tbuckley/cabot-search huggingface dataset:
Reduced lung function and risk of atrial fibrillation in The Copenhagen City Heart Study
Authors: P. Buch, J. Friberg, H. Scharling, P. Lange, E. Prescott
Journal: European Respiratory Journal (2003)

Chronic obstructive pulmonary disease has been associated with a high frequency of arrhythmias. Few studies have analysed the role of reduced lung function in predicting atrial fibrillation (AF). The aim of the present study was to investigate the relationship between forced expiratory volume in one second (FEV 1 ) and risk of first episode of AF in a prospective study. Data from 13,430 males and females without previous myocardial infarction, who participated in the Copenhagen City Heart Study, were analysed. New AF was assessed at re-examination after 5 yrs and by hospital admission for AF during a period of 13 yrs. Multivariate analyses were used with adjustment for cardiopulmonary risk factors. There were 62 new cases of AF at 5-yr follow-up (0.58%) and 290 cases (2.20%) diagnosed at hospitalisations. Risk of new AF at re-examination was 1.8-times higher for FEV 1 between 60–80% of predicted compared with FEV 1 ≥80% after adjustment for sex, age, smoking, blood pressure, diabetes and body mass index. The risk of AF hospitalisation was 1.3-times higher for FEV 1 between 60–80% and 1.8-times higher for FEV 1 &lt;60% compared with FEV 1 ≥80%, when additional adjustment was made for education, treatment with diuretics and chest pain at activity. The authors conclude that reduced lung function is an independent predictor for incident atrial fibrillation.
Association Between Sodium Intake and Change in Uric Acid, Urine Albumin Excretion, and the Risk of Developing Hypertension
Authors: John P. Forman, Lieneke Scheven, Paul E. de Jong, Stephan J.L. Bakker, Gary C. Curhan, Ron T. Gansevoort
Journal: Circulation (2012)

A high-sodium diet has little short-term effect on blood pressure in nonhypertensive individuals but, for unclear reasons, is associated with hypertension if consumed long term. We hypothesized that a chronically high sodium intake would be associated with increases in biomarkers of endothelial dysfunction, specifically serum uric acid (SUA) and urine albumin excretion (UAE), and that high sodium intake would be associated with incident hypertension among those with higher SUA and UAE.We prospectively analyzed the associations between sodium intake and the change in SUA (n=4062) and UAE (n=4146) among participants of the Prevention of Renal and Vascular End Stage Disease (PREVEND) study who were not taking antihypertensive medications. We also examined the association of sodium intake with the incidence of hypertension (n=5556) among nonhypertensive participants. After adjustment for confounders, each 1-g-higher sodium intake was associated with a 1.2-μmol/L increase in SUA (P=0.01) and a 4.6-mg/d increase in UAE (P<0.001). The relation between sodium intake and incident hypertension varied according to SUA and UAE. For each 1-g-higher sodium intake, the adjusted hazard ratio for developing hypertension was 0.98 (95% confidence interval, 0.89-1.08) among those in the lowest tertile of SUA and 1.09 (1.02-1.16) among those in the highest tertile. Corresponding hazard ratios were 0.99 (confidence interval, 0.93-1.06) among participants whose UAE was <10 mg/d and 1.18 (confidence interval, 1.07-1.29) among those whose UAE was >15 mg/d.Over time, higher sodium intake is associated with increases in SUA and UAE. Among individuals with higher SUA and urine UAE, a higher sodium intake is an independent risk factor for developing hypertension.
Involvement of Oxidative Stress–Induced DNA Damage, Endoplasmic Reticulum Stress, and Autophagy Deficits in the Decline of β-Cell Mass in Japanese Type 2 Diabetic Patients
Authors: Hiroki Mizukami, Kazunori Takahashi, Wataru Inaba, Kentaro Tsuboi, Sho Osonoi, Taro Yoshida, Soroku Yagihashi
Journal: Diabetes Care (2014)

