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[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe have preliminarily reported MTA2 expression in gastric cancer and its biological functions by using knockdown cell models, while the molecular mechanisms of MTA2 in regulating malignant behaviors are still unclear. MTA2 overexpression models were established by transfection assay in gastric cancer cells BGC-823 and MKN28. Cell proliferation assay, colony formation in soft agar, wound-healing assay and transwell migration assay were performed with MTA2 overexpression and negative control (NC) cells. Subcutaneous xenografts and pulmonary metastasis models by BGC-823/MTA2 and BGC-823/NC cells were used to observe the capacity of growth and metastasis in vivo. Differential gene expression in MTA2 knockdown and overexpression cells was analyzed by microarrays. IL-11, which demonstrated as differential expression in microarray, was detected by real-time PCR, western blot, ELISA and immunohistochemistry staining. Recombinant human IL-11 (rhIL-11) was administrated in cell proliferation and colony formation as rescue assay. The numbers of colonies in soft agar were significantly more in BGC-823/MTA2 and MKN28/MTA2 cells, comparing with those in their NC cells. Capabilities of cell proliferation, wound-healing and cell migration were not significantly changed in MTA2 overexpression cells. The sizes of subcutaneous xenografts and pulmonary metastases of BGC-832/MTA2 cells were significantly larger than those in BGC-823/NC group. Differential expression of IL-11 was identified by genome expression microarray both in MTA2 knockdown and overexpression cells. IL-11 expression was elevated in BGC-823/MTA2 cells, whereas reduced in SGC-7901/shMTA2 cells. Administration of rhIL-11 recovered colony formation capacity of SGC-7901/shMTA2 cells.\n\nQuestion:\nDoes mTA2 enhance colony formation and tumor growth of gastric cancer cells through IL-11?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo determine the prevalence and psychosocial correlates of ADHD among adolescents in Jos, Nigeria. A cross-sectional descriptive two-stage study of 487 randomly selected participants using Kiddie-Schedule for Affective Disorders and Schizophrenia-Present and Lifetime Version (K-SADS-PL), Raven's Standard Progressive Matrix (SPM) and the Children's Global Assessment Score (CGAS). The prevalence of ADHD was 8.8%. The subtypes found were inattentive (3.08%), hyperactive-impulsive (2.05%), and combined (3.08%); male:female ratio of 1.4:1. ADHD was significantly associated with use of substance by father (odds ratio [OR] = 0.35; 95% confidence interval [CI] = [0.154, 0.781]), use of substance by mother (OR = 0.2; 95% CI = [0.055, 0.711]), and lower education of mother (OR = 0.3 95% CI = [0.116, 0.693]). Poor quality of handwriting (χ\n\nQuestion:\nDoes prevalence and correlate of ADHD Among Adolescent Students in Nigeria?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nVery little is known about how compression bandages lose interface pressure. We hypothesized that the loss of interface pressure is correlated with the slippage of the bandages, and studied the interface pressure and slippage of three bandages over 8 hours. Twenty-Seven legs from 27 healthy volunteers were bandaged with short stretch bandages (SS), cohesive short stretch bandages (CS), and long stretch bandages (LS). Pressure sensors were placed above the ankle (B1), below the knee (D), and mid thigh (F). Interface pressures in a sitting position were recorded at the beginning, and 4 and 8 hours later. In 17 legs, the pressure sensor sites were marked, and their heights were measured on standing upright. SS and CS lost interface pressure quickly, but LS maintained pressure better than SS and CS at all sites. There was no pressure difference between SS and CS at the lower leg. However, CS maintained pressure better than SS at the mid thigh (44.6% vs. 54.4% pressure loss at 8 hours, respectively. P=0.037). There was a tendency toward less slippage with CS than SS at the mid thigh. In CS and LS, there was a linear correlation between the slippage of bandages and the interface pressure at the mid thigh (P <.01, in both).\n\nQuestion:\nIs interface pressure affected by slippage of bandages at thigh?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nRisk factors for intravenous immunoglobulin-induced renal failure (IVIg-RF) were suspected from case series studies. This study was aimed at quantifying the risk of IVIg-RF associated with exposure to drugs that modify intrarenal hemodynamics. We conducted a case-control study in the French Pharmacovigilance Database (FPVD). Adult IVIg-RF cases registered in the FPVD from 1996 to 2009 were reviewed. Controls were patients included in the FPVD for another IVIg adverse effect. Controls were matched for sucrose content of the preparation, year of adverse event and age. The predictors of IVIg-RF were exposure to angiotensin-converting enzyme inhibitors (ACE-I), angiotensin receptor antagonists (ARA), diuretics, age, gender and weight, IVIg delivered dose and infusion duration, chronic kidney disease, hypertension and diabetes mellitus. Acute IVIg-RF was defined as a calculated creatinine clearance less than 60 mL/min and, in the event of chronic kidney disease, (i) a more than 50% increase of serum creatinine, (ii) an indication of oligo-anuria or (iii) a requirement for dialysis. We selected 71 cases and 71 controls. Forty-nine percent of the cases required transient hemodialysis. In the final multivariate model, exposure to ACE-I and/or ARA was the sole independent predictor associated with IVIg-RF (OR = 7.9, 95%CI = 1.3-49.2). There was an interaction between 'diabetes mellitus' (OR = 7.7, 95%CI = 2.3-25.5) and 'chronic kidney disease' (OR = 13.0, 95%CI = 3.1-54.7), both being strong risk factors in univariate models (p < 0.001). Chronic hypertension was a risk factor for hemodialysis.\n\nQuestion:\nIs exposure to inhibitors of the renin-angiotensin system a major independent risk factor for acute renal failure induced by sucrose-containing intravenous immunoglobulins : a case-control study?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAlthough combination antiretroviral therapy (cART) dramatically reduces rates of AIDS and death, a minority of patients experience clinical disease progression during treatment. To investigate whether detection of CXCR4(X4)-specific strains or quantification of X4-specific HIV-1 load predict clinical outcome. From the Swiss HIV Cohort Study, 96 participants who initiated cART yet subsequently progressed to AIDS or death were compared with 84 contemporaneous, treated nonprogressors. A sensitive heteroduplex tracking assay was developed to quantify plasma X4 and CCR5 variants and resolve HIV-1 load into coreceptor-specific components. Measurements were analyzed as cofactors of progression in multivariable Cox models adjusted for concurrent CD4 cell count and total viral load, applying inverse probability weights to adjust for sampling bias. Patients with X4 variants at baseline displayed reduced CD4 cell responses compared with those without X4 strains (40 versus 82 cells/microl; P = 0.012). The adjusted multivariable hazard ratio (HR) for clinical progression was 4.8 [95% confidence interval (CI) 2.3-10.0] for those demonstrating X4 strains at baseline. The X4-specific HIV-1 load was a similarly independent predictor, with HR values of 3.7 (95% CI, 1.2-11.3) and 5.9 (95% CI, 2.2-15.0) for baseline loads of 2.2-4.3 and > 4.3 log10 copies/ml, respectively, compared with < 2.2 log10 copies/ml.\n\nQuestion:\nDo hIV-1 coreceptor usage and CXCR4-specific viral load predict clinical disease progression during combination antiretroviral therapy?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nSoutheast China is one of the sites of influenza origin. During 2003--2004, nine avian influenza outbreaks took place in Guangdong Province. But no human case was reported. To examine the status of potential human infection by human influenza (H1N1, H3N2) and avian influenza (H5N1, H7N7, H9N2) in the avian influenza epidemic area of Guangdong Province, China, we conducted a seroepidemiologic survey in the people of this area from April to June of 2004. Three out of 9 H5N1 avian influenza affected poultry areas in Guangdong were randomly selected, and the population living within 3 kilometers of the affected poultries were chosen as the survey subjects. One thousand two hundred and fourteen people were selected from 3 villages at random. Human and avian influenza antibody titers were determined by hemagglutination-inhibition (HI) test and microneutralization test (MNT). The positive rate of antibody to H5N1 was 3.03% in the occupational exposure group and 2.34% in general citizens group; that of H9N2 was 9.52% in the occupational exposure group and 3.76% in the general citizens group. Moreover one case in the occupational exposure group was positive for H7N7. One year later, all previously positive cases had become negative except for one H5N1-positive case.\n\nQuestion:\nDo potential infections of H5N1 and H9N2 avian influenza do exist in Guangdong populations of China?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nGastric cancer (GC) is an aggressive malignancy whose mechanisms of development and progression are poorly understood. The identification of prognosis-related genomic loci and genes may suffer from the relatively small case numbers and a lack of systematic validation in previous studies. Array-based comparative genomic hybridization (aCGH) coupled with patient clinical information was applied to identify prognosis-related loci and genes with high-frequency recurrent gains in 129 GC patients. The candidate loci and genes were then validated using an independent cohort of 384 patients through branched DNA signal amplification analysis (QuantiGene assays). In the 129 patients, a copy number gain of three chromosome regions-namely, 8q22 (including ESRP1 and CCNE2), 8q24 (including MYC and TNFRSF11B), and 20q11-q13 (including SRC, MMP9, and CSE1L)--conferred poor survival for patients. In addition, the correlation between the branched DNA signal amplification analysis results and the aCGH results was analyzed in 73 of these 129 patients, and MYC, TNFRSF11B, ESRP1, CSE1L, and MMP9 were found to be well correlated. Further validation using an independent cohort (n = 384) verified that only MYC and TNFRSF11B within 8q24 are related to survival. Patients with gains in both MYC and TNFRSF11B had poorer survival than those with no gains, particularly those with noncardia GC. Gains in both of these genes were also a significant independent prognostic indicator.\n\nQuestion:\nIs recurrent amplification of MYC and TNFRSF11B in 8q24 associated with poor survival in patients with gastric cancer?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIgE-mediated cross-linking of FcεRI results in the release of mediators stored in basophil granules, such as histamine and proteases, and in the de novo synthesis of sulfidoleukotrienes. In this study, we investigated the role of the histamine receptors, in particular that of the histamine H4 receptor (H4R), in modulating human basophil function. The mRNA expression of the histamine receptors was measured by real-time PCR. Migration of basophils was assessed using the modified Boyden chamber technique. The expression levels of CD63 and CD203c on the cell surface and the sulfidoleukotriene release were determined by flow cytometry and ELISA, respectively. We could show that highly purified basophils express the H1R, H2R, and H4R but not the H3R mRNA. Human basophils expressed higher H4R mRNA levels as compared to the expression levels of the H1R (P < 0.01). Histamine and the H4R agonist ST-1006 initiated active migration of basophils (P < 0.001). A significant reduction in FcεRI cross-linking-mediated surface expression of CD63 and CD203c was observed on basophils after pre-incubation with histamine or the specific H4R agonist ST-1006 (P < 0.01). The synthesis and release of sulfidoleukotrienes from basophils after activation with different stimuli, by FcεRI cross-linking or by stimulation with hymenoptera venom allergens, were significantly reduced by histamine or the H4R agonist ST-1006 (P < 0.05-0.001).\n\nQuestion:\nAre human basophil chemotaxis and activation regulated via the histamine H4 receptor?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThere is increasing interest in and physician support for the use of single-item screeners for problem drinking. In a representative sample of U.S. adults (n = 43,093) and within selected subgroups, past-year frequency of drinking 5+/4+ drinks and maximum drinks consumed on any day were evaluated as screeners for past-year alcohol dependence, any alcohol use disorder (AUD), and any AUD or hazardous drinking, using standard measures of screening performance. AUDs were defined according to DSM-IV criteria. Hazardous drinking was defined as consuming >14 drinks/wk or 5+ drinks on any day for men and >7 drinks/wk or 4+ drinks on any day for women. Optimal cutpoints for both screeners varied across population subgroups, and these variations should be taken into account in order to maximize screening performance. At the optimal cutpoints for the total population, the sensitivity and specificity of maximum drinks were 89% and 82% for dependence at > or =5 drinks, 90% and 79% for any AUD at > or =4 drinks, and 90% and 96% for any AUD or hazardous drinking at > or =4 drinks. Comparable values of sensitivity and specificity for 5+/4+ frequency were 90% and 83% at > or =3 times a year, 87% and 82% at > or =once a year, and 88% and 100% at > or =once a year, respectively. Specificity was lower when only past-year drinkers were considered. The 5+/4+ frequency screener yielded fairly low sensitivity in predicting alcohol problems among the elderly and among Blacks. Results supported a past-year reference period for frequency of 5+/4+ drinks and substantiated gender- and age-specific thresholds for defining risk drinking.\n\nQuestion:\nDo a comparison of two single-item screeners for hazardous drinking and alcohol use disorder?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nLong-term ethanol consumption is known to impair the ability of the liver to regenerate, but the molecular mechanisms are poorly understood. Multiple growth factors promote hepatocyte proliferation, some of which involve the insulin receptor substrate 1 (IRS-1)-mediated signal transduction pathway. To explore effects of ethanol on the IRS-1 signal liver growth in vivo, studies in transgenic mice overexpressing IRS-1 in the liver were performed because these mice show constitutive activation of the downstream signal transduction pathways leading to enhanced hepatocyte proliferation. Tyrosyl phosphorylation of IRS-1 and subsequent protein-protein interactions were examined in liver lysates from animals fed ethanol or control diet. Activity of phosphatidylinositol-3 kinase (PI3K) and mitogen-activated protein kinase (MAPK) was assessed by specific enzymatic assays. Hepatocyte proliferation was measured by incorporation of [3H]thymidine into liver DNA. Tyrosyl phosphorylation of IRS-1, association of IRS-1 with PI3K, and activation of downstream PI3K and MAPK pathways were greatly reduced as a result of long-term ethanol consumption. Ethanol virtually abolished the enhanced hepatocyte DNA synthesis induced by expression of the IRS-1 transgene.\n\nQuestion:\nDoes ethanol inhibit hepatocyte proliferation in insulin receptor substrate 1 transgenic mice?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe 6-minute walk test (6MWT) is commonly used to measure the functional exercise capacity in chronic patients with cardiovascular diseases. The purpose of this study was to determine whether the 6MWT is associated with the global assessment of functioning (GAF) score in patients with schizophrenia. A total of 68 male and 25 female in-patients with schizophrenia (34.6 ± 9.7 years; body mass index = 24.9 ± 4.4) performed a 6MWT and were assessed with the GAF scale and the Psychosis Evaluation tool for Common use by Caregivers (PECC). The mean distance walked on the 6MWT was 587.3 ± 98.4 m, while the mean GAF score was 52.0 ± 10.4. The Pearson's correlation coefficient between the 6MWT and the GAF score was 0.59 (P < 0.001), indicating a moderate association between both measures. The 6MWT was also significantly related to negative (r = -0.45, P < 0.001), depressive (r = -0.48, P < 0.001) and cognitive (r=, P) symptoms and with body mass index (r = -0.31, P < 0.005), smoking behaviour (r = -0.36, P < 0.001)) and dose of antipsychotic medication (r = -0.38, P < 0.001).\n\nQuestion:\nIs the functional exercise capacity correlated with global functioning in patients with schizophrenia?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe dual specificity phosphatase cdc25C was the first human cdc25 family member found to be essential in the activation of cdk1/cyclin B1 that takes place at the entry into mitosis. Human cdc25C is phosphorylated on Proline-dependent SP and TP sites when it becomes active at mitosis and the prevalent model is that this phosphorylation/activation of cdc25C would be part of an amplification loop with cdk1/cyclin B1. Using highly specific antibodies directed against cdc25C phospho-epitopes, pT67 and pT130, we show here that these two phospho-forms of cdc25C represent distinct pools with differential localization during human mitosis. Phosphorylation on T67 occurs from prophase and the cdc25C-pT67 phospho-isoform closely localizes with condensed chromosomes throughout mitosis. The phospho-T130 form of cdc25C arises in late G2 and associates predominantly with centrosomes from prophase to anaphase B where it colocalizes with Plk1. As shown by immunoprecipitation of each isoform, these two phospho-forms are not simultaneously phosphorylated on the other mitotic TP sites or associated with one another. Phospho-T67 cdc25C co-precipitates with MPM2-reactive proteins while pT130-cdc25C is associated with Plk1. Interaction and colocalization of phosphoT130-cdc25C with Plk1 demonstrate in living cells, that the sequence around pT130 acts as a true Polo Box Domain (PBD) binding site as previously identified from in vitro peptide screening studies. Overexpression of non-phosphorylatable alanine mutant forms for each isoform, but not wild type cdc25C, strongly impairs mitotic progression showing the functional requirement for each site-specific phosphorylation of cdc25C at mitosis.\n\nQuestion:\nAre distinct pools of cdc25C phosphorylated on specific TP sites and differentially localized in human mitotic cells?