC and colectomy in these patients." + }, + "questions": [ + { + "id": "0de6b85a-b98a-438b-9d8a-2fab7c73e53c", + "text": "What are the risk factors of Colorectal Cancer?", + "answers": [ + { + "answer_start": 1139, + "text": "Patients with at least one adenoma" + } + ] + } + ] +} \ No newline at end of file diff --git a/ffd1692b-afef-486f-ad86-113aea6b6af0.json b/ffd1692b-afef-486f-ad86-113aea6b6af0.json new file mode 100644 index 0000000000000000000000000000000000000000..ca2a2dbc37ea0c726414856b4b0ef2dd71fc013d --- /dev/null +++ b/ffd1692b-afef-486f-ad86-113aea6b6af0.json @@ -0,0 +1,36 @@ +{ + "id": "ffd1692b-afef-486f-ad86-113aea6b6af0", + "disease": { + "id": "H01714", + "names": [ + "Chronic obstructive pulmonary disease (COPD)", + "Emphysema" + ], + "dbLinks": { + "icd10": [ + "J43", + "J44" + ], + "mesh": [ + "D029424" + ] + }, + "category": "Lung disease" + }, + "article": { + "id": "25101718", + "text": "Pulmonary hypertension is associated with advanced chronic obstructive pulmonary disease (COPD), although pulmonary vascular changes occur early in the course of the disease. Pulmonary artery (PA) enlargement (PAE) measured by computed tomography correlates with pulmonary hypertension and COPD exacerbation frequency. Genome-wide association studies of PAE in subjects with COPD have not been reported. To investigate whether genetic variants are associated with PAE within subjects with COPD, we investigated data from current and former smokers from the COPDGene Study and the Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints study. The ratio of the diameter of the PA to the diameter of the aorta (A) was measured using computed tomography. PAE was defined as PA/A greater than 1. A genome-wide association study for COPD with PAE was performed using subjects with COPD without PAE (PA/A ≤ 1) as a control group. A secondary analysis used smokers with normal spirometry as a control group. Genotyping was performed on Illumina platforms. The results were summarized using fixed-effect meta-analysis. Both meta-analyses revealed a genome-wide significant locus on chromosome 15q25.1 in IREB2 (COPD with versus without PAE, rs7181486; odds ratio [OR] = 1.32; P = 2.10 × 10(-8); versus smoking control subjects, rs2009746; OR = 1.42; P = 1.32 × 10(-9)). PAE was also associated with a region on 14q31.3 near the GALC gene (rs7140285; OR = 1.55; P = 3.75 × 10(-8)). Genetic variants near IREB2 and GALC likely contribute to genetic susceptibility to PAE associated with COPD. This study provides evidence for genetic heterogeneity associated with a clinically important COPD vascular subtype." + }, + "questions": [ + { + "id": "28f25b38-5cec-4d9d-93bd-79f1eba96c64", + "text": "What are the risk factors for Chronic obstructive pulmonary disease (COPD)?", + "answers": [ + { + "answer_start": 1162, + "text": "genome-wide significant locus on chromosome 15q25.1 in IREB2" + } + ] + } + ] +} \ No newline at end of file diff --git a/fffb53ed-9cc6-4bb7-be8e-1930fae6a651.json b/fffb53ed-9cc6-4bb7-be8e-1930fae6a651.json new file mode 100644 index 0000000000000000000000000000000000000000..4b745a995dc0300b8df1a75c6ae3465188358027 --- /dev/null +++ b/fffb53ed-9cc6-4bb7-be8e-1930fae6a651.json @@ -0,0 +1,42 @@ +{ + "id": "fffb53ed-9cc6-4bb7-be8e-1930fae6a651", + "disease": { + "id": "H00409", + "names": [ + "Type 2 diabetes mellitus" + ], + "dbLinks": { + "icd10": [ + "E11" + ], + "mesh": [ + "D003924" + ] + }, + "category": "Metabolic disease; Endocrine disease" + }, + "article": { + "id": "24081730", + "text": "CONTEXT:\nPolycystic ovary syndrome (PCOS) affects 6%-21% of women. PCOS has been associated with an increased risk of dysglycemia including gestational diabetes mellitus (GDM) and type 2 diabetes mellitus (T2DM).\n\nOBJECTIVE:\nThe objective of the study was to assess the prevalence of dysglycemia and the impact of obesity in young reproductive-aged women with and without PCOS in a community-based cohort.\n\nDESIGN:\nThis was a cross-sectional analysis of data from a large longitudinal study (the Australian Longitudinal Study on Women's Health).\n\nSETTING:\nThe setting for the study was the general community.\n\nPARTICIPANTS:\nWomen were randomly selected from the national health insurance database. Standardized data collection occurred at five survey time points (years 1996, 2000, 2003, 2006, and 2009). Data from survey 4 (2006, n = 9145, 62% of original cohort aged 18-23 y) were examined for this study.\n\nMAIN OUTCOME MEASURES:\nSelf-reported PCOS, GDM, and T2DM were measured.\n\nRESULTS:\nIn women aged 28-33 years, PCOS prevalence was 5.8% [95% confidence interval (CI) 5.3%-6.4%]. The prevalence of GDM (in women reporting prior pregnancy) and T2DM was 11.2% and 5.1% in women with PCOS and 3.8% and 0.3% in women without PCOS, respectively (P for both \u003c .001). PCOS was associated with an increased odds of GDM and T2DM. After adjusting for age, body mass index, hypertension, smoking, and demographic factors, the odds of GDM (odds ratio 2.1, 95% CI 1.1-3.9, P = .02) and T2DM (odds ratio 8.8, 95% CI 3.9-20.1, P \u003c .001) remained increased in women reporting PCOS.\n\nCONCLUSIONS:\nIn a large community-based cohort of reproductive-aged women, PCOS was independently associated with a higher risk of GDM and T2DM, independent of body mass index. Aggressive screening, prevention, and management of dysglycemia is clearly warranted in women with PCOS." + }, + "questions": [ + { + "id": "83aa08f3-dba0-4211-a76f-a980d2f0c70c", + "text": "what are the risk factors of Type 2 diabetes mellitus?", + "answers": [ + { + "answer_start": 1647, + "text": "PCOS" + }, + { + "answer_start": 9, + "text": "Polycystic ovary syndrome (PCOS)" + }, + { + "answer_start": 1175, + "text": "women with PCOS" + } + ] + } + ] +} \ No newline at end of file