Deficits of β-cells characterize the islet pathology in type 2 diabetes. It is yet to be clear how the β-cell loss develops in type 2 diabetes. We explored the implication of oxidative stress, endoplasmic reticulum (ER)-induced stress, and autophagy deficit in the β-cell decline in Japanese type 2 diabetic patients.Pancreases from recent autopsy cases of 47 type 2 diabetic and 30 nondiabetic subjects were investigated on the islet structure with morphometric analysis. Volume densities of islet (Vi), β-cell (Vβ), and α-cell (Vα) were measured. To evaluate cell damage of endocrine cells, immunohistochemical expressions of oxidative stress-related DNA damage as expressed by γH2AX, ER stress-related cell damage as CCAAT/enhancer 1 binding protein-β (C/EBP-β), and autophagy deficit as P62 were semiquantified, and their correlations to islet changes were sought.Compared with nondiabetic subjects, Vβ was reduced in diabetic subjects. Contrariwise, there was an increase in Vα. There was a significant link between reduced Vβ and increased HbA1c levels (P < 0.01) and a trend of inverse correlation between Vβ and duration of diabetes (P = 0.06). Expressions of γH2AX, P62, and C/EBP-β were all enhanced in diabetic islets, and reduced Vβ correlated with the intensity of γH2AX expression but not with C/EBP-β or P62 expressions. Combined expressions of γH2AX, P62, and C/EBP-β were associated with severe reduction of Vβ.β-Cell deficit in type 2 diabetes was associated with increased oxidative stress and may further be augmented by autophagic deficits and ER stress.
The dilemma of Morbid Obesity
Authors: T. B. Van Itallie
Journal: JAMA (1981)

A NATIONWIDE survey in the United States completed in 1974 has shown that 15% of men and 25% of women aged 20 to 74 years were 20% or more overweight, based on standards derived from a representative population aged 20 to 29 years.<sup>1</sup>Among women aged 55 to 64 years, 35% were similarly overweight. The same survey showed that 5% of men and 7% of women were "severely" obese (ie, with a body fat content, determined by skinfold thickness, greater than the 95th percentile for men and nonpregnant women aged 20 to 29 years). When this criterion was applied to body weight, it was found that the severely obese men were 30% or more above average weight for their height and age, while the severely obese women were 50% or more above average weight. Of this subset, between 8% and 10% (about 600,000 people) had a body weight twice
A VIRAL AGENT ISOLATED FROM A CASE OF "NON-PARALYTIC POLIOMYELITIS" AND PATHOGENIC FOR SUCKLING MICE: ITS POSSIBLE RELATION TO THE COXSACKIE GROUP OF VIRUSES
Authors: F. Sargent Cheever, Joan B. Daniels, E. Freeman Hersey
Journal: The Journal of Experimental Medicine (1950)

1. A viral agent, Powers, causing myocarditis, adipositis, pancreatitis, hepatitis, and encephalomyelitis but not myositis in suckling mice 1 to 2 days old has been isolated from the stool of a patient in whom the clinical diagnosis was "non-paralytic poliomyelitis." 2. Serological evidence linking the virus to the clinical disease observed was clear only in the case of "non-paralytic poliomyelitis" from which it was isolated. 3. The possible relation of this agent to the Coxsackie group of viruses is discussed. No serological relationship with the Connecticut 5, Ohio R, and High Point strains was demonstrated. 4. A second virus, Matulaitis, has been isolated from a concurrent case of "non-paralytic poliomyelitis" in the same area. Lesions produced in infant mice by the two agents show certain differences.
Pneumocystis carinii pneumonia with pleurisy, platypnoea and orthodeoxia
Authors: P N Newton
Journal: Thorax (2003)

We present a patient who collapsed with chest pain and dyspnoea on a transatlantic flight. She was found to have Pneumocystis carinii pneumonia (PCP) and human immunodeficiency virus infection. Platypnoea and orthodeoxia, which have not been previously reported in association with PCP, were major features of her illness. The PCP predominantly affected her lung bases and it is likely that gravity increased intrapulmonary blood flow through poorly ventilated lung bases with failure of pulmonary vasoconstriction to increase upper zone perfusion, exacerbating desaturation on sitting up. The partial DNA sequence of the infecting P carinii was identical to previously described isolates.
Prevention of fetal loss in experimental antiphospholipid syndrome by in vivo administration of recombinant interleukin-3.
Authors: P Fishman, E Falach-Vaknine, R Zigelman, R Bakimer, B Sredni, M Djaldetti, Y Shoenfeld
Journal: Journal of Clinical Investigation (1993)