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThis study sought to examine the effects of long-term estrogen therapy on vascular function in male to female transsexuals and to compare the findings with those observed in men and premenopausal women. Gender differences in coronary artery disease have largely been attributed to the beneficial effects of estrogen on vascular function and plasma lipids in women. However, the effects of estrogen on the male vasculature have not been widely studied. We compared the effects of estrogen on vascular function in 14 male to female transsexuals, 14 age-matched men and 15 premenopausal women. Flow-mediated vasodilation and response to nitroglycerin were assessed in the brachial artery using noninvasive ultrasound. Flow-mediated vasodilation was similar in transsexuals and women but greater than that in men ([mean +/- SE] 11.5 +/- 1.3% and 9.4 +/- 1.1% vs. 5.2 +/- 1.0% respectively, p < 0.005). Responses to nitroglycerin were also greater in transsexuals and women than in men (21.6 +/- 1.7% and 21.0 +/- 0.9% vs. 14.5 +/- 1.2%, respectively, p = 0.0005). These differences persisted even after adjusting for vessel size. Despite similar total cholesterol levels, transsexuals had high density lipoprotein cholesterol levels similar to those in women and greater than those observed in men (1.76 +/- 0.12 and 1.82 +/- 0.11 mmol/liter vs. 1.35 +/- 0.07 mmol/liter, respectively, p < 0.005). Moreover, triglyceride levels were greater in transsexuals than in men and women, and low density lipoprotein cholesterol (LDL-C) particle size was smaller (25.7 +/- 0.2 nm vs. 26.2 +/- 0.1 and 26.6 +/- 0.1 nm, respectively, p = 0.0001). Serum testosterone (an index of estrogen therapy in transsexuals) was markedly suppressed in transsexuals and similar to that in women. Univariate analysis revealed that there was a strong inverse correlation between serum testosterone and flow-mediated vasodilation (r(s) = -0.48, p < 0.005). Multivariate analysis revealed that the best combination of predictors of flow-mediated vasodilation was serum testosterone, vessel size and LDL-C (R2 = 0.3, p < 0.005).\n\nQuestion:\nDoes long-term estrogen therapy improve vascular function in male to female transsexuals?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAvoiding danger and finding food are closely related behaviours that are essential for surviving in a natural environment. Growing evidence supports an important role of gut-brain peptides in modulating energy homeostasis and emotional-affective behaviour. For instance, postprandial release of pancreatic polypeptide (PP) reduced food intake and altered stress-induced motor activity and anxiety by activating central Y4 receptors. We characterized [K(30) (PEG2)]hPP2-36 as long-acting Y4 receptor agonist and injected it peripherally into wildtype and Y4 receptor knockout (Y4KO) C57Bl/6NCrl mice to investigate the role of Y4 receptors in fear conditioning. Extinction and relapse after extinction was measured by spontaneous recovery and renewal. The Y4KO mice showed impaired cued and context fear extinction without affecting acquisition, consolidation or recall of fear. Correspondingly, peripheral injection of [K(30) (PEG2)]hPP2-36 facilitated extinction learning upon fasting, an effect that was long-lasting and generalized. Furthermore, peripherally applied [K(30) (PEG2)]hPP2-36 before extinction inhibited the activation of orexin-expressing neurons in the lateral hypothalamus in WT, but not in Y4KO mice.\n\nQuestion:\nAre pancreatic polypeptide and its central Y4 receptors essential for cued fear extinction and permanent suppression of fear?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe cardiopulmonary exercise test (CPX) is an affordable tool for risk prediction in patients with chronic heart failure (CHF). We aimed to determine the role of CPX parameters in predicting the risk of incidence of sustained ventricular arrhythmias (SVA) in CHF. Sixty-one consecutive patients with CHF enrolled in the Daunia Heart Failure Registry underwent CPX and were followed for 327 ± 247 days. Clinical follow-up was performed every month and anticipated in case of re-hospitalisation for cardiac disease. Incidence of SVA was evaluated by direct clinical examination (ECG, ambulatory ECG). Patients with episodes of SVA (N 14) showed lower values of pVO2 and PetCO2, and higher values of VE/VCO2, VE/VCO2 slope, and VE%. After correction for age, gender, diabetes, ischaemic heart disease and left ventricular ejection fraction, peak VO2 (hazard ratio (HR) 0.68, 95 % confidence interval (CI) 0.51-0.91, p < 0.05), VE% (HR 1.38, 95 % CI 1.04-1.84, p < 0.05), VE/VCO2 (HR 1.38, 95 % CI 1.04-1.82, p < 0.05), VE/VCO2 slope (HR 1.77, 95 % CI 1.31-2.39, p < 0.01), PetCO2 (HR 0.66, 95 % CI 0.50-0.88, p < 0.01) were found as predictors of SVA. At Kaplan-Meier analysis, lower event-free rates were found in subjects with peak VO2 values below median (log rank p < 0.05), values of VE/VCO2 above mean (p < 0.05), higher VE/VCO2 slope tertiles (p <0.05), and values of PetCO2 below median (p < 0.05).\n\nQuestion:\nDoes cardiopulmonary exercise test predict sustained ventricular arrhythmias in chronic heart failure?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe aim of our study is to identify the contribution of hematopoietic-derived cells to burn-wound healing in a non-severe injury. There are many conflicting reports of the contribution of bone marrow-derived cells to wound healing and whether these are hematopoietic or mesenchymal in origin. The role of hematopoietic lineage cells is investigated in this study in the context of the response to burn injury. Transgenic mice expressing the LacZ reporter gene in all cells of the hematopoietic lineage underwent a non-severe full-thickness burn injury (8 % of total body surface area). Wounds were assessed for LacZ-positive cells at days 7, 14, and 28 post-injury by using whole-mount staining. Cells were also cultured from the wounds at each time point and analysed for expression of fibroblast and myofibroblast markers. At day 7, positive cells were identified in the wounds representing the inflammatory response. Some dermal cells were also identified at this early stage. At day 14, positive cells were also identified and were cultured from the wound tissue samples. However, by day 28, no positive cells could be detected or cultured from the healed wound tissue. Isolated LacZ-positive cells did not express collagen 1 or α-smooth muscle actin proteins, indicating that they had not differentiated into dermal fibroblast-type cells.\n\nQuestion:\nAre cells from the hematopoietic lineage only present transiently during healing in a mouse model of non-severe burn injury?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo identify the subgroup of high-risk papillary thyroid microcarcinoma (PTMC) inclined to lymph node metastasis (LNM). Patients who underwent total thyroidectomy with central neck dissection and had a pathologic diagnosis of PTMC between 2003 and 2010 at Wuhan Union Hospital were identified. The frequency of LNM was retrospectively analyzed according to the clinicopathological features. For multifocal lesions, total tumor diameter (TTD) was calculated as the sum of the maximal diameter of each lesion. Last, a meta-analysis was performed with respect to multifocality and LNM in the PTMCs. The proportion of LNM was similar between multifocal PTMCs with TTD ≤ 1 cm and unifocal tumors with diameter ≤ 1 cm (37.5 vs. 30%, P = 0.463). LNM frequency was also similar between multifocal PTMCs with 1 < TTD ≤ 2 cm (TTD greater than 1 cm but less than or equal to 2 cm) and unifocal tumors with 1 < diameter ≤ 2 cm (56.8 vs. 64.9%, P = 0.330). However, LNM frequency was significantly higher in multifocal PTMCs with TTD > 1 cm than unifocal tumors with diameter ≤ 1 cm (60.4 vs. 30%, P < 0.001). A meta-analysis of nine publications plus our own data with a total 1,586 PTMCs demonstrated that multifocality was significantly associated with LNM risk (odds ratio 1.9, 95% confidence interval 1.5-2.4).\n\nQuestion:\nDo multifocality and total tumor diameter predict central neck lymph node metastases in papillary thyroid microcarcinoma?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nEarly, effective lactate clearance has been shown to be associated with improved mortality in patients with trauma, burns, and sepsis. We investigated whether early, high lactate clearance was associated with reduced mortality in post-cardiac arrest patients. We performed a retrospective analysis of post-cardiac arrest patients in an urban emergency department. Inclusion criteria included pre-hospital cardiac arrest patients over the age of 18. Exclusion criteria were traumatic arrest, successful resuscitation prior to the arrival of emergency medical services, and cardiac arrest in the presence of pre-hospital providers. Primary endpoints consisted of survival to 24h and survival to hospital discharge. A total of 79 patients were analyzed with a mean age of 64+/-17 and mean APACHE II score of 37.7+/-5. Of the 79 patients, 27 (34%) died within 24h and 66 (84%) died during the hospital course. The mean initial lactate level for the overall group was 15+/-5.2mmol/dl with a mean lactate of 14.4+/-5.1mmol/dl in the survivors and 16+/-5.3mmol/dl in the non-survivors (p>0.05). Lactate clearance at both 6 and 12h was significantly higher for both 24-h and overall in-hospital survival (p<0.05). A multivariable analysis showed that high lactate clearance at 12h was predictive of 24-h survival (p<0.05).\n\nQuestion:\nIs effective lactate clearance associated with improved outcome in post-cardiac arrest patients?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo investigate serum bone biomarkers in rats with intrauterine growth restriction (IUGR) in order to determine the effects of puerarin on bone metabolism. A rat model of IUGR was induced using a low protein diet during pregnancy. The offspring were given puerarin or an identical volume of saline via subcutaneous abdominal injection. All rats were studied at 1, 3, and 8 weeks of age. Serum biomarkers of bone formation, including insulin-like growth factor-1 (IGF-1), bone-specific alkaline phosphatase (BALP), osteocalcin (OC), osteoprotegerin (OPG), receptor-activator of nuclear factor-κB Iigand (RANKL), as well as blood levels of calcium and phosphorus were measured. Serum BALP, OPG, IGF-1, and OC levels, as well as the OPG/RANKL ratio, were lower in the IUGR group compared with the control group at 1 week of age (P = 0.024, 0.011, 0.014, 0.004, and 0.002, respectively). At 3 weeks of age, the serum BALP and OC levels were higher in the protein-restricted group compared with the control group (P = 0.003 and 0.001, respectively). A comparison between the IUGR plus puerarin intervention group and the IUGR group revealed differences in the levels of BALP and IGF-1 at 3 weeks of age (P = 0.008 and 0.003, respectively). In addition, serum OPG and OC levels and the OPG/RANKL ratio were higher at 8 weeks of age (P = 0.044, 0.007, and 0.016, respectively). No differences in serum calcium and phosphorus levels were observed among the three groups.\n\nQuestion:\nDoes puerarin affect bone biomarkers in the serum of rats with intrauterine growth restriction?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIntra-hepatic metabolism of lipids is subject to hormonal, metabolic and neural regulation, but little is known about the latter. Catecholamines stimulate the output of glucose and inhibit the release of very low density lipoproteins (VLDL) from the liver. To investigate the effects and involved mechanism of liver denervation on the levels of serum and liver lipids. Two groups of male rats were taken as control and cases and the liver was denerved chemically by 90% phenol in the case group. On the fourth day of the operation, blood samples were taken and the liver homogenized for lipid and glycogen analyses. Cholesterol, triglyceride, HDLc and glucose were measured enzymatically. Total phospholipids were analyzed by the measuring of liberated inorganic phosphate in organic phase. Glycogen was extracted by ethanol and analyzed by phenol/sulphuric acid reagent. In a separate experiment, the rate of triglyceride secretion was measured in vivo by using tyloxapol and compared in two groups. The serum concentrations of triglyceride (73.7 ± 6.3 vs. 45.8 ± 1.6 mg/dL, P ≤ 0.003) and cholesterol (87.7 ± 3.7 vs. 67.4 ± 2.2mg/dL, P ≤ 0.001) were significantly higher in the denerved compared with the control group. The serum glucose showed a significant decrease (170.5 ± 5.4 vs. 140.6 ± 10.7 mg/dL, P ≤ 0.04) in the denerved group while HDLc had no significant difference between the two groups. Denerved rats compared to the control rats had the higher levels of hepatic glycogen (201.1 ± 20.6 vs. 100.7 ± 19.9 mg/g liver, P ≤ 0.02). The contents of liver triglyceride, cholesterol and total phospholipids did not differ significantly between two groups. The mean rate of triglyceride secretion from the liver increased in the denerved group (276.1 ± 16.1 vs. 230.6 ± 7.7 mg/dL.h, P ≤ 0.03).\n\nQuestion:\nDoes liver denervation increase the levels of serum triglyceride and cholesterol via increases in the rate of VLDL secretion?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIt has been reported that human FOXP3(+) CD4 Tregs express GARP-anchored surface latency-associated peptide (LAP) after activation, based on the use of an anti-human LAP mAb. Murine CD4 Foxp3(+) Tregs have also been reported to express surface LAP, but these studies have been hampered by the lack of suitable anti-mouse LAP mAbs. We generated anti-mouse LAP mAbs by immunizing TGF-β(-/-) animals with a mouse Tgfb1-transduced P3U1 cell line. Using these antibodies, we demonstrated that murine Foxp3(+) CD4 Tregs express LAP on their surface. In addition, retroviral transduction of Foxp3 into mouse CD4(+)CD25(-) T cells induced surface LAP expression. We then examined surface LAP expression after treating CD4(+)CD25(-) T cells with TGF-β and found that TGF-β induced surface LAP not only on T cells that became Foxp3(+) but also on T cells that remained Foxp3(-) after TGF-β treatment. GARP expression correlated with the surface LAP expression, suggesting that surface LAP is GARP-anchored also in murine T cells.\n\nQuestion:\nDoes tGF-β induce surface LAP expression on murine CD4 T cells independent of Foxp3 induction?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe assessed the prognostic value of baseline prostate specific antigen (PSA) for outcome after high energy transurethral thermotherapy in patients with lower urinary tract symptoms. Data were collected prospectively in 404 consecutive patients treated with high energy transurethral thermotherapy with the Prostatron device (EDAP-Technomed, Lyon, France). Patients were followed a minimum of 1 year. At baseline certain criteria were assessed, including pretreatment PSA, uroflowmetry, ultrasound measurement of prostatic volume, voided and post-void residual urine volume, and International Prostate Symptom Score (I-PSS) and quality of life scores. Outcome assessment included I-PSS, quality of life score and uroflowmetry of peak urine flow. Linear regression analyses were performed to correlate baseline PSA with improved clinical parameters at 12 months of followup. Logistic regression analyses and receiver operating characteristics curves characterized the ability of baseline PSA to discriminate patients with a more or less favorable outcome. An evident linear association was identified for prostate size at baseline and PSA. After 1 year 36 patients were treated again due to transurethral thermotherapy failure and 16 had died, which was not related to lower urinary tract symptoms or treatment for lower urinary tract symptoms. To include re-treated patients in the analyses we considered that their I-PSS, quality of life and peak urine flow values at 1 year were unchanged compared with baseline. Of the 388 evaluable patients an improvement of 50% or more in I-PSS, quality of life and peak urine flow was observed in 57%, 62% and 44%, respectively. Absolute mean changes at 1 year were -9.7, -2 and 5.2 ml. per second for I-PSS, quality of life and peak urine flow, respectively. Neither linear nor logistic regression analysis showed any clinically relevant correlation between baseline PSA and changes in I-PSS (r = -0.004), quality of life (r = -0.135) or peak urine flow (r = 0.105) at 1 year. Receiver operating characteristics curves failed to distinguish more or less favorable outcomes in all evaluated parameters.\n\nQuestion:\nDoes baseline prostatic specific antigen predict the outcome of high energy transurethral microwave thermotherapy?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAlthough 2-chloroprocaine continues to be a useful drug for epidural anesthesia in obstetrics, it has the anomalous action of decreasing the analgesic effectiveness of subsequently administered epidural fentanyl. Some investigators have suggested that 2-chloroprocaine may act at an opioid receptor site to antagonize the effects of fentanyl. The purpose of our studies was to investigate this hypothesis. Radioligand binding assays using the mu and kappa opioid receptor-selective radioligands [3H]-DAMGO and [3H]-U69,593, respectively, were performed to determine the potencies of lidocaine, 2-chloroprocaine, and 2-chloroprocaine metabolites at the mu and kappa opioid receptor sites. Electrophysiologic experiments in in vitro hippocampal slice preparations were then used to examine the effects of 2-chloroprocaine at these opioid receptor subtypes. Lidocaine caused a partial reduction of [3H]-DAMGO binding, which was dose-limited owing to the solubility of lidocaine. 2-Chloroprocaine caused complete displacement of [3H]-DAMGO binding, with a median effective concentration of 1.44 +/- 0.36 mM. The EC50 values for [3H]-U69,593 displacement were 177 +/- 47 microM for 2-chloroprocaine and 2.53 +/- 0.48 mM for lidocaine. Assuming a competitive interaction between anesthetic and opioid, the Ki value for 2-chloroprocaine was 435 microM at mu receptors and 49 microM at kappa receptors. In the mu activity bioassay, 2-chloroprocaine reversed the increased neuronal excitability caused by fentanyl, but this effect was further reduced by naloxone. In addition, 2-chloroprocaine did not reverse the after depolarization caused by fentanyl. In the kappa activity bioassay, 2-chloroprocaine produced effects similar to the kappa agonist U69, 593, but these were not antagonized by naloxone.\n\nQuestion:\nIs the hypothesis that antagonism of fentanyl analgesia by 2-chloroprocaine mediated by direct action on opioid receptors?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nProliferative activity in tumors depends on regulation of the cell cycle. p27(Kip1) (p27) plays a pivotal role as a negative regulator of the cell cycle. A decrease in p27 expression has been reported in many kinds of tumors, but little is known regarding p27 in patients with renal cell carcinoma (RCC). Expression of p27 and the related cyclins (cyclin A, cyclin E, and cyclin D1) was examined immunohistochemically in 67 patients with of clear cell RCC. The Ki-67 labeling index (MIB-1 LI) and clinicopathologic parameters related to a poor prognosis also were analyzed. To determine their prognostic significance, univariate and multivariate survival analyses were performed. In tumors, there was considerable immunoreactivity for cyclin A, cyclin D1, and MIB-1, and the mean values for each were 1.08%, 16.1%, and 1.5%, respectively. Cyclin E expression was rare. The expression of p27 was correlated strongly with the expression of cyclin A (correlation coefficient, 0.432; P < 0.0004) and cyclin D1 (correlation coefficient, 0.476; P < 0.0004). Also, an inverse correlation was present between p27 expression and tumor size (P = 0.0377). In univariate analysis, the unfavorable prognostic factors were high TNM stage (P < 0.0001), large tumor size (P = 0.0016), high histologic grade (P = 0.0104), and low p27 expression (P < 0.0001). In multivariate analysis, high TNM stage (P = 0.0035) and low p27 expression (P = 0.0235) were independent prognostic factors for disease specific survival in patients with RCC.\n\nQuestion:\nIs low expression of p27 ( Kip1 ) associated with tumor size and poor prognosis in patients with renal cell carcinoma?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nShort uncemented metaphyseally anchored femoral endoprostheses are becoming popular and are proposed to be less invasive than longer conventional implants. However, it is proposed here that shortening femoral endoprostheses can increase the risk of periprosthestic fracture. A simple analytical model of a femoral hip implant was developed to estimate the risk of bone overload for varying implant size, implantation geometry, implantation force and bone quality. The load capacity of a particular short implant design in poor quality cadaveric bone specimens was also measured experimentally, to validate the model. The model demonstrated a high risk of bone overload for a short endoprosthesis in poor quality bone. The experimental results and a clinical example of failure, to which the model was applied, supported this finding. Bone stresses increased with decreasing implant length and diameter, varus implantation, incomplete seating and high implantation forces, approaching the strength of good quality bone in extreme cases.\n\nQuestion:\nDoes biomechanics of short hip endoprostheses -- the risk of bone failure increase with decreasing implant size?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo identify genetic causes of malformations of the müllerian ducts. Retrospective laboratory study. University hospital. A total of 167 patients with disorders of the müllerian ducts: 116 patients with Mayer-Rokitansky-Küster-Hauser syndrome and 51 patients with fusion disorders of the müllerian ducts. The control group was composed of 94 fertile women with at least one child. Sequential analysis of RBM8A and TBX6 in a group of 167 clinically well-defined patients with disorders of the müllerian ducts. Identification of rare variants in RBM8A and TBX6. In total, we detected four RBM8A variants in 13 patients with disorders of the müllerian ducts and two heterozygous TBX6 variants in 5 of 167 patients.\n\nQuestion:\nAre variations in RBM8A and TBX6 associated with disorders of the müllerian ducts?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIn this study, we determine the prevalence and the prognostic value of the class III beta-tubulin microtubule protein examined immunohistochemically, in tumors of 40 patients with carcinomas of unknown primary site treated with paclitaxel-based chemotherapy. Immunohistochemical intensity of staining and percentage of cells were quantified. Clinical characteristics, response to chemotherapy, progression-free survival, and overall survival were assessed for relationships with the expression of class III beta-tubulin. The response rate was 17.9% (seven partial responses among 39 valuable patients), while eleven patients had a stable disease (28.2%) and 21 patients progressed on therapy (53.8%). Patients with high class III beta-tubulin expression were more resistant to taxane-based chemotherapy, defined as progression under treatment, while patient characteristics were not found to be correlated with response to chemotherapy. Patients whose tumors expressed high levels of class III beta-tubulin isotype had shorter overall survival, while there was a trend for an association with progression free survival. Multivariate analysis showed that class III beta-tubulin expression was independently correlated with progression free survival and overall survival.\n\nQuestion:\nIs class III beta-tubulin a marker of paclitaxel resistance in carcinomas of unknown primary site?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nGynodioecy, the co-occurrence of female and hermaphroditic individuals, is thought to be an intermediate step between hermaphroditism and separate sexes, a major transition in flowering plants. Because retaining females in a population requires that they have increased seed fitness (to compensate for the lack of pollen fitness), factors that affect seed fitness are of great importance to the evolution of this mating system and have often been studied. However, factors negatively affecting female fitness are equally important and have been largely neglected. One such factor stems from female flowers being less attractive to insects than hermaphrodite flowers, thereby decreasing their relative fitness. To test the severity and consequences of this type of pollinator discrimination in Geranium maculatum, experimental populations with the range of sex ratios observed in nature were created, ranging from 13 % to 42 % females. Pollinators were observed in order to measure the strength of discrimination, and pollen deposition and seed production of both sexes were measured to determine the fitness consequences of this discrimination. Additionally a comparison was made across the sex ratios to determine whether discrimination was frequency-dependent. It was found that female flowers, on average, were visited at half of the rate of hermaphrodite flowers, which decreased their pollen receipt and seed production. Additionally, females were most discriminated against when rare, due to both changes in the pollinators' behaviour and a shift in pollinator composition.\n\nQuestion:\nDoes frequency-dependent pollinator discrimination act against female plants in the gynodioecious Geranium maculatum?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe previously showed that immunization of mice with plasmid DNA (pDNA) encoding the Escherichia coli beta-galactosidase gene (pCMV-LacZ) induces a Th1 response, whereas beta-galactosidase (beta-gal) in saline or alum induces a Th2 response. Furthermore, the Th1 response dominates over the Th2 response and downregulates preexisiting IgE antibody formation. Here, we determined by passive transfer of CD4+ or CD8+ lymphocytes and by immunizing beta2-microglobulin knockout (beta2-M KO) mice whether CD4+ and/or CD8+ cells from pDNA-immunized mice suppress IgE antibody production. BALB/c mice were injected with either CD4+ or CD8+ lymphocytes from naive beta-gal-in-alum or pCMV-LacZ-immunized mice, then immunized with beta-gal in alum, and the IgE antibody formation was determined. Second, C57BL/6 wild-type (WT) or beta2-M KO mice were immunized with beta-gal orpCMV-LacZ, and the IgE antibody production was assessed. Passive transfer of both CD4+ and CD8+ lymphocytes from pDNA-immunized mice suppressed the IgE antibody response by 90% compared to transfer of CD4+ T cells from naive or beta-galin-alum immunized mice. beta2-M KO mice produced 3 times more IgE than the WT control mice both in the primary and secondary response.\n\nQuestion:\nIs inhibition of IgE antibody formation by plasmid DNA immunization mediated by both CD4+ and CD8+ T cells?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nArtesunate plus sulfadoxine-pyrimethamine (AS + SP) has been Somalia's national treatment policy since 2006. Routine monitoring of first-line malaria treatment is needed to ensure appropriate national malaria treatment policy and early detection of drug resistance. For this purpose, we conducted therapeutic efficacy studies of AS + SP for the treatment of uncomplicated malaria in Somalia in 2011. Studies were conducted in three sentinel sites. Eligible patients were evaluated for clinical and parasitological outcomes according to the WHO standard protocol. Molecular surveillance was conducted on resistance conferring mutations in the P.falciparum dihydrofolate reductase (dfhr) and dihydropteroate synthase (dhps) genes. The proportion of PCR-corrected treatment failures was high in Jamame (22%, 95% CI: 13.7-32.8%) and low (<5%) in Janale and Jowhar. All patients cleared parasites by day 3. Molecular markers associated with SP resistance were detected in all three sites. Treatment failure was associated with the presence of the double mutant dhps A437G/K540E (OR = 22.4, 95% CI: 5.1-98.1), quadruple mutant dhfr N51I/S108N+dhps A437G/K540E (OR = 5.5, 95% CI: 2.3-13.6), quintuple mutant dhfr N51I/C59R/S108N+dhps A437G/K540E (OR = 3.5, 95% CI: 1.4-8.8) and younger age (OR=0.86, 95% CI: 0.76-0.96).\n\nQuestion:\nIs treatment of uncomplicated malaria with artesunate plus sulfadoxine-pyrimethamine failing in Somalia : evidence from therapeutic efficacy studies and Pfdhfr and Pfdhps mutant alleles?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo analyze the relationship between maternal, cord blood and neonatal procalcitonin (PCT) levels in preterm deliveries with and without histologically proven chorioamnionitis (HCA). 91 mother-infant pairs from 24+0 to 33+0 gestational weeks were analyzed. Procalcitonin was measured in all mothers within 24 hours before and subsequently in cord blood and in neonates within the first two hours after delivery. PCT levels were analysed in relationship to HCA and clinical outcome. HCA was confirmed in 28 cases (31%). We found no differences in PCT values between HCA positive and negative groups in maternal blood (0.1±0.1 vs 0.09±0.09 ng/L, P = 0.76). PCT values in cord blood and neonates were significantly higher in the HCA positive compared to HCA negative group (0.23±0.1 vs 1.2±2.7 ng/L, P < 0.001 and 0.89±3.4 vs 4.2±9.3 ng/L, P < 0.0001 respectively). PCT values in neonates were significantly higher than those of cord blood. Levels were not influenced by the mode of delivery, gestational age or premature rupture of membranes. Chorioamnionitis was more frequently associated with early onset neonatal sepsis (36% in HCA group vs 5% in non HCA group, P < 0.0001). Comparison of other clinical data revealed no differences between HCA positive and negative groups.\n\nQuestion:\nIs procalcitonin more likely to be released by the fetus rather than placental tissue during chorioamnionitis?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe purpose of this study was to identify risk factors for poor clinical outcome after surgical resection of small lung adenocarcinoma. Clinical records of 127 patients who had pathologic stage IA lung adenocarcinoma 20 mm or less and who had undergone a lobectomy with mediastinal lymph node dissection were reviewed. The percentage of non-bronchioloalveolar carcinoma (non-BAC) components quantified objectively, and epidermal growth factor receptor gene (EGFR) mutation determined by polymerase chain reaction-based assay were retrospectively linked with clinical data. Based on the percentage of non-BAC component, 127 patients were classified as follows: 26 in group I, BAC, 46 in group II mixed subtype with >or= 50% BAC, 18 in group III, mixed subtype with under 50% BAC, and 37 in group IV, mixed subtype with all non-BAC components or a pure pattern of one of the non-BAC components. Groups I and II were considered to be a \"low non-BAC component type\" and groups III and IV were considered to be a \"high non-BAC component type.\" EGFR mutations in exon19 and exon21 were observed in 64 patients (50.4%). In terms of recurrence, the high non-BAC component type was the only independent factor for recurrence (p = 0.029). Regarding survival, the high age (p = 0.028) and high non-BAC component type (p = 0.046) were independent risk factors for poor overall survival. They were also independent risk factors for poor disease-free survival (p = 0.025 and p = 0.027, respectively).\n\nQuestion:\nIs non-BAC component but not epidermal growth factor receptor gene mutation associated with poor outcomes in small adenocarcinoma of the lung?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nOur previous studies show that β2-adrenergic receptor (β2-AR) is highly expressed in most Her2-overexpressing breast cancers. However, the mechanisms underlying upregulation of the β2-AR expression in Her2-overexpressing breast cancer cells are not fully understood. The clinical significance of the β2-AR overexpression in breast cancer is unclear. Human breast cancer cells MCF-7 and MCF-7/Her2 were transfected with the let-7 mimics or inhibitors. The expression of β2-AR was analyzed by Western blot. The β2-AR status in primary and metastatic sites of breast cancer and the human breast cancer tissue microarrays containing 49 primary tumors and 50 metastatic lymph node tissues was analyzed by immunohistochemistry. The correlation of lymph node metastasis with the β2-AR level was determined in 59 primary tumor tissues from the patients with Her2-positive breast cancer. The clinical prognostic significance of the β2-AR overexpression in the patients with Her2-positive breast cancers was evaluated by a retrospective study. The let-7f level in Her2-overexpressing breast cancer cells SKBR3 and BT474 was significantly lower than that in MCF-7 cells, which express low level of Her2. Ectopic expression of Her2 in MCF-7 cells (MCF-7/Her2) represses the expression of microRNA let-7f, which is previously identified to regulate baseline β2-AR expression. The treatment with MEK1/2 inhibitors PD98059 or PD184352 effectively restored the let-7f level, suggesting that Her2-overexpression-mediated ERK constitutive activation inhibited let-7f, leading to the upregulation of the β2-AR expression. The transfection with the let-7f mimics markedly downregulated the β2-AR level, whereas the let-7 inhibitor significantly upregulated the β2-AR expression in both parental MCF-7 and MCF-7/Her2 cells. In addition, treatment of MCF-7/Her2 cells with isoproterenol resulted in a concentration-dependent reduction of the let-7f expression, demonstrating that the inhibitory effect of Her2 overexpression on let-7f can be reinforced by agonist-triggered β2-AR activation. We further demonstrate that high level of β2-AR associates with lymph node metastasis and poor outcome in the patients with Her2-positive breast cancer.\n\nQuestion:\nDoes a Her2-let-7-β2-AR circuit affect prognosis in patients with Her2-positive breast cancer?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe aim of this study was to determine the association between serum concentrations of brain-derived neurotrophic factor (BDNF), neuron-specific enolase (NSE), and S100β and the occurrence of delirium in critically ill patients. This case-control study included 30 patients with delirium and 30 matched controls in a 16-bed general intensive care unit (ICU). Serum BDNF, NSE, and S100 concentrations were determined by enzyme-linked immunosorbent assay assays at the time of ICU admission and on the day before delirium was diagnosed. Delirium was diagnosed by confusion assessment method for the ICU. At ICU admission, serum BDNF levels were significantly higher in delirious patients than in nondelirious controls (2.89 ± 1.48 vs 1.79 ± 0.89 ng/mL, respectively). When we compared serum S100 levels, there were no significant differences between the groups. Neuron-specific enolase values were significantly higher in the delirious patients than in the nondelirious controls (0.79 ± 0.03 ng/mL vs 0.59 ± 0.01 ng/mL, respectively). When patients who earlier developed delirium were separately analyzed, it was determined that serum NSE and BDNF levels at admission were significant higher only in this group.\n\nQuestion:\nAre brain-derived neurotrophic factor and neuron-specific enolase , but not S100β , levels associated to the occurrence of delirium in intensive care unit patients?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAdrenomedullin and endothelin-1 are hormones with opposing effects on the cardiovascular system. Adrenomedullin acts as a vasodilator and seems to be important for the initiation and continuation of the hyperdynamic circulatory response in sepsis. Endothelin-1 is a vasoconstrictor and has been linked to decreased cardiac performance. Few studies have studied the relationship between adrenomedullin and endothelin-1, and morbidity and mortality in septic shock patients. High-sensitivity troponin T (hsTNT) is normally used to diagnose acute cardiac injury but is also prognostic for outcome in intensive care. We investigated the relationship between mid-regional pro-adrenomedullin (MR-proADM), C-terminal pro-endothelin-1 (CT-proET-1), and myocardial injury, measured using transthoracic echocardiography and hsTNT in septic shock patients. We were also interested in the development of different biomarkers throughout the ICU stay, and how early measurements were related to mortality. Further, we assessed if a positive biomarker panel, consisting of MR-proADM, CT-proET-1, and hsTNT changed the odds for mortality. A cohort of 53 consecutive patients with septic shock had their levels of MR-proADM, CT-proET-1, hsTNT, and left ventricular systolic functions prospectively measured over 7 days. The relationship between day 1 levels of MR-proADM/CT-proET-1 and myocardial injury was studied. We also investigated the relationship between biomarkers and early (7-day) and later (28-day) mortality. Likelihood ratios, and pretest and posttest odds for mortality were calculated. Levels of MR-proADM and CT-proET-1 were significantly higher among patients with myocardial injury and were correlated with left ventricular systolic dysfunction. MR-proADM and hsTNT were significantly higher among 7-day and 28-day non-survivors. CT-proET-1 was also significantly higher among 28-day but not 7-day non-survivors. A positive biomarker panel consisting of the three biomarkers increased the odds for mortality 13-fold to 20-fold.\n\nQuestion:\nAre adrenomedullin and endothelin-1 associated with myocardial injury and death in septic shock patients?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWHAT'S KNOWN ON THE SUBJECT? AND WHAT DOES THE STUDY ADD?: To date, only a few studies have addressed the long-term oncological outcomes of radical prostatectomy (RP) in patients with pathological Gleason score ≥ 8 prostate cancer. According to these reports, some individuals with pathological Gleason score ≥ 8 may benefit from RP, with cancer-control outcomes comparable with those of patients with low- and intermediate-risk prostate cancer. The presence of pathological Gleason score 8-10 represents a poor prognostic factor in the outcome of men with prostate cancer. However, in patients with specimen-confined disease, RP and bilateral PLND provided long-term cancer-control outcomes similar to those of patients with more favourable disease characteristics. To evaluate the outcomes of patients with pathological Gleason score 8-10 prostate cancer subjected to radical prostatectomy (RP). To determine the prognostic factors associated with cancer-specific survival (CSS) in this subset of patients. The study included 580 consecutive patients with pathological Gleason sum 8-10 prostate cancer treated with RP and pelvic lymph node dissection (PLND) at a single European institution between July 1988 and April 2010. All patients had detailed pathological and follow-up data. Pathological Gleason score was determined by a single expert genitourinary pathologist. Biochemical recurrence (BCR) was defined PSA concentration of ≥ 0.2 ng/mL and rising. Kaplan-Meier plots were used to graphically explore BCR-free survival as well as CSS and overall survival (OS) rates. Moreover, univariable and multivariable Cox regression models were fitted to test the predictors of CSS. The mean (median, range) age at surgery was 66.1 (66.4, 41-85) years. The mean (median, range) total PSA concentration was 29.6 (11.1, 0.5-1710) ng/mL. Pathological Gleason score was 8 in 238 (41.0%), 9 in 330 (56.9%) and 10 in 12 (2.1%) patients. Overall, 119 (20.5%), 124 (21.4%), 281 (48.4%) and 56 (9.7%) patients had pT2, pT3a, pT3b and pT4 prostate cancer, respectively. Overall, 275 (47.4%) had LN invasion, while 150 (25.1%) patients had specimen-confined disease (defined as pT2cR0 pN0 or pT3aR0 pN0 prostate cancer). The mean (median, range) follow-up was 53 (47, 1-226) months. At 5 and 10 years after RP, BCR-free survival was 76.7% and 49.6%, respectively. Similarly, the 5- and 10-year CSS rates were 87.3% and 69.5%, respectively. Patients with specimen-confined disease (P < 0.001) and patients with negative LNs (P = 0.012) had significantly better CSS rates than their counterparts with less favourable pathological characteristics. In multivariable Cox regression models, only the presence of specimen-confined disease achieved independent predictor status (P = 0.001).