Antiphospholipid antibodies are strongly associated with arte- rial and venous thrombosis and with fetal loss.Recently an experimental model for antiphospholipid syndrome (APLS) was established in our laboratory.In this model, mice are immu- nized passively or actively with anticardiolipin antibodies and acquire the syndrome, which is characterized by prolonged ac- tivated partial thromboplastin time (APTT), thrombocytopenia, low fecundity rate, and fetal loss.In a normal process of pregnancy, lymphokines affect fetal implantation and development.Cytokines from the colony stim- ulating factor family, like GM-CSF and IL-3, were shown to be positive signals for implantation and to promote placental devel- opment and fetal growth.Given our preliminary findings of low IL-3 in mice with APLS and the efficacy of IL-3 in preventing fetal loss in a strain of mice prone to fetal resorption, our aim in the present study was to examine the effect of murine recombinant IL-3 (mrIL-3) on pregnant mice induced with experimental APLS.Mice were passively transfused to the tail vein, 24 h following mating, with anticardiolipin antibodies.The mice were divided into two groups: one group was injected intraperitoneally with mrIL-3 on days 6.5, 8.5, and 10.5 after mating, while the con- trol group was injected with PBS.When the mice were killed on day 15 of pregnancy a 32%±4.2resorption rate was observed in the anti-cardiolipin-immunized group, which was reduced to 4%±0.3 following treatment with mrIL-3.The thrombocyto- penia associated with the experimental APLS was also corrected following lymphokine administration.IL-3 may be effective in prevention of recurrent fetal loss in APLS.(
Smokers with the<i>CHRNA</i>Lung Cancer–Associated Variants Are Exposed to Higher Levels of Nicotine Equivalents and a Carcinogenic Tobacco-Specific Nitrosamine
Authors: Loïc Le Marchand, Kiersten S. Derby, Sharon E. Murphy, Stephen S. Hecht, Dorothy Hatsukami, Steven G. Carmella, Maarit Tiirikainen, Hansong Wang
Journal: Cancer Research (2008)

Abstract A locus at 15q24/15q25.1, which includes the nicotinic acetylcholine receptor A subunits 3 and 5 (CHRNA3 and CHRNA5) genes, has recently been associated with lung cancer risk, self-reported number of cigarettes smoked per day, and a nicotine dependence scale. It is not clear whether the association with lung cancer is direct or mediated through differences in smoking behavior. We used urinary biomarkers to test whether two linked lung cancer risk variants in CHRNA3 (rs1051730) and CHRNA5 (rs16969968) are associated with intensity of smoking and exposure to a tobacco-specific carcinogenic nitrosamine per cigarette dose. We studied 819 smokers and found that carriers of these variants extract a greater amount of nicotine (P = 0.003) and are exposed to a higher internal dose of 4-(methylnitrosamino)-I-(3-pyridyl)-1-butanone (P = 0.03) per cigarette than noncarriers. Thus, smokers who carry the CHRNA3 and CHRNA5 variants are expected to be at increased risk for lung cancer compared with smokers who do not carry these alleles even if they smoked the same number of cigarettes. Number of cigarettes per day, even if it could be accurately assessed, is not an adequate measure of smoking dose. [Cancer Res 2008;68(22):9137–40]
Myocardial Ischemia/Reperfusion Injury in NADPH Oxidase–Deficient Mice
Authors: Michaela R. Hoffmeyer, Steven P. Jones, Christopher R. Ross, Brent Sharp, Matthew B. Grisham, F. Stephen Laroux, Timothy J. Stalker, Rosario Scalia, David J. Lefer
Journal: Circulation Research (2000)

Abstract —Previous studies have suggested that oxygen-derived free radicals are involved in the pathophysiology of myocardial ischemia/reperfusion (MI/R) injury. Specifically, neutrophils have been shown to mediate postischemic ventricular arrhythmias and myocardial necrosis. We hypothesized that MI/R injury would be reduced in the absence (−/−) of NADPH oxidase. Heterozygous control mice (n=23) and NADPH oxidase –/– mice (n=24) were subjected to 30 minutes of coronary artery occlusion and 24 hours of reperfusion. Myocardial area at risk per left ventricle was similar in heterozygous control hearts (55±3%) and NADPH oxidase –/– hearts (61±4%). Contrary to our hypothesis, the size of infarct area at risk was similar in the heterozygous control mice (42±4%) and NADPH oxidase –/– mice (34±5%) ( P =not significant). In addition, echocardiographic examination of both groups revealed that left ventricle fractional shortening was similar in NADPH oxidase –/– mice (n=8; 27±2.5%) and heterozygous control mice (n=10; 23.3±3.3%) after MI/R. Superoxide production, as detected by cytochrome c reduction, was significantly impaired ( P &lt;0.01) in NADPH oxidase –/– mice (n=6) compared with heterozygous mice (n=7) (0.04±0.03 versus 2.2±0.08 nmol O 2 ·min –1 ·10 6 cells –1 ). Intravital microscopy of the inflamed mesenteric microcirculation demonstrated that leukocyte rolling and adhesion were unaffected by the absence of NADPH oxidase. Oyster glycogen-stimulated neutrophil transmigration into the peritoneum was also similar in both the heterozygous control mice and NADPH oxidase –/– mice ( P =not significant). These findings suggest that NADPH oxidase does not contribute to the development of myocardial injury and dysfunction after MI/R.
Epidemiological, clinical and histological evaluation of HCV serotypes in the patients with chronic HCV infection
Authors: S. Pavic, N. Svirtlih, J. Simonovic, Lj. Jemuovic, M. Bozic, Lj. Dokic, M. Diordjevic, P. Nikolic, S. Zerjav, I. Boricic
Journal: Journal of Hepatology (2000)
Prone Position in Acute Respiratory Distress Syndrome. Rationale, Indications, and Limits
Authors: Luciano Gattinoni, Paolo Taccone, Eleonora Carlesso, John J. Marini
Journal: American Journal of Respiratory and Critical Care Medicine (2013)