\n\nQuestion:\nDoes radical prostatectomy represent an effective treatment in patients with specimen-confined high pathological Gleason score prostate cancer?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCardiac hypertrophy has been demonstrated to decreases the ATP-sensitive potassium channels (K(ATP)), the major protective mechanism following the energy depletion, a common condition seen during the reperfusion after open heart surgery. In this study we have demonstrated the role of ischemic preconditioning (IP) in preventing the reperfusion injury of the hypertrophied heart by activation of the depleted K(ATP) channels. Pressure overload left ventricular hypertrophy was induced in 6 weeks old male Wistar rats by supra renal transverse abdominal aortic constriction and the study was conducted 10-12 weeks later. Hypertrophied rats were subjected to IP protocols by four episodes of 3 min ischemia each being separated by 10 min reperfusion, followed by 30 min of sustained ischemia and 120 min of reperfusion with or without treating the rats with K(ATP) channel antagonists 5-hydroxydecanoic acid (10 mg/kg per i.v.) or glibenclamide (1 mg/kg per i.v.), 10 min before the sustained ischemia. IP resulted in (a) less incidence of ventricular arrhythmias (b) less area of myocardial infarction (9.3% vs. 48.1%, IP to control) (c) less tissue water content (76.5% vs. 94.8%, IP to control) (d) well preserved myocardial ATP content (P<0.001 from control) content and (e) much fewer apoptotic cells (4.7% vs. 13.2%, IP to control). Pre treating the rats with the K(ATP) channel inhibitors before sustained ischemia resulted in inhibition of these protective effects of IP on cardiac hypertrophy.\n\nQuestion:\nDoes ischemic preconditioning prevent reperfusion heart injury in cardiac hypertrophy by activation of mitochondrial KATP channels?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe study was aimed to investigate the inhibitory effect and mechanism of astragaloside IV (ASI) on the activation of microglial cells. After pre-incubated with ASI for 2 h, microglial cells BV-2 were stimulated with interferon-γ (IFN-γ) for 1. 5 h and 24 h, respectively. Secretion of nitric oxide (NO) in the medium was measured by Griess method. Production of tumor necrosis factor alpha (TNF-α) was detected by ELISA approach. Cellular gene expressions of CD11b, TNF-α, interleukin 1β (IL-1β) and induced nitric oxide synthase (iNOS) were examined by quantitative-PCR analysis. Total and phosphorylation of STAT1, IκB and NF-κB was analyzed by Western blot method. ASI could significantly inhibit the increased secretion of TNF-α and NO from BV-2 cells upon IFN-γ stimulation (P < 0.001). Further study showed that ASI significantly down-regulated gene expression of IL-1β and TNF-α (P < 0.01, P < 0.05) and exhibited a trend to reduce that of iNOS. IFN-γ and ASI have no obvious effect on gene expression of CD11b. Moreover, ASI inhibited the phosphorylation of STAT1, IκB and NF-κB elicited by IFN-γ stimulation.\n\nQuestion:\nDoes [ Astragaloside IV regulate STAT1/IκB/NF-κB signaling pathway to inhibit activation of BV-2 cells ]?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nRecent investigations have revealed that populations of macrophages and dendritic cells (DCs) are present in the stroma and epithelium of the cornea, although the precise phenotype and distribution are still controversial. CX(3)CR1, the sole receptor for the chemokine fractalkine, is expressed by these monocyte-derived cells. Transgenic CX(3)CR1(GFP) mice, in which either one (heterozygous) or both (homozygous) copies of the CX(3)CR1 gene were replaced by enhanced green fluorescent protein (eGFP), were used to characterize monocyte-derived cells in the mouse cornea and to determine whether the expression of this receptor influences the recruitment of these cells into the normal cornea. Wholemount corneas were immunostained with anti-leukocyte antibodies to the phenotypic markers major histocompatibility complex (MHC) class II, CD169, CD68, CD11b, and CD45 and analyzed by epifluorescence and confocal microscopy. The density of intraepithelial MHC class II(+) cells was quantified in wild-type, CX(3)CR1(+/GFP) heterozygous, CX(3)CR1(GFP/GFP) homozygous, and CX(3)CR1-knockout mice. There was a significant reduction in the number of MHC class II(+) cells (putative DCs) in the corneal epithelium of CX(3)CR1-deficient mice (P < 0.009) compared with wild-type mice, and the few cells that were present did not possess classic dendriform morphology. No GFP(+) MHC class II(-) cells were noted in the epithelium. Dual immunostaining of corneas in both heterozygous and homozygous (CX(3)CR1-deficient) mice revealed GFP(+) cells with a more pleomorphic morphology throughout the entire corneal stroma that were CD11b(+) CD169(+), and had variable degrees of expression of CD68 andMHC class II. The immunophenotype and morphology of these intrastromal cells is strongly indicative of a macrophage phenotype.\n\nQuestion:\nDoes the chemokine receptor CX3CR1 mediate homing of MHC class II-positive cells to the normal mouse corneal epithelium?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMany epidemiological studies have revealed a positive correlation between medical radiation exposure and the reproductive health in female childhood cancer survivors. However, because of variations in the samples size, such studies showed partly inconsistent conclusions. The aim of this meta-analysis was to clarify the association between radiotherapy and the risk of reproductive health impairment for female who survived from childhood cancer. Fourteen cohort studies involving childhood radiotherapy were selected as the exposure of interest and the impaired reproductive health condition during the childbearing age as the outcome. Among meta-analysis of observational studies found in Pubmed and Embase from 1900 to 2014, we evaluated those relevant observational studies which surveyed the association of medical radiation and reproductive health in female childhood cancer survivors. Review Manager 5.2 and STATA 12.0 software were used to perform the meta-analysis. Study-specific estimations for each outcome were combined into a pooled relative risk (RR) with 95% confidence interval (CI) by a meta-analytic approach. Based on a random-effects meta-analysis, significant association between infertility (RR = 1.28, 95% CI = 1.16-1.42), acute ovarian failure (AOF) (RR = 9.51, 95% CI = 5.03-17.96), low level of anti mullerian hormone (AMH) (<1 ng/mL) (RR = 14.79, 95% CI = 3.36-66.64), stillbirth (RR = 1.19, 95% CI = 1.02-1.39) and low birth weight (RR = 2.22, 95% CI = 1.55-3.17) were identified. Conversely, no significant results were found in abortion and congenital malformations.\n\nQuestion:\nIs exposure to radiation therapy associated with female reproductive health among childhood cancer survivors : a meta-analysis study?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe clinical syndrome of frailty identified through the assessment of weight loss, gait speed, grip strength, physical activity, and physical exhaustion has been used to identify patients with reduced reserves. We hypothesized that frailty is useful in predicting adverse outcomes in optimized elective elderly colorectal surgery patients. A prospective study was conducted at 2 centers (Singapore and Japan). All patients over 75 years of age undergoing colorectal resection were assessed for the presence of the syndrome of frailty. All these patients had already had their comorbidities optimized for surgery. The outcome measure was postoperative major complications (defined as Clavien-Dindo type II and above complications). Eighty-three patients were studied from February 2008 to April 2010. The mean age was 81.5 years (range 75-93 years). The mean comorbidity index was 3.37 (range 0-11). Twenty-six (31.3%) patients were an American Society of Anesthesiologists (ASA) score of 3 and above. Chi-square analysis revealed that the odds ratio of postoperative major complications was 4.083 (95% confidence interval, 1.433-11.638) when the patient satisfied the criteria for frailty. Albumin <35, ASA >3, comorbidity index >5, and Physiologic and Operative Severity Score for the enUmeration of Mortality and Morbidity (POSSUM) scores were not predictive of postoperative major complications.\n\nQuestion:\nIs assessment for frailty useful for predicting morbidity in elderly patients undergoing colorectal cancer resection whose comorbidities are already optimized?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nChemokines and chemokine receptors play important roles in autoimmune diseases; however, their role in immune thrombocytopenia (ITP) is unclear. High-dose dexamethasone (HD-DXM) may become a first-line therapy for adult patients with ITP, but the effect of HD-DXM on chemokines in ITP patients is unknown. Our aim was to investigate the mechanism of pulsed HD-DXM for management of ITP, specifically regarding the chemokine pathways. Th1-/Th2-associated chemokine and chemokine receptor profiles in ITP patients before and after pulsed HD-DXM was studied. Plasma levels of CCL5 and CXCL11 (Th1-associated) and of CCL11 (Th2-associated) were determined by ELISA. Gene expression of these three chemokines and their corresponding receptors CCR5, CXCR3, and CCR3, in peripheral blood mononuclear cells (PBMCs) was determined by quantitative RT-PCR. Thirty-three of the thirty-eight ITP patients responded effectively to HD-DXM (oral, 40 mg/day, 4 days). In ITP patients, plasma CXCL11 levels increased, while CCL11 and CCL5 decreased compared to controls (P < 0.05). Similarly, gene expression of CXCL11 and its receptor CXCR3 increased, while CCL11 and CCR3 decreased (P < 0.05). CCL5 expression did not significantly change; however, expression of its receptor CCR5 increased (P < 0.05). Interestingly, in the patients who responded to pulsed HD-DXM, CXCL11 and CXCR3 expression was down-regulated, while CCL11 and CCR3 expression was up-regulated (P < 0.05). Meanwhile, CCL5 expression was up-regulated and CCR5 was down-regulated by HD-DXM (P < 0.05).\n\nQuestion:\nDoes pulsed high-dose dexamethasone modulate Th1-/Th2-chemokine imbalance in immune thrombocytopenia?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo discuss the important role of actin polymerization in calcium ionophore A23187-induced human acrosome reaction and its mechanism. Each spermatozoon specimen was divided into five groups, treated with A23187 3 micromol/L in Group A, Phalloidin 40 micromol/L and A23187 3 micromol/L in Group B, SLO 0.5 U/ml and A23187 3 micromol/L in Group C, SLO 0.5 U/ ml, Phalloidin 40 micromol/L and A23187 3 micromol/L in Group D, and nothing added in Grpup E. Then the percentage of the human acrosome reaction was assessed with Rhodamine-PSA (10 microg/ml). The difference of the human spermatozoon acrosome reaction was significant (P < 0.01) among the 5 groups with or without SLO, Phalloidin and calcium ionophore A23187 but not between Groups A and B (P > 0.01).\n\nQuestion:\nDoes [ Phalloidin play an important role in calcium ionophore A23187-induced human acrosome reaction ]?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPosttranslational modification, such as phosphorylation, plays an essential role in regulating activation of endothelial NO synthase (eNOS). In the present study, we aim to determine whether eNOS could be phosphorylated and regulated by a novel serine/threonine-protein kinase Pim1 in vascular endothelial cells (ECs). Using immunoprecipitation and protein kinase assays, we demonstrated that Pim1 specifically interacts with eNOS, which leads to a marked phosphorylation of eNOS at Ser-633 and increased production of nitric oxide (NO). Intriguingly, in response to VEGF stimulation, eNOS phosphorylation at Ser-633 exhibits two distinct phases: transient phosphorylation occurring between 0 and 60 min and sustained phosphorylation occurring between 2 and 24 h, which are mediated by the protein kinase A (PKA) and Pim1, respectively. Inhibiting Pim1 by either pharmacological inhibitor SMI-4a or the dominant-negative form of Pim1 markedly attenuates VEGF-induced tube formation, while Pim1 overexpression significantly increases EC tube formation and migration in an NO-dependent manner. Importantly, Pim1 expression and eNOS phosphorylation at Ser-633 were substantially decreased in high glucose-treated ECs and in the aorta of db/db diabetic mice. Increased Pim1 expression ameliorates impaired vascular angiogenesis in diabetic mice, as determined by an ex vivo aortic ring assay.\n\nQuestion:\nDoes pim1 kinase promote angiogenesis through phosphorylation of endothelial nitric oxide synthase at Ser-633?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nDespite numerous clinical trials no efficacious medications for methamphetamine (MA) have been identified. Neuroinflammation, which has a role in MA-related reward and neurodegeneration, is a novel MA pharmacotherapy target. Ibudilast inhibits activation of microglia and pro-inflammatory cytokines and has reduced MA self-administration in preclinical research. This study examined whether ibudilast would reduce subjective effects of MA in humans. Adult, non-treatment seeking, MA-dependent volunteers (N=11) received oral placebo, moderate ibudilast (40 mg), and high-dose ibudilast (100mg) via twice-daily dosing for 7 days each in an inpatient setting. Following infusions of saline, MA 15 mg, and MA 30 mg participants rated 12 subjective drug effects on a visual analog scale (VAS). As demonstrated by statistically-significant ibudilast × MA condition interactions (p<.05), ibudilast reduced several MA-related subjective effects including High, Effect (i.e., any drug effect), Good, Stimulated and Like. The ibudilast-related reductions were most pronounced in the MA 30 mg infusions, with ibudilast 100mg significantly reducing Effect (97.5% CI [-12.54, -2.27]), High (97.5% CI [-12.01, -1.65]), and Good (97.5% CI [-11.20, -0.21]), compared to placebo.\n\nQuestion:\nDoes ibudilast attenuate subjective effects of methamphetamine in a placebo-controlled inpatient study?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThree years ago a consultant geriatrician began regular visits to the coloproctology and general surgery wards of an acute Trust every weekday, to assist staff with the medical management, rehabilitation and discharge planning of patients aged 65 years and above. The length of stay of these patients in the first 10 months of the appointment was compared with younger concurrent controls and with historical controls in the preceding 10 months. The mean length of stay for the 4146 patients aged 16 years and above in a 10-month intervention period was 1.3 days shorter (95% confidence interval (CI) 0.86-1.74 days) than for the 4002 patients in the 10-month control period. This pattern was consistent across all ages and types of surgery, including major colorectal resection.\n\nQuestion:\nDoes the benefit of geriatric intervention in surgery-increased throughput necessarily need more beds?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nOsteoprotegerin is a novel member of the tumor necrosis factor receptor superfamily and a soluble decoy receptor of the receptor activator of nuclear factor-kappaB ligand. Recent experimental research has implicated osteoprotegerin in atherogenesis, but epidemiological confirmation of this concept is sparse. As part of the prospective, population-based Bruneck Study, severity, initiation, and progression of atherosclerosis were assessed in carotid arteries. Cases of incident cardiovascular disease and vascular mortality were carefully recorded over a 10-year period (1990 to 2000). Osteoprotegerin levels were measured in samples obtained at baseline and during follow-up. Serum osteoprotegerin showed a strong association with numerous vascular risk factors, including age, diabetes, markers of systemic inflammation, chronic infection, and smoking. In multivariate analyses, osteoprotegerin was significantly related to severity and 10-year progression of carotid atherosclerosis. Furthermore, a high level of osteoprotegerin was an independent risk factor for incident cardiovascular disease (adjusted relative risk for the top versus bottom tertile group for osteoprotegerin 2.2 [1.3 to 3.8]; P=0.001) and vascular mortality (adjusted relative risk for the top versus bottom tertile group for osteoprotegerin 3.1 [1.2 to 8.2]; P=0.010) but not for mortality due to nonvascular causes.\n\nQuestion:\nIs osteoprotegerin a risk factor for progressive atherosclerosis and cardiovascular disease?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe outcome of patients with metastatic colorectal carcinoma (mCRC) following first line therapy is poor, with median survival of less than one year. The purpose of this study was to identify candidate therapeutically targetable somatic events in mCRC patient samples by whole genome sequencing (WGS), so as to obtain targeted treatment strategies for individual patients. Four patients were recruited, all of whom had received > 2 prior therapy regimens. Percutaneous needle biopsies of metastases were performed with whole blood collection for the extraction of constitutional DNA. One tumor was not included in this study as the quality of tumor tissue was not sufficient for further analysis. WGS was performed using Illumina paired end chemistry on HiSeq2000 sequencing systems, which yielded coverage of greater than 30X for all samples. NGS data were processed and analyzed to detect somatic genomic alterations including point mutations, indels, copy number alterations, translocations and rearrangements. All 3 tumor samples had KRAS mutations, while 2 tumors contained mutations in the APC gene and the PIK3CA gene. Although we did not identify a TCF7L2-VTI1A translocation, we did detect a TCF7L2 mutation in one tumor. Among the other interesting mutated genes was INPPL1, an important gene involved in PI3 kinase signaling. Functional studies demonstrated that inhibition of INPPL1 reduced growth of CRC cells, suggesting that INPPL1 may promote growth in CRC.\n\nQuestion:\nDoes whole genome sequencing reveal potential targets for therapy in patients with refractory KRAS mutated metastatic colorectal cancer?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo test the hypothesis that length of cranial nerve irradiated is a major factor predicting the risk of cranial nerve injury following radiosurgery and to identify any other significant related treatment factors. Ninety-two patients (93 acoustic tumors) were treated with a 201 source Cobalt-60 gamma unit from 1987 to 1990 and prospectively followed. The range of minimum tumor dose was 12-20 Gy and maximum dose 24-50 Gy. Univariate and multivariate analyses were used to evaluate any correlations between tumor measurements and treatment factors, with the development of trigeminal and facial neuropathies following radiosurgery. The risks of trigeminal and facial neuropathy following radiosurgery were associated with the pon-petrous distance and mid porous transverse tumor diameters respectively (anatomically related to the irradiated length of cranial nerves V and VII respectively) in both univariate (p = .002 for V and p = .026 for VII) and multivariate (p = .004 for V and p = .055 for VII) analyses. Tumor volume, other tumor measurements, maximum dose, minimum tumor dose, and tumor dose inhomogeneity were not significantly related to either trigeminal or facial neuropathy in univariate and multivariate analyses.\n\nQuestion:\nDoes cranial nerve length predict the risk of delayed facial and trigeminal neuropathies after acoustic tumor stereotactic radiosurgery?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe microbiota of the mammalian gastrointestinal (GI) tract consists of diverse populations of commensal bacteria that interact with host physiological function. Dysregulating these populations, through exogenous means such as antibiotics or dietary changes, can have adverse consequences on the health of the host. Studies from laboratories such as ours have demonstrated that exposure to psychological stressors disrupts the population profile of intestinal microbiota. To date, such studies have primarily focused on prolonged stressors (repeated across several days) and have assessed fecal bacterial populations. It is not known whether shorter stressors can also impact the microbiota, and whether colonic mucosa-associated populations can also be affected. The mucosa-associated microbiota exist in close proximity to elements of the host immune system and the two are tightly interrelated. Therefore, alterations in these populations should be emphasized. Additionally, stressors can induce differential responses in anxiety-like behavior and corticosterone outputs in variant strains of mice. Thus, whether stressor exposure can have contrasting effects on the colonic microbiota in inbred C57BL/6 mice and outbred CD-1 mice was also examined. In the present study, we used high throughput pyrosequencing to assess the effects of a single 2-hour exposure to a social stressor, called social disruption (SDR), on colonic mucosa-associated microbial profiles of C57BL/6 mice. The data indicate that exposure to the stressor significantly changed the community profile and significantly reduced the relative proportions of two genera and one family of highly abundant intestinal bacteria, including the genus Lactobacillus. This finding was confirmed using a quantitative real-time polymerase chain reaction (qPCR) technique. The use of qPCR also identified mouse strain-specific differences in bacterial abundances. L. reuteri, an immunomodulatory species, was decreased in stressor-exposed CD-1 mice, but not C57BL/6 mice.\n\nQuestion:\nDoes exposure to a social stressor disrupt the community structure of the colonic mucosa-associated microbiota?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nRemifentanil is commonly used to replace nitrous oxide in general anesthesia to avoid the side effects of the latter. However, there are reports that intraoperative remifentanil infusion can lead to acute opioid tolerance. In this study, the authors tried to determine the dose of remifentanil comparable in efficacy to 70% nitrous oxide and to evaluate its effect on postoperative pain and morphine consumption after colorectal surgery using isoflurane anesthesia. Sixty adult patients undergoing open colorectal surgery were randomly assigned to receive either remifentanil or 70% nitrous oxide along with isoflurane anesthesia. After morphine analgesia titration in the postanesthesia care unit, patient-controlled analgesia was commenced. Morphine consumption and pain were scored at rest and during cough or movement for 24 h. The mean remifentanil infusion rate was 0.17 mug . kg . min. The median visual analog pain score on arrival in the postanesthesia care unit was 1 (0-10) in the nitrous oxide group and 3 (0-9) in the remifentanil group (P < 0.05). Otherwise, there was no difference in pain scores at 5, 10, and 15 min and no difference in the total morphine consumption during the stay in the postanesthesia care unit. The two groups had similar total morphine consumption in the first 24 h and pain scores at rest and during movement. The incidence of postoperative nausea and vomiting was 10% in both groups. There was no difference in the sedation scores.\n\nQuestion:\nDoes intraoperative remifentanil infusion increase postoperative opioid consumption compared with 70 % nitrous oxide?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nHigher parity is associated with increased subclinical cardiovascular disease (CVD) in mid-life and older women and with increased CVD risk overall. The relationship between parity, subclinical CVD, and infertility in young women with overweight and obesity has been infrequently evaluated. Reproductive histories were obtained in 191 (66%) young women with overweight and obesity (BMI 25-39.9 kg/m(2) ) participating in a weight loss trial. Baseline carotid intima-media thickness (IMT) and inter-adventitial diameter (IAD) were assessed via B-mode ultrasound. Linear regression was used to estimate the relationship between parity and carotid measures, adjusted for demographic, cardiovascular, and reproductive risk factors. Nulliparous women (n = 70, age 34.9 ± 7.1) had increased common carotid IAD (0.230 mm, SE 0.08, P = 0.003) and mean common carotid artery (CCA) IMT (0.031 mm, SE 0.01, P = 0.007) compared with parous women (n = 102, age 39.5 ± 4.9), persisting after adjustment for age, race, and CVD risk factors. No other reproductive factors were statistically significantly associated.\n\nQuestion:\nIs nulliparity associated with less healthy markers of subclinical cardiovascular disease in young women with overweight and obesity?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe objective of the present study was to investigate the effect of vitamin A supplementation on serum Th17 (IL-6, IL-17, IFNγ) and Treg (TGF-β, IL-10) related cytokines in obese and non-obese women. In a randomized double blind placebo controlled design, 56 obese women were randomly assigned to receive either an oral dose of 25,000 IU retinyl palmitate or placebo per day for 4 months. Twenty eight ages matched non-obese women were also received vitamin A. At the study entry, anthropometric variables were measured and serum Th17 and Treg related cytokine profile were determined at baseline and 4 months after intervention. Significantly higher baseline concentrations of IL-6 were observed in obese compared with non-obese women (P < 0.05). However, the initial concentrations of other cytokines were not significantly different between groups. The mean concentrations of IL-17 and TGF-β were significantly decreased after vitamin A supplementation in non-obese and obese women respectively. Positive relationships between IL-17 and IL-10 (r = 0.42, P < 0.001), TGF-β and IL-17 (r = 0.35, P < 0.001) and between IL-10 and IFN-γ (r = 0.41, P = 0.002) in total participants were also observed.\n\nQuestion:\nDoes vitamin A supplementation reduce the Th17-Treg - Related cytokines in obese and non-obese women?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nEstablishment of the left-right axis is important for positioning organs asymmetrically in the developing vertebrate-embryo. A number of factors like maternally deposited molecules have emerged essential in initiating the specification of the axis; the downstream events, however, are regulated by signal-transduction and gene-expression changes identifying which remains a crucial challenge. The EGF-CFC family member Cryptic, that functions as a co-receptor for some TGF-beta ligands, is developmentally expressed in higher mammals and mutations in the gene cause loss or change in left-right axis asymmetry. Despite the strong phenotype, no transcriptional-regulator of this gene is known till date. Using promoter-analyses tools, we found strong evidence that the developmentally essential transcription factor Snail binds to the human Cryptic-promoter. We cloned the promoter-region of human Cryptic in a reporter gene and observed decreased Cryptic-promoter activation upon increasing Snail expression. Further, the expression of Cryptic is down-regulated upon exogenous Snail expression, validating the reporter assays and the previously identified role of Snail as a transcriptional repressor. Finally, we demonstrate using gel-shift assay that Snail in nuclear extract of PANC1 cells interacts with the promoter-construct bearing putative Snail binding sites and confirm this finding using chromatin immunoprecipitation assay.\n\nQuestion:\nIs left-right axis asymmetry determining human Cryptic gene transcriptionally repressed by Snail?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTissue plasminogen activator (tPA) treatment for acute ischaemic stroke (AIS) should be given as soon as possible, preferably within 60 min after arrival at hospital. There is great variation in door-to-needle times (DNTs) internationally, nationally and even within the same hospital. Various strategies for improving treatment delays have been presented. The role of emergency physicians (EPs) in treating AIS has been under discussion in recent years. Emergency Medicine (EM) officially became a specialty in Finland in 2013. Practical education of EPs in Kanta-Häme Central Hospital began in October 2012, together with reorganization of the in-hospital treatment path for AIS patients. The main change was shifting the on-call duty regarding stroke patients from internists or neurologists to EPs after the third quarter of 2013. This was a retrospective study. The data, concerning the characteristics of tPA-treated patients, DNTs and onset-to-treatment times (OTTs) was collected from electronic and paper records. The period studied was 1 year before and 1 year during reorganization, i.e. 2012 and 2013. During the study period a total of 64 tPA treatments were given, 31 before and 33 during reorganization. The median DNT was 54 min in 2012, while it was 28 min in 2013 (p < 0.001). The median OTTs were 139 and 101 min before and during the start of reorganization, respectively (p < 0.001).\n\nQuestion:\nDoes stroke thrombolysis given by emergency physicians cut in-hospital delays significantly immediately after implementing a new treatment protocol?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nIt has been proposed that differentiation between M. bovis and M. tuberculosis is possible by using a PCR assay for the 500bp fragment present only in the M. bovis genome. Forty clinical samples and 16 clinical isolates from the Department of Microbiology, as well as 4 clinical isolates obtained from another laboratory, were tested for the purpose of this study. As controls we tested 2 M. bovis (M. bovis BCG Pasteur TMC1011 and M. bovis BCG Copenhagen), 1 H37Rv M. tuberculosis strain, 2 M. avium (ATCC15765 and ATCC1975, respectively) and 1 M. paratuberculosis (ATCC19698) strains. None of the mtp40- negative clinical isolates amplified the 500bp fragment, whereas 4 out of 17 mtp40-positive clinical isolates scored positive for the 500bp fragment. All clinical isolates scored positive for IS6110, mtp40, the pncA and oxyR PCR's. All but one of the clinical isolates amplified the 500bp fragment. Sequence analysis of the pncA and oxyR PCR products revealed the presence of nucleotide C at position 169 and G at position 285 respectively, suggesting M. tuberculosis as the causative agent.\n\nQuestion:\nIs the 500-base-pair fragment of the putative gene RvD1-Rv2031c also present in the genome of Mycobacterium tuberculosis?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nMicroRNAs (miRNAs) are a class of small RNAs that are implicated in the control of eukaryotic gene expression by binding to the 3'UTR of target mRNAs. Several algorithms have been developed for miRNA target prediction however, experimental validation is still essential for the correct identification of miRNA targets. We have recently predicted that Neuropilin2a (Nrp2a), a vascular endothelial growth factor receptor which is essential for normal developmental angiogenesis in zebrafish, is a dre-miR-2188 target. Here we show that dre-miR-2188 targets the 3'-untranslated region (3'UTR) of Nrp2a mRNA and is implicated in proper intersegmental vessel development in vivo. Over expression of miR-2188 in zebrafish embryos down regulates Nrp2a expression and results in intersegmental vessel disruption, while its silencing increases Nrp2a expression and intersegmental vessel sprouting. An in vivo GFP sensor assay based on a fusion between the GFP coding region and the Nrp2a 3'UTR confirms that miR-2188 binds to the 3'UTR of Nrp2a and inhibits protein translation.\n\nQuestion:\nDoes dre-miR-2188 targets Nrp2a and mediate proper intersegmental vessel development in zebrafish embryos?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nLow biocompatibility of peritoneal dialysis fluids (PDF) contributes to mesothelial injury. We investigated whether the heat shock proteins (HSP)-27, HSP-72, and HSP-90 are differentially induced upon exposure of mesothelial cells to PDF and whether this was affected by selective modulation of the physicochemical properties of PDF. Human mesothelial cells (Met5A and primary human mesothelial cells) were exposed to acidic lactate and glucose-monomer based PDF (CAPD2 and CAPD3), to control culture media, or to a neutral lactate and glucose-monomer-based PDF with reduced levels of glucose degradation products (BALANCE). Expression of HSP-27, HSP-72, and HSP-90 and cellular distribution of HSP-72 were assessed by Western blotting and immunocytochemistry. Mesothelial cells exhibited strong constitutive expression of HSP-27 and to a lesser extent HSP-72 and HSP-90. Exposure of the cells to CAPD2 and CAPD3 resulted in strong up-regulation of HSP-72. HSP-27 levels were slightly increased, but HSP-90 levels were unchanged upon exposure to CAPD2 or CAPD3. In contrast, exposure of the cells to BALANCE did not affect HSP-27 or HSP-72 expression. The acidic pH and glucose degradation products were found to be principal in mediating increased HSP-72 expression upon exposure to PDF.\n\nQuestion:\nDoes peritoneal dialysate fluid composition determine heat shock protein expression patterns in human mesothelial cells?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAutosomal dominant optic atrophy is a hereditary disorder characterized by progressive loss of vision and caused by mutations in a dynamin-related gene, OPA1, which translates into a protein with a mitochondrial leader sequence. In this study the OPA1 gene and its protein were localized in the rat and mouse retina, and its rat orthologue, rOpa1, was identified. The rOpa1 cDNA was isolated by using reverse transcribed cDNA from total RNA obtained from a rat retinal ganglion cell line. The spatial and temporal expression patterns of OPA1 and its gene product were investigated by RNA in situ hybridization and immunohistochemistry in mouse and rat retinas. To characterize further the OPA1-positive neurons, retinal ganglion cells were retrogradely labeled by an immunogold fluorescent tracer or double labeled with OPA1 and choline acetyltransferase or calbindin antibodies. Protein sequence alignment revealed a 96% identity between rat and human OPA1 mRNA. OPA1 expression was found as early as postnatal day 3 in the developing rodent retina. In the mature retina, the OPA1 gene and its protein were found not only in retinal ganglion cells, but also in starburst amacrine cells and horizontal cells, both of which are involved in lateral signal processing within the retina. However, OPA1 was absent from mitochondria rich nerve fibers and photoreceptor indicating a specific role for OPA1 in signal processing rather than in the requirement of mitochondrial energy supply in the retina.\n\nQuestion:\nIs oPA1 , the disease gene for autosomal dominant optic atrophy , specifically expressed in ganglion cells and intrinsic neurons of the retina?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo study the molecular mechanisms of nm23-H1 for regulating PKC signal pathway before and after transfection with nm23-H1 gene. Using Western-blot, Boyden-chamber, MTT and laser scanning confocal microscopy (LSCM) techniques to detect the distribution of PKC in cytosol and plasma membrane, changes of invasion and proliferation activity, PKC translocation status and changes of intracellular Ca(2+) concentration among different human pulmonary carcinoma cells with transfected or untransfected nm23-H1 gene, and changes of the three cell lines after treatment with Calphostin C, a PKC inhibitor. (1) The expression of PKCalpha, PKCbeta II on L9981 and L9981-pLXSN cell membrane, which was in activated status, was remarkably higher than those in L9981-nm23-H1 cell line (P < 0.001). The expression of PKCalpha, PKCbeta II in cytosol in L9981 and L9981-pLXSN cell lines, which was in inactivated status, was lower than those in L9981-nm23-H1 cell line (P < 0.001). It means that the PKC signal pathway was activated in L9981 and L9981-pLXSN cell lines. (2) PKCalpha and PKCbeta II mainly located in nuclei and perinuclear area in L9981 and L9981-pLXSN cells, which were in active status, and the Ca(2+) concentration in these cells was obviously higher than that in L9981-nm23-H1 cell line (P < 0.01). In L9981-nm23-H1 cell line, which was transfected with nm23-H1 gene, PKCalpha and PKCbeta II mainly located in soluble cytosolic section, in an inactive status. (3) The invasion and proliferation ability of L9981 and L9981-pLXSN lung cancer cells was higher than that of L9981-nm23-H1 cell line (P < 0.001). There was no statistically significant difference between L9981 and L9981-pLXSN cell lines (P > 0.05). (4) After treated with PKC inhibitor Calphstin C, the expression of PKC and PKCbeta II in membrane in L9981 and L9981-pLXSN cell lines was down-regulated (P < 0.001), PKCalpha and PKCbeta II were mainly located in cytosolic area, mainly in an inactive status, and the Ca(2+) concentration was found to be decreased in all the three cell lines. The invasion and proliferation ability of the three lung cancer cell lines were obviously decreasing (P < 0.001). However, the invasion and proliferation ability of L9981-nm23-H1 lung cancer cell line was still lower than that of L9981 and L9981-pLXSN lung cancer cell lines (P < 0.001). There was also no significant difference between L9981 and L9981-pLXSN cell lines (P > 0.05).\n\nQuestion:\nDoes [ nm23-H1 gene inhibit lung cancer cell invasion through down-regulation of PKC signal pathway ]?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nFine motor skill impairments are common in autism spectrum disorder (ASD), significantly affecting quality of life. Sensory inputs reaching the primary motor cortex (M1) from the somatosensory cortex (S1) are likely involved in fine motor skill and specifically motor learning. However, the role of these connections has not been directly investigated in humans. This study aimed to investigate, for the first time, the role of the S1-M1 connections in healthy subjects in vivo and whether microstructural alterations are associated with motor impairment in ASD. Sixty right-handed neurotypical adult men aged 18 to 45 years, and 60 right-handed age- and sex-matched subjects diagnosed with ASD underwent fine motor skill assessment and scanning with diffusion tensor imaging (DTI). The streamlines of the hand region connecting S1-M1 of the motor-sensory homunculus were virtually dissected using TrackVis, and diffusion properties were extracted. The face/tongue region connections were used as control tracts. The ASD group displayed lower motor performances and altered DTI measurements of the hand-region connection. Behavioral performance correlated with hand-region DTI measures in both groups, but not with the face/tongue connections, indicating anatomical specificity. There was a left-hemisphere association of motor ability in the control group and an atypical rightward shift in the ASD group.