Section:ChooseTop of pageAbstract <<PathophysiologyProne Positioning and Ven...Clinical EvidenceConclusionsReferencesCITING ARTICLES
Racial and Ethnic Disparities in Patient-Provider Communication, Quality-of-Care Ratings, and Patient Activation Among Long-Term Cancer Survivors
Authors: Nynikka R.A. Palmer, Erin E. Kent, Laura P. Forsythe, Neeraj K. Arora, Julia H. Rowland, Noreen M. Aziz, Danielle Blanch-Hartigan, Ingrid Oakley-Girvan, Ann S. Hamilton, Kathryn E. Weaver
Journal: Journal of Clinical Oncology (2014)

We examined racial and ethnic disparities in patient-provider communication (PPC), perceived care quality, and patient activation among long-term cancer survivors.In 2005 to 2006, survivors of breast, prostate, colorectal, ovarian, and endometrial cancers completed a mailed survey on cancer follow-up care. African American, Asian/Pacific Islander (Asian), Hispanic, and non-Hispanic white (white) survivors who had seen a physician for follow-up care in the past 2 years (n = 1,196) composed the analytic sample. We conducted linear and logistic regression analyses to identify racial and ethnic differences in PPC (overall communication and medical test communication), perceived care quality, and patient activation in clinical care (self-efficacy in medical decisions and perceived control). We further examined the potential contribution of PPC to racial and ethnic differences in perceived care quality and patient activation.Compared with white survivors (mean score, 85.16), Hispanic (mean score, 79.95) and Asian (mean score, 76.55) survivors reported poorer overall communication (P = .04 and P < .001, respectively), and Asian survivors (mean score, 79.97) reported poorer medical test communication (P = .001). Asian survivors were less likely to report high care quality (odds ratio, 0.47; 95% CI, 0.30 to 0.72) and reported lower self-efficacy in medical decisions (mean score, 74.71; P < .001) compared with white survivors (mean score, 84.22). No disparity was found in perceived control. PPC was positively associated with care quality (P < .001) and self-efficacy (P < .001). After adjusting for PPC and other covariates, when compared with whites, Asian disparities remained significant.Asian survivors report poorer follow-up care communication and care quality. More research is needed to identify contributing factors beyond PPC, such as cultural influences and medical system factors.
Atrogin-1 and MuRF1 regulate cardiac MyBP-C levels via different mechanisms
Authors: Giulia Mearini, Christina Gedicke, Saskia Schlossarek, Christian C. Witt, Elisabeth Krämer, Peirang Cao, Marcelo D. Gomes, Stewart H. Lecker, Siegfried Labeit, Monte S. Willis, Thomas Eschenhagen, Lucie Carrier
Journal: Cardiovascular Research (2009)

AimsFamilial hypertrophic cardiomyopathy (FHC) is frequently caused by cardiac myosin-binding protein C (cMyBP-C) gene mutations, which should result in C-terminal truncated mutants. However, truncated mutants were not detected in myocardial tissue of FHC patients and were rapidly degraded by the ubiquitin-proteasome system (UPS) after gene transfer in cardiac myocytes. Since the diversity and specificity of UPS regulation lie in E3 ubiquitin ligases, we investigated whether the muscle-specific E3 ligases atrogin-1 or muscle ring finger protein-1 (MuRF1) mediate degradation of truncated cMyBP-C.
Angiogenic Acceleration of Neu Induced Mammary Tumor Progression and Metastasis
Authors: Robert G. Oshima, Jacqueline Lesperance, Varinia Munoz, Lionel Hebbard, Barbara Ranscht, Niki Sharan, William J. Muller, Craig A. Hauser, Robert D. Cardiff
Journal: Cancer Research (2004)