\n\nQuestion:\nDoes impaired Communication Between the Motor and Somatosensory Homunculus be Associated With Poor Manual Dexterity in Autism Spectrum Disorder?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nOncogene HCCR-1 functions as a negative regulator of the p53 and contributes to tumorigenesis of various human tissues. However, it is unknown how HCCR-1 contributes to the cellular and biochemical mechanisms of human tumorigenesis. In this study, we showed how the expression of HCCR-1 is modulated. The luciferase activity assay indicated that the HCCR-1 5'-flanking region at positions -166 to +30 plays an important role in HCCR-1 promoter activity. Computational analysis of this region identified two consensus sequences for the T-cell factor (TCF) located at -26 to -4 (Tcf1) and -136 to -114 (Tcf2). Mutation at the Tcf1 site led to a dramatic decrease in promoter activity. Mobility shift assays (EMSA) revealed that nuclear proteins bind to the Tcf1 site, but not to the Tcf2 site. LiCl, Wnt signal activator by GSK-3beta inhibition, significantly increased reporter activities in wild-type Tcf1-containing constructs, but were without effect in mutant Tcf1-containing constructs in HEK/293 cells. In addition, endogenous HCCR-1 expression was also increased by treatment with GSK-3beta inhibitor, LiCl or AR-A014418 in HEK/293 and K562 cells. Finally, we also observed that the transcription factor, TCF, and its cofactor, beta-catenin, bound to the Tcf1 site.\n\nQuestion:\nDoes tCF/beta-catenin play an important role in HCCR-1 oncogene expression?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCompared with surgery alone, preoperative radiotherapy and 5-fluorouracil-based chemotherapy (combined-modality therapy; CMT) improves outcomes in patients with locally advanced rectal cancer. Although numerous studies have focused on identifying molecular markers of prognosis in the primary rectal cancer before CMT, our aim was to identify markers of prognosis in residual rectal cancer after preoperative CMT. Sixty-seven patients with locally advanced (T3-4 and/or N1) rectal cancer were treated with preoperative radiotherapy (median, 5040 cGy) with or without 5-fluorouracil-based chemotherapy. Residual tumor in the resected specimen, available for 52 patients, was analyzed for tumor-node-metastasis stage, lymphovascular and/or perineural invasion, and immunohistochemical expression of p27, p21, p53, Ki-67, retinoblastoma gene, cyclin D1, and bcl-2. Recurrence-free survival (RFS) was determined by the Kaplan-Meier method and compared by the log-rank test. With a median follow-up of 69 months, the overall 5-year RFS was 74%. RFS was significantly worse for patients with positive p27 expression (P = .005), T3-4 tumors (P = .02), and positive lymph nodes (P = .04) in the irradiated specimen. On multivariate analysis, positive p27 expression remained an independent negative prognostic factor for RFS (P = .04). None of the other proteins was significantly associated with RFS.\n\nQuestion:\nDoes expression of p27 in residual rectal cancer after preoperative chemoradiation predict long-term outcome?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe objective of this study was to determine the relationship between multidrug resistance and sensitivity to paclitaxel (PTX) in ovarian cancer. We used human ovarian adenocarcinoma cell lines, KF, a PTX-resistant cell line (KFTx), SK-OV-3, and KOC7c. Additionally, 27 patients with ovarian cancer who had residual disease were examined. All patients underwent postoperative chemotherapy consisting of 175 mg/m(2) PTX and area under curve (AUC) 5 carboplatin. The sensitivity of the cells to PTX or cisplatin (CDDP) was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. mRNA expression of multidrug resistance gene-1 (MDR-1) and multidrug resistance-associated protein-1 (MRP-1) and MRP-2 was determined by reverse transcription-polymerase chain reaction. beta-Tubulin polymerization and Bcl-2 phosphorylation were examined by Western blot analysis. Compared with KF, the IC(50) to PTX was 5.5-fold higher for KFTx, 0.3-fold for SK-OV-3, and 52.1-fold for KOC7c. The IC(50) to CDDP was 0.7-, 4.2-, and 5.8-fold, respectively. Expression of the MDR-1 gene was clearly observed in KFTx and KOC7c. Expression of MRP-1 was observed in SK-OV-3 and KOC7c. Expression of MRP-2 was detected only in KOC7c. CDDP enhanced beta-tubulin polymerization induced by PTX in CDDP-sensitive cells. Bcl-2 phosphorylation appeared after exposure to IC(50) PTX in all cells. Twenty-one patients responded to chemotherapy and six did not. Expression of the MDR-1 gene for nonresponders was significantly higher than that for responders (260.0 +/- 191.6 vs 9.3 +/- 21.8). With the cutoff value of MDR-1 expression at 100, the predictive value for chemoresponse was 96%. Expression of the MRP-1 and MRP-2 genes did not differ between nonresponders and responders.\n\nQuestion:\nIs multidrug resistance gene-1 a useful predictor of Paclitaxel-based chemotherapy for patients with ovarian cancer?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAlthough chronic kidney disease is associated with a high prevalence of cardiovascular disease, the relationship between coronary artery spasm and renal dysfunction has not been elucidated. We evaluated 139 patients with chest pain at rest who had no significant organic stenosis on coronary angiograms and who underwent coronary spasm provocation tests using acetylcholine or ergonovine. The results of the provocation tests revealed that 59 patients had vasospastic angina (VSA), and that 80 did not (non-VSA). We analyzed the association between VSA and renal dysfunction using the estimated glomerular filtration rate (eGFR). The eGFR was significantly lower in the VSA group than in the non-VSA group (P = 0.013). The patients were assigned to quartiles (Q) 1, 2, 3 and 4 based on eGFR (ml·min⁻¹·1.73 m²) < 64.1, 64.1-74.7, 74.8-85.0 and ≥ 85.1, respectively, in each of which the prevalence of VSA was 57%, 53%, 34% and 26%, respectively. The prevalence of VSA was significantly higher in Q1 than in Q4 (P = 0.008). Logistic regression analysis showed that the independent factors associated with the presence of VSA were a lower eGFR (P = 0.011) and male gender (P = 0.001).\n\nQuestion:\nIs low glomerular filtration rate associated with high prevalence of vasospastic angina?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nBiomarkers predictive of pathological complete response (pCR) to neoadjuvant chemotherapy (NACT) of breast cancer are urgently needed. Using a training/validation approach for detection of predictive biomarkers in HER2-negative breast cancer, pre-therapeutic core biopsies from four independent cohorts were investigated: Gene array data were analysed in fresh frozen samples of two cohorts (n=86 and n=55). Quantitative reverse transcription polymerase chain reaction (qRT-PCR) was performed in formalin-fixed, paraffin-embedded (FFPE) samples from two neoadjuvant phase III trials (GeparTrio, n=212, and GeparQuattro, n=383). A strong predictive capacity of thymosin beta 15 (TMSB15A) gene expression was evident in both fresh frozen cohorts (P<0.0001; P<0.0042). In the GeparTrio FFPE training cohort, a significant linear correlation between TMSB15A expression and pCR was apparent in triple-negative breast cancer (TNBC) (n=61, P=0.040). A cutoff point was then defined that divided TNBC into a low and a high expression group (pCR rate 16.0% vs 47.2%). Both linear correlation of TMSB15A mRNA levels (P=0.017) and the pre-defined cutoff point were validated in 134 TNBC from GeparQuattro (pCR rate 36.8% vs 17.0%, P=0.020). No significant predictive capacity was observed in luminal carcinomas from GeparTrio and GeparQuattro.\n\nQuestion:\nIs thymosin beta 15A ( TMSB15A ) a predictor of chemotherapy response in triple-negative breast cancer?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe neurotrophins, which include nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), NT-4/5 and NT-6, are a family of proteins that play fundamental roles in the differentiation, survival and maintenance of peripheral and central neurons. Much research has focused on the role of neurotrophins as target-derived, retrogradely transported trophic molecules. Although there is recent evidence that BDNF and NT-3 can be transported in an anterograde direction along peripheral and central axons, there is as yet no conclusive evidence that these anterograde factors have direct post-synaptic actions. We report that BDNF travels in an anterograde direction along the optic nerve. The anterogradely transported BDNF had rapid effects on retinal target neurons in the superior colliculus and lateral geniculate nucleus of the brain. When endogenous BDNF within the developing superior colliculus was neutralised, the rate of programmed neuronal death increased. Conversely, provision of an afferent supply of BDNF prevented the degeneration of geniculate neurons after removal of their cortical target.\n\nQuestion:\nIs brain-derived neurotrophic factor an anterograde survival factor in the rat visual system?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nCalcitonin gene-related peptide (CGRP) is a potent vasodilator, implicated in the pathogenesis of migraine. CGRP activates a receptor complex comprising, calcitonin receptor-like receptor (CLR) and receptor activity-modifying protein 1 (RAMP1). In vitro studies indicate recycling of CLR●RAMP1 is regulated by degradation of CGRP in early endosomes by endothelin-converting enzyme-1 (ECE-1). However, it is not known if ECE-1 regulates the resensitization of CGRP-induced responses in functional arterial tissue. CLR, ECE-1a-d and RAMP1 expression in rat mesenteric artery smooth muscle cells (RMA-SMCs) and mesenteric arteries was analysed by RT-PCR and by immunofluorescence and confocal microscopy. CGRP-induced signalling in cells was examined by measuring cAMP production and ERK activation. CGRP-induced relaxation of arteries was measured by isometric wire myography. ECE-1 was inhibited using the specific inhibitor, SM-19712. RMA-SMCs and arteries contained mRNA for CLR, ECE-1a-d and RAMP1. ECE-1 was present in early endosomes of RMA-SMCs and in the smooth muscle layer of arteries. CGRP induced endothelium-independent relaxation of arteries. ECE-1 inhibition had no effect on initial CGRP-induced responses but reduced cAMP generation in RMA-SMCs and vasodilation in mesenteric arteries responses to subsequent CGRP challenges.\n\nQuestion:\nDoes endosomal proteolysis regulate calcitonin gene-related peptide responses in mesenteric arteries?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo compare the incidence, temporal trends and cause of burn hospitalisations between urban, rural and remote regions in Western Australia, 1983-2008. De-identified linked hospital morbidity and mortality records for all persons hospitalised for an index burn in Western Australia were analysed 1983-2008. Annual age-specific incidence and age standardised rates were estimated. Poisson regression analyses were used to estimate temporal trends in hospital admissions by urban, rural and remote region. Of 23,450 burn-related hospital admissions 1983-2008, 14,007 (59.7%) were in urban, 5442 (23.1%) rural and 4021 (17.2%) remote hospital regions. Hospitalisation rates were higher in rural (Incidence rate ratio (IRR), 95% CI: 1.5, 1.4-1.6) and remote (IRR, 95%C: 2.1, 2.0-2.2) regions compared to urban. Age-standardised rates of burn hospital admissions declined from 1983 to 2008 for each region with 26-year declines of 56% (95% CI: 51-60) for remote, 71% (95% CI: 68-73) for rural, and 9% (95% CI: 4-14) for admissions in urban regions. Scald was the most common cause for urban admissions while flame the most common cause for rural and remote burn admissions.\n\nQuestion:\nDo urban compared with rural and remote burn hospitalisations in Western Australia?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo evaluate the correlation between anterior chamber inflammation and the central foveal thickness of the retina in a homogenous uveitic group (seronegative spondyloarthropathy (subgroup: ankylosing spondylitis)) of patients with the first acute anterior unilateral uveitic attack. Central foveal thickness (FT) and perifoveal retinal thickness were recorded by optical coherence tomography (Optovue RTVue-100), and the difference between the two eyes was calculated. Statistical analysis was performed by Mathworks Matlab software. Anterior chamber inflammation was measured by laser flare photometry (Kowa FM-600). A statistically significant (p < .05) increase was found in retinal thickness in all OCT subfields in acute anterior uveitic eyes compared to healthy fellow eyes. There was a linear correlation between the degree of inflammation (laser flare photometry values) and central foveal thickness (r = .900, p < .001).\n\nQuestion:\nDo macular Changes Correlate with the Degree of Acute Anterior Uveitis in Patients with Spondyloarthropathy?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nQuantification of plasma noncholesterol sterols allows the study of cholesterol absorption and synthesis. A pattern of low cholesterol absorption and high synthesis has been demonstrated in patients with obesity and insulin resistance. To understand the relationship between cholesterol absorption/synthesis and visceral obesity, we investigated surrogate markers of cholesterol absorption (campesterol and sitosterol) and synthesis (lathosterol) in dyslipidaemic patients with different representation of abdominal fat, estimated by ultrasonographic measurement of visceral fat area (VFA). In 126 patients with primary hyperlipaemias, plasma sitosterol, campesterol and lathosterol were determined by gas chromatography coupled with mass spectrometry. Visceral and subcutaneous fats were evaluated by ultrasonography. The study population was divided into two groups on the basis of VFA median values, below/equal and above 154 cm(2) . RESULTS Patients with higher VFA had significantly higher lathosterol levels (median 109 vs. 76 × 10(2) μmol/mmol cholesterol P < 0·004), body mass index, waist circumference, blood pressure, triglycerides, insulin, homoeostatic model assessment (HOMA)-IR and lower high-density lipoprotein (HDL)-C. VFA was positively correlated with lathosterol (ρ = 0·35, P < 0·001) and negatively with HDL-C (ρ = -0·43, P < 0·001), campesterol (ρ = -0·23, P = 0.01) and sitosterol (ρ = -0·35, P < 0·001). VFA was an independent predictor of lathosterol values (β = 0·389, P < 0·0001, P of the model < 0·0001);age, systolic blood pressure, BMI, waist circumference, triglycerides, HDL-C and HOMA failed to enter the final equation.\n\nQuestion:\nDoes visceral fat positively correlate with cholesterol synthesis in dyslipidaemic patients?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nBeta-hydroxyisovalerylshikonin (beta-HIVS), a compound isolated from the traditional oriental medicinal herb Lithospermum radix, is an ATP non-competitive inhibitor of protein-tyrosine kinases, such as v-Src and EGFR, and it induces apoptosis in some lines of human tumor cells. We investigated the effect of beta-HIVS on three endometrial cancer cell lines, two ovarian cancer cell lines, and normal human endometrial epithelial cells. Endometrial and ovarian cancer cells were treated with various concentrations of beta-HIVS, and its effect on cell growth, cell cycle, apoptosis, and related measurements was investigated. The 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay showed that all endometrial and ovarian cancer cell lines were sensitive to the growth-inhibitory effect of beta-HIVS, although normal endometrial epithelial cells were viable after treatment with the same doses of beta-HIVS that induced growth inhibition in endometrial and ovarian cancer cells. Cell-cycle analysis indicated that their exposure to beta-HIVS decreased the proportion of cells in the S phase and increased the proportion in the G0/G1 phases of the cell cycle. Induction of apoptosis was confirmed by annexin V staining of externalized phosphatidylserine and loss of the transmembrane potential of mitochondria. This induction occurred in concert with altered expression of genes related to cell growth, malignant phenotype, and apoptosis.\n\nQuestion:\nDoes beta-hydroxyisovalerylshikonin have a profound anti-growth activity in human endometrial and ovarian cancer cells?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nChemokines are potent proinflammatory and immune modulators. Increased expression of chemokines, eg, monocyte chemoattractant protein-1 (MCP-1), has recently been described in clinical and experimental heart failure. The present report is aimed at exploring the expression, localization, and binding site regulation of MCP-1, a member of the C-C chemokine family, in a rat model of volume-overload congestive heart failure (CHF). An aortocaval fistula was surgically created between the abdominal aorta and inferior vena cava. Rats with CHF were further subdivided into compensated and decompensated subgroups. Northern blot analysis and real-time quantitative polymerase chain reaction demonstrated upregulation of MCP-1 mRNA expression correlating with the severity of CHF (288+/-22, 502+/-62, and 826+/-138 copies/ng total RNA for sham, compensated, and decompensated animals, respectively; n=5, P:<0.05). MCP-1 protein was localized by immunohistochemistry in cardiomyocytes, vascular endothelium and smooth muscle cells, infiltrating leukocytes, and interstitial fibroblasts, and its intensity increased with severity of CHF. In addition, rats with CHF displayed a significant decrease of (125)I-labeled MCP-1 binding sites to myocardium-derived membranes (384.3+/-57.0, 181.3+/-8.8, and 123.3+/-14.1 fmol/mg protein for sham, compensated, and decompensated animals, respectively).\n\nQuestion:\nIs monocyte chemoattractant protein-1 upregulated in rats with volume-overload congestive heart failure?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nSuper-obese patients can achieve adequate weight loss with long limb Roux-en-Y gastric bypass (RYGB). These patients, however, might need longer intestinal limbs to control co-morbidities such as type 2 diabetes, lipid disorders, hypertension, sleep apnea, and gastroesophageal reflux disorder. A total of 105 patients with a body mass index of > or =50 kg/m(2) were randomly divided into 2 similar groups regarding sex, age, and number of co-morbidities. All underwent laparoscopic Roux-en-Y gastric bypass. In group 1, the length of the biliary limb was 50 cm and the length of the Roux limb was 150 cm. In group 2, the length of the biliary limb was 100 cm and the length of the Roux limb was 250 cm. The follow-up for both group was 48 months. Diabetes was controlled in 58% of group 1 and in 93% of group 2 (P <0.05). Lipid disorders improved in 57% of group 1 and in 70% of group 2 (P <0.05). No statistical difference was found in the control or improvement of hypertension, sleep apnea, or gastroesophageal reflux disorder. The excess weight loss was faster in group 1 but was similar in both groups at 48 months (70% in group 1 and 74% in group 2), with no statistical difference.\n\nQuestion:\nIs long-long limb Roux-en-Y gastric bypass more efficacious in treatment of type 2 diabetes and lipid disorders in super-obese patients?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nEstrogen synthesis is an important function of the mammalian ovary. Estrogen plays important roles in many biological processes, including follicular development, oocyte maturation and endometrial proliferation, and dysfunctions in estrogen synthesis contribute to the development of polycystic ovary syndrome and premature ovarian failure. Classical signaling cascades triggered by follicle-stimulating hormone induce estrogen synthesis via the upregulation of Cyp19a1 in granulosa cells (GCs). This study aimed to determine the effect of microRNA-132 (miR-132) on estradiol synthesis in GCs. Primary mouse GCs were collected from ovaries of 21-day-old immature ICR mice through follicle puncture. GCs were cultured and treated with the stable cyclic adenosine monophosphate analog 8-Br-cAMP or transfected with miR-132 mimics, Nurr1-specific small interfering RNA oligonucleotides and Flag-Nurr1 plasmids. Concentrations of estradiol and progesterone in culture medium were determined by an automated chemiluminescence-based assay. Quantitative real time PCR and western blot were performed to identify the effect of miR-132 on Cyp19a1, Cyp11a1 and an orphan nuclear receptor-Nurr1 expression in GCs. Direct suppression of Nurr1 via its 3'-untranslated region by miR-132 were further verified using luciferase reporter assays. The expression level of miR-132 in cultured mouse GCs was significantly elevated during 48 h of treatment with 8-Br-cAMP. The synthesis of estradiol increased after the overexpression of miR-132 in mouse GCs. The real-time PCR results demonstrated that miR-132 induced the expression of Cyp19a1 significantly. Nurr1, an orphan nuclear receptor that suppresses Cyp19a1 expression, was found to be a direct target of miR-132. Nurr1 was suppressed by miR-132, as indicated by a luciferase assay and Western blotting. The knockdown of Nurr1 primarily elevated the synthesis of estradiol and partially attenuated the miR-132-induced estradiol elevation, and the ectopic expression of Flag-Nurr1 abrogated the stimulatory effect of miR-132 on estradiol synthesis in mouse GCs.\n\nQuestion:\nDoes microRNA-132 promote estradiol synthesis in ovarian granulosa cells via translational repression of Nurr1?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nInitiation of enamel formation requires reciprocal signaling between epithelially and mesenchymally derived cells. In this study, we used a transgenic mouse model which drives overexpression of an activated form of TGF-beta2 under control of the osteocalcin promoter, to investigate the role of TGF-beta2 in the dental mesenchyme, on enamel formation. Dentin and enamel were imaged by scanning electron microscopy (SEM) and atomic force microscopy (AFM). Dentin mechanical properties were characterized for hardness and elasticity, following nanoindentation with a modified AFM. Pores found in enamel were quantified and compared using image analysis software (Scion Imagetrade mark). The elastic modulus of dentin was significantly reduced in the male TGF-beta2 overexpressor mice as compared to male wildtype mice, with no significant differences between female mice. Similarly, there were significantly more pores in enamel of the male transgenic mice as compared to male wildtype mice, with no significant differences between female mice. In situ hybridization of the continuously erupting incisor confirmed that osteocalcin expression was limited to the odontoblast cell layer at all stages of tooth formation.\n\nQuestion:\nDoes elevated TGF-beta2 signaling in dentin result in sex related enamel defects?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAnthocyanins have been reported to have beneficial effects on obesity and obesity-related metabolic disorders (e.g., insulin resistance and dyslipidemia). The objective of this study was to examine the beneficial effects of sweet cherry anthocyanins (SWCN) on high-fat diet-induced liver steatosis and investigate the underlying molecular mechanism. C57 BL/6 J mice were fed low-fat diet, high-fat diet, or high-fat diet supplemented with SWCN of 200 mg/kg for 15 wk. The hepatic gene expression profile was analyzed by DNA microarray analysis. SWCN supplementation alleviated high-fat diet-induced liver steatosis in mice. Microarray analysis of hepatic gene expression profiles indicated that SWCN treatment significantly changed the expression profiles of 1119 genes which were enriched in 16 pathways, such as PPAR signaling pathway, steroid biosynthesis, fatty acid metabolism, and biosynthesis of unsaturated fatty acids.\n\nQuestion:\nDoes dietary sweet cherry anthocyanins attenuate diet-induced hepatic steatosis by improving hepatic lipid metabolism in mice?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe poor prognosis associated with epithelial ovarian cancer (EOC) is due to the lack of overt early symptoms and the absence of reliable diagnostic screening methods. Since many tumors over express angiogenic regulators, the purpose of this study was to determine whether elevated levels of the angiogenic or angiostatic molecules vascular endothelial growth factor (VEGF), hepatocyte growth factor (HGF), endostatin (ES), and angiostatin (AS) were elevated in plasma and urine from patients with EOC. VEGF, HGF, ES and AS were assayed by ELISA in samples from pilot cohort consisting of healthy women (N=48; pre-menopausal N=23, post-menopausal N=25), women with benign gynecological disease (N=54), patients with primary peritoneal cancer (PP) (N=2) and EOC (N=35). Wherever possible, parallel serum samples were measured for CA125 levels by ELISA. AS was the angioregulator that independently discriminated EOC patients from healthy individuals. Levels of urinary AS (uAS) from healthy individuals or women with benign gynecological disease averaged 21.4 ng/mL+/-3.7 and 41.5 ng/mL+/-8.8, respectively. In contrast, uAS averaged 115 ng/mL+/-39.2 and 276 ng/mL+/-45.8 from women with Stage I (N=6) and late stage (N=31) EOC, respectively. Furthermore, uAS was elevated in EOC patients regardless of tumor grade, stage, size, histological subtype, creatinine levels, menopausal status, or patient age, but appeared to complement CA125 measurements.\n\nQuestion:\nAre urinary angiostatin levels elevated in patients with epithelial ovarian cancer?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nWe investigated the myocardial protective effect of sevoflurane in patients receiving off-pump coronary artery bypass grafting (OPCABG) and the role of brain natriuretic peptide (BNP). Forty-eight patients receiving elective OPCABG were randomly assigned to a control group, and to 0.75 MAC, 1.0 MAC and 1.5 MAC sevoflurane groups. Blood samples were collected and levels of BNP and cardiac troponin I (cTnI) were measured before anesthesia, and immediately, 24, 48 and 72 h after surgery. Dopamine was necessary to maintain blood pressure in the sevoflurane groups, but not in the control group (p < 0.002). 1.0 MAC sevoflurane significantly decreased post-surgical cTnI levels (p < 0.001). 0.75 MAC had no significant effect, and increasing sevoflurane concentrations to 1.5 MAC caused no further decrease in cTnI concentrations. There was no significant difference in BNP level among the groups (p = 0.227) or between any two groups, although values of BNP showed a significant correlation with cTnI values in control subjects immediately after (r = 0.847) and 24 h after (r = 0.661) surgery.\n\nQuestion:\nDoes sevoflurane at 1 MAC provide optimal myocardial protection during off-pump CABG?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nGadolinium-ethoxybenzyl-diethylenetriamine pentaacetic acid (Gd-EOB-DTPA) is an MRI contrast agent with perfusion and hepatoselective properties. The purpose of the study was to examine uptake of Gd-EOB-DTPA in the hepatobiliary phase in hepatocellular carcinoma (HCC). A retrospective analysis of 22 patients with HCC who underwent preoperative Gd-EOB-DTPA-enhanced MRI was performed. Enhancement ratios (ERs) and expression levels of the organic anion transporter (OATP) 1B3 protein were examined. Gd-EOB-DTPA accumulated in the hepatobiliary phase in 6 of the 22 cases. All 6 Gd-EOB-DTPA-positive cases were moderately differentiated HCC, but 11 other moderately differentiated HCCs did not show Gd-EOB-DTPA uptake. Histopathologically, 4 Gd-EOB-DTPA-positive HCCs and 5 Gd-EOB-DTPA-negative HCCs produced bile. HCCs with Gd-EOB-DTPA uptake overexpressed OATP1B3 compared with HCCs without Gd-EOB-DTPA uptake, and OATP1B3 levels were significantly correlated with ERs (r=0.91, P<0.0001).\n\nQuestion:\nDoes expression of OATP1B3 determine uptake of Gd-EOB-DTPA in hepatocellular carcinoma?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nBackgroung/Aim: Breast cancer resistance protein [BCRP/ATP-binding cassette subfamily G member 2 (ABCG2)] is a member of the ATP-binding cassette transporter family, used as a maker of cancer stem cells (CSCs) and thought to be responsible for drug resistance by pumping them out of cells. However, its precise role in various cancer types has been controversial, and the aim of this study was to investigate the expression of ABCG2 in hepacellular carcinoma (HCC) and relate the results to established prognostic factors. We conducted analysis of 181 HCC and paired-match adjacent normal liver tissue by immunohistochemistry from tissue array of slides. The mean score for ABCG2 expression was higher in tumor than in adjacent normal liver tissue of HCC patients (p<0.001). There was a statistically significant correlation between ABCG2 expression and age, differentiation status and hepatitis B surface antigen (p=0.031, p=0.015 and p=0.033, respectively). Additionally, increased expression of ABCG2 in HCC and its statistically significant correlation with hepatitis B surface antigen was found in elderly (p=0.039), not in younger patients (p=0.518). Importantly, by using Kaplan-Meier and Cox regression analysis, overall survival in patients with high expression of ABCG2 was found reduced in elderly patients (p=0.029 and p=0.081, respectively).\n\nQuestion:\nDoes aBCG2 Overexpression confer Poor Outcomes in Hepatocellular Carcinoma of Elderly Patients?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nPostconditioning (PostC) maneuvers allow post-ischemic accumulation of autacoids, which may trigger protection. Intermittent infusion of either bradykinin or diazoxide during early reperfusion triggered PostC protection via redox signaling. Here we tested whether intermittent adenosine (ADO) may trigger PostC-like cardioprotection. Isolated rat hearts underwent 30 min ischemia and 120 min reperfusion. PostC (5 cycles of 10-s reperfusion/ischemia) or short-term ADO treatment were performed immediately after the 30 min ischemia. Non-selective ADO receptor-antagonist (8-SPT) was infused during PostC maneuvers. Left ventricular pressure was monitored, and infarct size was evaluated by using nitro-blue-tetrazolium staining. In Control hearts after ischemia/reperfusion, infarct size was 64% +/- 4% of risk-area. PostC reduced infarct size to 28% +/- 3% (P < 0.01). PostC protection was abolished by 3 min of the infusion of 8-SPT during PostC maneuvers. Since 3 min of ADO infusion (1 mum or 30 mum) did not trigger PostC protection, protocol with intermittent ADO infusion (5 cycles of 10-s buffer-no-ADO/buffer-plus-ADO) was used to mimic PostC. Also intermittent ADO did not attenuate infarct size (75% +/- 2%; P = NS versus ADO and Control; P < 0.01 versus PostC). Despite disparities on infarct size, post-ischemic systolic function was similar among groups.\n\nQuestion:\nDoes intermittent adenosine at the beginning of reperfusion trigger cardioprotection?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nAtherosclerosis is an inflammatory disease of multifactorial origin, in which immune cells together with metabolic risk factors may initiate, propagate, and activate lesions in the arterial tree. We investigated the role of auto-antibodies against endothelial cells in patients with previous myocardial infarction. One hundred and four patients were studied four to five years after acute myocardial infarction (aged 36-84 years) and 83 sex-matched healthy controls (aged 32-70 years). Anti-endothelial cells IgM and IgG auto-antibodies (AECA) were quantified in plasma using flow cytometry. IgM and IgG AECA were significantly higher (23.08 ± 0.81 and 10.63 ± 0.31 channel shifts, respectively; p < 0.001) in patients as compared to controls (13.40 ± 0.95 and 3.53 ± 0.54 channel shifts, respectively). Further, patients who got an invasive treatment had significantly higher levels of AECA as compared to patients with only medical treatment. Plasma concentration of IgG was positively (p < 0.05) correlated to the levels of high-sensitivity C-reactive protein (hsCRP).\n\nQuestion:\nAre anti-endothelial cell antibodies increased in patients with previous myocardial infarction?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nFollowing tobacco and alcohol, cannabis is the most commonly used substance during pregnancy. Given the high prevalence of concurrent cannabis and tobacco use as well as the health consequences associated with prenatal substance use, we sought to document the relative contributions of psychosocial and psychiatric factors commonly associated with cannabis use in predicting a lifetime cannabis use disorder (CUD) among women who had quit smoking tobacco as a result of pregnancy. Pregnant former tobacco smokers (n=273) enrolled in a larger randomized controlled trial for postpartum tobacco relapse prevention completed semi-structured psychiatric interviews and self-reported demographic, pregnancy, health, psychosocial, and tobacco use factors during their third trimester of pregnancy. In total, 14% (n=38) of women met criteria for a lifetime CUD. The strongest predictors of a lifetime CUD were a history of having multiple psychiatric disorders (OR=36.44; 95% CI=5.03-264.27; p<0.001) followed by a lifetime alcohol use disorder (OR=3.54; 95% CI=1.27-9.87; p<0.05). In addition, more frequent attempts to quit smoking tobacco (OR=1.12; 95% CI=1.01-1.25; p<0.05) and lower self-efficacy about weight management after quitting smoking tobacco (OR=0.78; 95% CI=0.62-0.97; p<0.05) also were significantly associated with a lifetime CUD.\n\nQuestion:\nDoes prevalence and correlate of a lifetime cannabis use disorder among pregnant former tobacco smokers?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nSpecimens of endometrial biopsies can sometimes present with an artifact within blood, composed of optically clear vacuoles mimicking adipose tissue, pseudolipomatosis. This artifact can be mistaken for adipose tissue and lead to an overdiagnosis of uterine perforation. We describe the case of pseudolipomatosis seen within the evacuated products of conception from a missed abortion. Areas of vacuolization in the blood clot mimicked adipose tissue. However, the vacuoles varied in size and did not contain adipocytes.\n\nQuestion:\nDoes pseudolipomatosis in Endometrial Specimens Represent Uterine Perforation?\n\nAnswer:", "role": "user" }, { "content": "no", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo examine the longitudinal relationship between cumulative exposure to anticholinergic medications and memory and executive function in older men. Prospective cohort study. A Department of Veterans Affairs primary care clinic. Five hundred forty-four community-dwelling men aged 65 and older with diagnosed hypertension. The outcomes were measured using the Hopkins Verbal Recall Test (HVRT) for short-term memory and the instrumental activity of daily living (IADL) scale for executive function at baseline and during follow-up. Anticholinergic medication use was ascertained using participants' primary care visit records and quantified as total anticholinergic burden using a clinician-rated anticholinergic score. Cumulative exposure to anticholinergic medications over the preceding 12 months was associated with poorer performance on the HVRT and IADLs. On average, a 1-unit increase in the total anticholinergic burden per 3 months was associated with a 0.32-point (95% confidence interval (CI)= 0.05-0.58) and 0.10-point (95% CI=0.04-0.17) decrease in the HVRT and IADLs, respectively, independent of other potential risk factors for cognitive impairment, including age, education, cognitive and physical function, comorbidities, and severity of hypertension. The association was attenuated but remained statistically significant with memory (0.29, 95% CI=0.01-0.56) and executive function (0.08, 95% CI=0.02-0.15) after further adjustment for concomitant non-anticholinergic medications.\n\nQuestion:\nIs cumulative anticholinergic exposure associated with poor memory and executive function in older men?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe chemokine CCL5 plays a critical role as neutrophil and macrophage activator do in atherosclerosis and myocardial infarction. Thus, we investigated whether the treatment with a neutralizing monoclonal antibody (mAb) to mouse CCL5 would provide therapeutic benefit when provoking a coronary-associated ischaemic event. C57Bl/6 mice were submitted to left coronary artery permanent ligature. Then, various parameters were monitored for up to 21 days. At5 min and 3 days after coronary occlusion, mice received one intravenous injection of the rat anti-mouse CCL5 mAb or isotype IgG control. Infarct size was assessed histologically and by measuring serum cardiac troponin I levels. Kinetics of CCL5 tissue expression, leucocyte infiltration, matrix metalloproteinase (MMP) levels, and collagen deposition were histologically assessed. Serum chemokine levels were measured by enzyme-linked immunosorbent assay. Cardiac function and dimensions were assessed by magnetic resonance imaging (MRI). Chronic ischaemia increased both circulating and intracardiac levels of CCL5. At 24 h, treatment with the anti-CCL5 mAb resulted in a smaller infarct size and reduced circulating levels of chemokines. This effect was associated with reduction of neutrophil and macrophage infiltration within the infarcted myocardium. After 3 days of chronic ischaemia, anti-CCL5 mAb treatment reduced cardiac MMP-9. At 7 days, collagen content was significantly lower. At 21 days, neutralizing CCL5 improved mouse survival, cardiac myocyte size, and cardiac function.\n\nQuestion:\nDoes cC chemokine CCL5 play a central role impacting infarct size and post-infarction heart failure in mice?