The Neu (ErbB2, HER2) member of the epidermal growth factor receptor family is implicated in many human breast cancers. We have tested the importance of increased angiogenic signaling in the NeuYD [mouse mammary tumor virus (MMTV)-Neu(ndl)-YD5] mammary tumor model. Transgenic mice expressing vascular endothelial growth factor (VEGF)(164) from the MMTV promoter were generated. These mice expressed VEGF(164) RNA and protein at 20- to 40-fold higher levels throughout mammary gland development but exhibited normal mammary gland development and function. However, in combination with the NeuYD oncogene, VEGF(164) expression resulted in increased vascularization of hyperplastic mammary epithelium and dramatic acceleration of tumor appearance from 111 to 51 days. Gene expression profiling also indicated that the VEGF-accelerated tumors were substantially more vascularized and less hypoxic. The preferential vascularization of early hyperplastic portions of mammary epithelia in NeuYD;MMTV-VEGF animals was associated with NeuYD RNA expression, disorganization of the tight junctions, and overlapping transgenic VEGF expression. NeuYD;MMTV-VEGF(164) bigenic, tumor-bearing animals resulted in an average of 10 tumor cell colonies/lung lodged within vascular spaces. No similar lung colonies were found in control NeuYD mice with similar tumor burdens. Overall, these results demonstrate the angiogenic restriction of early hyperplastic mammary lesions. They also reinforce in vivo the importance of activated Neu in causing disorganization of mammary luminal epithelial cell junctions and provide support for an invasion-independent mechanism of metastasis.
Genetically modified plants and human health
Authors: Suzie Key, Julian K-C Ma, Pascal MW Drake
Journal: Journal of the Royal Society of Medicine (2008)

Summary Genetically modified (or GM) plants have attracted a large amount of media attention in recent years and continue to do so. Despite this, the general public remains largely unaware of what a GM plant actually is or what advantages and disadvantages the technology has to offer, particularly with regard to the range of applications for which they can be used. From the first generation of GM crops, two main areas of concern have emerged, namely risk to the environment and risk to human health. As GM plants are gradually being introduced into the European Union there is likely to be increasing public concern regarding potential health issues. Although it is now commonplace for the press to adopt ‘health campaigns’, the information they publish is often unreliable and unrepresentative of the available scientific evidence. We consider it important that the medical profession should be aware of the state of the art, and, as they are often the first port of call for a concerned patient, be in a position to provide an informed opinion. This review will examine how GM plants may impact on human health both directly – through applications targeted at nutrition and enhancement of recombinant medicine production – but also indirectly, through potential effects on the environment. Finally, it will examine the most important opposition currently facing the worldwide adoption of this technology: public opinion.
Detection of DNA Copy Number Changes and Oncogenic Signaling Abnormalities from Gene Expression Data Reveals <i>MYC</i> Activation in High-Grade Papillary Renal Cell Carcinoma
Authors: Kyle A. Furge, Jindong Chen, Julie Koeman, Pamela Swiatek, Karl Dykema, Kseniji Lucin, Richard Kahnoski, Ximing J. Yang, Bin Tean Teh
Journal: Cancer Research (2007)

Abstract Papillary renal cell carcinoma (RCC) represents 10% to 15% of adult renal neoplasms; however, the molecular genetic events that are associated with the development and progression of sporadic papillary RCC remain largely unclear. Papillary RCCs can be divided into two subtypes based on histologic, cytogenetic, and gene expression differences. Type 1 tumors (∼60–70%) are generally low grade with favorable outcome, whereas type 2 tumors (∼30–40%) are associated with increased cytogenetic complexity, high tumor grade, and poor prognosis. In this study, computational analysis of gene expression data derived from papillary RCC revealed that a transcriptional signature indicative of MYC pathway activation is present in high-grade type 2 papillary RCC. The MYC signature is associated with amplification of chromosome 8q and overexpression of MYC that maps to chromosome 8q24. The importance of MYC activation was confirmed by both pharmacologic and short interfering RNA–mediated inhibition of active Myc signaling in a cell line model of type 2 papillary RCC. These results provide both computational and genetic evidence that activation of Myc is associated with the aggressiveness of papillary type 2 RCC. Therefore, it will be useful to consider inhibition of components of the MYC signaling pathway as avenues for therapeutic intervention in high-grade papillary RCC. [Cancer Res 2007;67(7):3171–6]