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nChronic activation of the angiotensin II (AngII) type 1 receptor (AT-1) is a central event in the development of chronic kidney disease (CKD), in part through enhanced expression of TGF-beta, and AT-1 receptor blockade inhibits the progression to CKD in a variety of disease states. The AT-1 receptor is a heptahelical Gaq/11-coupled receptor that initiates phospholipase C activity and release of intracellular calcium; recent data suggest that the AT-1 receptor can also activate the epidermal growth factor receptor (EGFR), although the roles of specific EGF-mediated signaling cascades in AT-1 effects on mesangial cell biology are uncertain. We hypothesized that 2 EGFR-activated pathways, PI3 kinase and MAP kinase, are stimulated by the AT-1 receptor and, in part, regulate the effects of AngII on TGF-beta1 levels in mesangial cells. We examined the effects of AT-1 receptor activation on EGFR, PI3 kinase, and MAP kinase activation in murine mesangial cells. Upon achieving 60-80% confluence, the medium was changed to low-serum for 48 hr and cells were exposed to either the AT-1 receptor blocker, losartan, the EGFR blocker, AG1478, or control medium, and then stimulated with AngII. Similar experiments were performed using LY294002 and U0126, specific inhibitors of PI3 kinase and MEK, respectively. Total cellular protein lysates and RNA were isolated. Activation of the receptors and pathways was evaluated by immunoblotting and levels of TGF-beta mRNA were measured using real-time quantitative RT-PCR. AngII induced autophosphorylation of EGFR (pY1068) and activated Akt and ERK, downstream targets of PI3 kinase and MAP kinase, respectively. AngII-mediated EGFR autophosphorylation was inhibited by losartan and AG1478. AG1478 also inhibited both basal and AngII-mediated activation of Akt and ERK. Finally, AngII-mediated increase in TGF-beta mRNA was inhibited by losartan, AG1478, LY249002, and U0126.\n\nQuestion:\nDoes angiotensin II regulation of TGF-beta in murine mesangial cells involve both PI3 kinase and MAP kinase?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nRetinoic acid (RA), the bioactive derivative of Vitamin A, by epigenetically controlling transcription through the RA-receptors (RARs), exerts a potent antiproliferative effect on human cells. However, a number of studies show that RA can also promote cell survival and growth. In the course of one of our studies we observed that disruption of RA-receptor alpha, RARalpha, abrogates the RA-mediated growth-inhibitory effects and unmasks the growth-promoting face of RA (Ren et al., Mol. Cell. Biol., 2005, 25:10591). The objective of this study was to investigate whether RA can differentially govern cell growth, in the presence and absence of RARalpha, through differential regulation of the \"rheostat\" comprising ceramide (CER), the sphingolipid with growth-inhibitory activity, and sphingosine-1-phosphate (S1P), the sphingolipid with prosurvival activity. We found that functional inhibition of endogenous RARalpha in breast cancer cells by using either RARalpha specific antagonists or a dominant negative RARalpha mutant hampers on one hand the RA-induced upregulation of neutral sphingomyelinase (nSMase)-mediated CER synthesis, and on the other hand the RA-induced downregulation of sphingosine kinase 1, SK1, pivotal for S1P synthesis. In association with RA inability to regulate the sphingolipid rheostat, cells not only survive, but also grow more in response to RA both in vitro and in vivo. By combining genetic, pharmacological and biochemical approaches, we mechanistically demonstrated that RA-induced growth is, at least in part, due to non-RAR-mediated activation of the SK1-S1P signaling.\n\nQuestion:\nDoes disruption of retinoic acid receptor alpha reveal the growth promoter face of retinoic acid?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nSome intestinal flora are known to synthesize folate. The aim of this study was to determine whether folate synthesized by small intestinal flora is assimilated by the human host. Subjects with atrophic gastritis and healthy volunteers were studied before and after omeprazole administration. A double-lumen perfusion tube was placed in the duodenum. 3H-labeled P-aminobenzoic acid, a precursor substrate for bacterial folate synthesis, was perfused. Downstream intestinal aspirates and a 48-hour urine collection were obtained. Atrophic gastritis and omeprazole administration were associated with increases in duodenal pH and in small intestinal flora. Bacterially synthesized folates were isolated from the intestinal aspirates. Tritiated 5-methyltetrahydrofolate, a major metabolite of folate, was isolated from the urine of omeprazole-treated subjects in greater quantities than from drug-free subjects (P<0.01); the quantity of tritiated 5-methyltetrahydrofolate in the urine of the subjects with atrophic gastritis was similarly elevated.\n\nQuestion:\nIs folate synthesized by bacteria in the human upper small intestine assimilated by the host?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe pathogenesis of bilirubin encephalopathy and Alzheimer's disease appears to result from accumulation of unconjugated bilirubin (UCB) and amyloid-beta (Abeta) peptide, respectively, which may cause apoptosis. Permeabilization of the mitochondrial membrane, with release of intermembrane proteins, has been strongly implicated in cell death. Inhibition of the mitochondrial permeability is one pathway by which ursodeoxycholate (UDC) and tauroursodeoxycholate (TUDC) protect against apoptosis in hepatic and nonhepatic cells. In this study, we further characterize UCB- and Abeta-induced cytotoxicty in isolated neural cells, and investigate membrane perturbation during incubation of isolated mitochondria with both agents. In addition, we evaluate whether the anti-apoptotic drugs UDC and TUDC prevent any changes from occurring. Primary rat neuron and astrocyte cultures were incubated with UCB or Abeta peptide, either alone or in the presence of UDC. Apoptosis was assessed by DNA fragmentation and nuclear morphological changes. Isolated mitochondria were treated with each toxic, either alone or in combination with UDC, TUDC, or cyclosporine A. Mitochondrial swelling was measured spectrophotometrically and cytochrome c protein levels determined by Western blot. Incubation of neural cells with both UCB and Abeta induced apoptosis (p < 0.01). Coincubation with UDC reduced apoptosis by > 50% (p < 0.05). Both toxins caused membrane permeabilization in isolated mitochondria (p < 0.001); whereas, pretreatment with UDC was protective (p < 0.05). TUDC was even more effective at preventing matrix swelling mediated by Abeta (p < 0.01). UDC and TUDC markedly reduced cytochrome c release associated with mitochondrial permeabilization induced by UCB and Abeta, respectively (p < 0.05). Moreover, cyclosporine A significantly inhibited mitochondrial swelling and cytochrome c efflux mediated by UCB (p < 0.05).\n\nQuestion:\nDo bilirubin and amyloid-beta peptide induce cytochrome c release through mitochondrial membrane permeabilization?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo determine if shoulder dystocia can be predicted in babies born weighing 3.5 kg or more. A case-control study nested in a perinatal database of 899 mothers and their babies who weighed 3.5 kg or more. All were term pregnancies and delivered vaginally. A case was defined as any baby that encountered shoulder dystocia at delivery. Controls were deliveries over the same period that were not complicated by shoulder dystocia. A logistic regression model was created with macrosomia, parity, previous delivery of more than 3.5 kg, diabetes in pregnancy, prolonged labor, prolonged second stage and instrumental delivery as the independent variables. The adjusted odds ratio and the receiver operator characteristics (ROC) curves were used to see if these variables, both individually and as a model, were associated with or were discriminative enough to predict shoulder dystocia; an ROC curve of more than 0.7 showing good prediction. There were 36 cases of shoulder dystocia during the study period, an incidence of 4%. Previous delivery of more than 3.5 kg, prolonged labor and prolonged second stage were not associated with shoulder dystocia. Although diabetes and instrumental delivery were independently and significantly associated with shoulder dystocia their importance as a predictor became relevant only in the presence of macrosomia.\n\nQuestion:\nIs macrosomia the only reliable predictor of shoulder dystocia in babies weighing 3.5 kg or more?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nRenal osteodystrophy is one of the major complications in patients with chronic renal failure. Large C-PTH fragments are secreted from the parathyroid glands and exert antagonistic actions against PTH-(1-84). The PTH-(1-84)/large C-PTH fragments ratio reflects both biosynthesis and processing of PTH; however the alteration of the ratio under vitamin D therapy has not been investigated. Seventeen hemodialysis patients with intact PTH levels of >300 pg/ml were enrolled. Calcitriol or maxacalcitol were administered intravenously for 78 weeks. Intact PTH, PTH-(1-84), and the PTH-(1-84)/large C-PTH fragments ratio were measured at 0, 13, 26, 52 and 78 weeks. Intact PTH and PTH-(1-84) levels, which were 492.0 +/- 115.7 and 303.4 +/- 105.4 pg/ml, respectively, at baseline, significantly decreased at the end of the study to 268.9 +/- 121.9 (p < 0.0001) and 190.7 +/- 106.9 pg/ml (p = 0.0008), respectively. In contrast, large C-PTH fragments, which were 152.7 +/- 53.5 pg/ml at baseline, did not significantly change at 78 weeks (144.5 +/- 72.2 pg/ml, p = 0.7612). Consequently, the PTH-(1-84)/large C-PTH fragments ratio was significantly reduced from 2.25 +/- 1.31 to 1.47 +/- 0.89 (p = 0.0004).\n\nQuestion:\nDoes intravenous vitamin D therapy reduce PTH- ( 1-84 ) /large C fragments ratio in chronic hemodialysis patients?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nA disease resembling the human spondylarthropathies develops in HLA-B27-transgenic rats. This disease in rats is mediated by CD4+ T cells, but antigen-presenting cells (APCs) may also play a role. Dendritic cells (DCs) have been reported to be defective in allogeneic mixed lymphocyte culture in this model. Here, we further investigated the functional defect of APCs. DCs and B cells from nontransgenic, HLA-B27 (33-3)-transgenic, and HLA-B7 (120-4)-transgenic rats were used to stimulate T cells. Surface expression of HLA-B transgene and rat molecules on APCs and the formation of conjugates between DCs and T cells were monitored by flow cytometry. We observed a strikingly defective stimulation of allogeneic and syngeneic T lymphocytes by APCs from HLA-B27 but not HLA-B7 rats, even if stimulation was driven in the presence of anti-T cell receptor (TCR) antibody. We found no evidence that HLA-B27 DCs were immature, lacked production of some diffusible factor, or produced an inhibitory factor for T cells. When comparing the levels of expression of class II major histocompatibility complex, CD2, intercellular adhesion molecule 1, lymphocyte function-associated antigen 1, B7, and CD40 molecules at the surface of DCs from 33-3, 120-4, and nontransgenic rats, we found little difference. However, HLA-B27-transgenic DCs formed fewer conjugates with T cells than did nontransgenic DCs. Furthermore, the proportion of conjugates formed between DCs and T cells, as well as the difference between nontransgenic and HLA-B27-transgenic DCs, were in large part reduced by blocking CD86 on DCs.\n\nQuestion:\nIs defective costimulatory function a striking feature of antigen-presenting cells in an HLA-B27-transgenic rat model of spondylarthropathy?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nThe worldwide epidemic of obesity is a major public health concern and is persuasively linked to the rising prevalence of diabetes and cardiovascular disease. Obesity is often associated with an abnormal lipoprotein profile, which may be partly negated by pioglitazone intervention, as this can influence the composition and oxidation characteristics of low-density lipoprotein (LDL). However, as pioglitazone's impact on these parameters within high-density lipoprotein (HDL), specifically HDL(2&3), is absent from the literature, this study was performed to address this shortcoming. Twenty men were randomized to placebo or pioglitazone (30 mg/day) for 12 weeks. HDL(2&3) were isolated by rapid-ultracentrifugation. HDL(2&3)-cholesterol and phospholipid content were assessed by enzymatic assays and apolipoprotein AI (apoAI) content by single-radial immunodiffusion. HDL(2&3) oxidation characteristics were assessed by monitoring conjugated diene production and paraoxonase-1 activity by spectrophotometric assays. Compared with the placebo group, pioglitazone influenced the composition and oxidation potential of HDL(2&3). Specifically, total cholesterol (P < 0.05), phospholipid (P < 0.001) and apoAI (P < 0.001) were enriched within HDL(2). Furthermore, the resistance of HDL(2&3) to oxidation (P < 0.05) and the activity of paroxonase-1 were also increased (P < 0.001).\n\nQuestion:\nDoes pioglitazone protect HDL ( 2 & 3 ) against oxidation in overweight and obese men?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo investigate the expressions of Galectin-3 (Gal-3), Bcl-2 and Bax in human pituitary adenomas, and to explore the interrelation among them. RT-PCR and immunohistochemistry were applied to detect the mRNA and protein expressions of Gal-3, Bcl-2 and Bax in surgically excised human pituitary adenoma tissues, including invasive and non-invasive pituitary adenomas, and the correlation analysis was performed. The Gal-3 and Bcl-2 expressions in the invasive pituitary group were significantly higher than those in the non-invasive group, and the expression of Bax had no significant difference between the two groups. Pearsonos correlation analyses showed that the Gal-3 expression was positively correlated with Bcl-2, but was not correlated with Bax, which was inversely correlated with expression of Bcl-2.\n\nQuestion:\nDoes expression of galectin-3 correlate with apoptosis in pituitary adenoma cells?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nHeat shock protein 70 (HSP70) was previously found to be highly expressed in cervical squamous cell carcinoma (SCC) tissues compared with normal tissues by proteomic analyses. The present study investigated the roles of HSP70 in malignant behaviors and chemosensitivity to cisplatin in cervical SCC cells in vitro. Effects of HSP70 knockdown on activities of cell migration, cell invasion and cell proliferation, cell cycle status, and apoptosis were examined using siRNA in two human cervical cancer cells (SiHa and SKG II). Furthermore, the effect of HSP70 knockdown on the apoptotic effect by cisplatin was examined. HSP70 knockdown significantly suppressed activities of cell migration, cell invasion and cell proliferation. The cell cycle was arrested at the S- and G2/M-phases with the increase in apoptosis by HSP70 knockdown. Although cisplatin had no apoptotic effect in the control cell, it showed a dose-dependent apoptotic effect in the HSP70 knockdown cells in SiHa. In SKG II, 5 μg/mL of cisplatin induced apoptosis, and the apoptotic effect by cisplatin was enhanced by HSP70 knockdown.\n\nQuestion:\nIs heat shock protein 70 involved in malignant behaviors and chemosensitivities to cisplatin in cervical squamous cell carcinoma cells?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nEndothelial progenitor cells (EPCs) play an important role in tissue repairing and regeneration in ischemic organs, including the brain. However, the cause of EPC migration and the function of EPCs after ischemia are unclear. In this study, we demonstrated the effects of EPCs on ischemic brain injury in a mouse model of transient middle cerebral artery occlusion (tMCAO). Circulating human EPCs were characterized with immunofluorescent staining and flow cytometry. EPCs (1 x 10(6)) were injected into nude mice after 1 hour of tMCAO. Histological analysis and behavioral tests were performed from day 0 to 28 days after tMCAO. EPCs were detected in ischemic brain regions 24 hours after tMCAO. EPC transplantation significantly reduced ischemic infarct volume at 3 days after tMCAO compared with control animals (p < 0.05). CXCR4 was expressed in the majority of EPCs, and stromal-derived factor-1 (SDF-1) induced EPC migration, which was blocked by pretreated EPCs with AMD3100 in vitro. SDF-1 was upregulated in ischemic brain. Compared with control animals, injecting AMD3100-pretreated EPCs resulted in a larger infarct volume 3 days after tMCAO, suggesting that SDF-1-mediated signaling was involved in EPC-mediated neuroprotection. In addition, EPC transplantation reduced mouse cortex atrophy 4 weeks after tMCAO and improved neurobehavioral outcomes (p < 0.05). EPC injection potently increased angiogenesis in the peri-infarction area (p < 0.05).\n\nQuestion:\nDoes endothelial progenitor cell transplantation improve long-term stroke outcome in mice?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nTo evaluate the role of a positive BTA stat Test result in patients with negative cystoscopic findings. Five hundred one consecutive patients in follow-up for bladder cancer were studied. A voided urine sample was obtained before cystoscopy and split for culture, cytology, and BTA stat testing. In the case of a positive BTA stat Test, but negative cystoscopic findings, patients underwent additional investigations. Of 501 patients, 133 (26.5%) had bladder cancer recurrence at cystoscopy, of which the BTA stat Test detected 71 (53.4%); only 21 of the cases (17.9%) were detected by cytologic examination. Of the remaining 368 patients with no visible tumor at cystoscopy, 96 (26.1%) had a positive BTA stat Test result. Fifty-five of those (57.3%) underwent intravenous urography or renal ultrasound and random biopsies, and an additional 9 recurrences (16.4%) were detected. Of those 46 patients who had a true false-positive BTA stat Test, 3 (3 of 43, 7.0%) had recurrence at the next follow-up cystoscopy, 4 (8.7%) had a urine infection, and 8 (17.4%) had ongoing intravesical instillations; the latter two percentages were significantly higher than among those with true-negative BTA stat Test results (0% and 6.8%, respectively).\n\nQuestion:\nDoes analysis of false-positive BTA STAT test result in patients followed up for bladder cancer?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]

[ { "content": "Given a question, a reference context and an answer, the goal is to answer the question given the reference context. The label is within the category of yes, no, or maybe.\n\nContext:\nDifferent microarray studies have compiled gene lists for predicting outcomes of a range of treatments and diseases. These have produced gene lists that have little overlap, indicating that the results from any one study are unstable. It has been suggested that the underlying pathways are essentially identical, and that the expression of gene sets, rather than that of individual genes, may be more informative with respect to prognosis and understanding of the underlying biological process. We sought to examine the stability of prognostic signatures based on gene sets rather than individual genes. We classified breast cancer cases from five microarray studies according to the risk of metastasis, using features derived from predefined gene sets. The expression levels of genes in the sets are aggregated, using what we call a set statistic. The resulting prognostic gene sets were as predictive as the lists of individual genes, but displayed more consistent rankings via bootstrap replications within datasets, produced more stable classifiers across different datasets, and are potentially more interpretable in the biological context since they examine gene expression in the context of their neighbouring genes in the pathway. In addition, we performed this analysis in each breast cancer molecular subtype, based on ER/HER2 status. The prognostic gene sets found in each subtype were consistent with the biology based on previous analysis of individual genes.\n\nQuestion:\nDoes prediction of breast cancer prognosis using gene set statistics provide signature stability and biological context?\n\nAnswer:", "role": "user" }, { "content": "yes", "role": "assistant" } ]