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Caroline E. Dale Jaroslav A. Hubacek Tom M. Palmer Hynek Pikhart Anne Peasey Annie Britton Pia Horvat Ruzena Kubinova Sofia Malyutina Andrzej Pajak Abdonas Tamosiunas Aparna Shankar Archana Singh‐Manoux Mikhail Voevoda Mika Kivimaki Aroon D. Hingorani Michael G. Marmot Juan P. Casas Martin Bobak 《Addiction (Abingdon, England)》2014,109(9):1462-1471
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Michael V. Holmes Ruth Frikke-Schmidt Daniela Melis Robert Luben Folkert W. Asselbergs Jolanda M.A. Boer Jackie Cooper Jutta Palmen Pia Horvat Jorgen Engmann Ka-Wah Li N. Charlotte Onland-Moret Marten H. Hofker Meena Kumari Brendan J. Keating Jaroslav A. Hubacek Vera Adamkova Ruzena Kubinova Martin Bobak Kay-Tee Khaw Børge G. Nordestgaard Nick Wareham Steve E. Humphries Claudia Langenberg Anne Tybjaerg-Hansen Philippa J. Talmud 《Atherosclerosis》2014
Background
Conflicting evidence exists on whether smoking acts as an effect modifier of the association between APOE genotype and risk of coronary heart disease (CHD).Methods and results
We searched PubMed and EMBASE to June 11, 2013 for published studies reporting APOE genotype, smoking status and CHD events and added unpublished data from population cohorts. We tested for presence of effect modification by smoking status in the relationship between APOE genotype and risk of CHD using likelihood ratio test.In total 13 studies (including unpublished data from eight cohorts) with 10,134 CHD events in 130,004 individuals of European descent were identified. The odds ratio (OR) for CHD risk from APOE genotype (ε4 carriers versus non-carriers) was 1.06 (95% confidence interval (CI): 1.01, 1.12) and for smoking (present vs. past/never smokers) was OR 2.05 (95%CI: 1.95, 2.14). When the association between APOE genotype and CHD was stratified by smoking status, compared to non-ε4 carriers, ε4 carriers had an OR of 1.11 (95%CI: 1.02, 1.21) in 28,789 present smokers and an OR of 1.04 (95%CI 0.98, 1.10) in 101,215 previous/never smokers, with no evidence of effect modification (P-value for heterogeneity = 0.19). Analysis of pack years in individual participant data of >60,000 with adjustment for cardiovascular traits also failed to identify evidence of effect modification.Conclusions
In the largest analysis to date, we identified no evidence for effect modification by smoking status in the association between APOE genotype and risk of CHD. 相似文献4.
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Bobak M Pikhart H Kubinova R Malyutina S Pajak A Sebakova H Topor-Madry R Nikitin Y Caan W Marmot M 《Occupational and environmental medicine》2005,62(8):546-550
Background: Psychosocial factors at work are thought to influence health partly through health behaviours. Aims: To examine the association between effort-reward imbalance and job control and several alcohol related measures in three eastern European populations. Methods: A cross-sectional study was conducted in Novosibirsk (Russia), Krakow (Poland), and Karvina (Czech Republic). The participants completed a questionnaire that included effort-reward at work, job control, and a number of sociodemographic variables. Annual alcohol intake, annual number of drinking sessions, the mean dose of alcohol per drinking session, and binge drinking (⩾80 g of ethanol in one session at least once a week) were based on graduated frequencies in the questionnaire. Data were also available on problem drinking (⩾2 positive answers on CAGE questionnaire) and negative social consequences of drinking. All male participants in full employment (n = 694) were included in the present analyses. Results: After controlling for age and centre, all indices of alcohol consumption and problem drinking were associated with the effort-reward ratio. Adjustment for material deprivation did not change the results but adjustment for depressive symptoms reduced the estimated effects. Job control was not associated with any of the alcohol related outcomes. Conclusions: The imbalance of effort-reward at work is associated with increased alcohol intake and problem drinking. The association appears to be partly mediated by depressive symptoms, which might be either an antecedent or a consequence of men''s drinking behaviour. 相似文献
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Rosolova H Cech J Simon J Spinar J Jandova R Widimský sen J Holubec L Topolcan O 《European journal of heart failure》2005,7(5):780-783
BACKGROUND AND AIM: The European Society of Cardiology initiated the EuroHeart Failure Survey to obtain more data about the quality of care in patients hospitalised with suspected heart failure (HF). The Czech Republic was 1 of the 24 European Society countries included in the survey. The aim of this report is to extend the original follow-up period of 12 weeks out to 4 years to assess mortality. METHODS: All admitted patients were screened according to the EuroHeart Survey Protocol, over a 6-week period in six hospitals in Pilsen, Prague and Brno in the year 2000. Annual mortality and cause of death were obtained from the Prague Institute for Health Statistical Information (UZIS Praha). RESULTS: A total of 2365 patients were screened and about 25% of all admitted patients fulfilled the criteria for HF. About 14% of patients died between admission and the 12-week follow-up, 36% of male and 42% of female patients died during the 4-year follow-up (2000-2003). Cardiovascular diseases were the main causes of death (92%). Deceased patients were significantly older, had lower haemoglobin and total plasma cholesterol level, and had renal insufficiency and higher levels of big endothelin and BNP than the survivors. Mortality risk was increased independently by positive history of previous myocardial infarction OR=2.39 (1.59-3.59), by age OR=1.03 (1.01-1.05) and by plasma creatinine level OR=1.04 (1.01-1.07). Treatment with diuretics and digoxin was associated with a higher risk of death; by contrast, a protective effect of beta-blockers and statins was found in these HF patients. CONCLUSION: Patients with HF were older and had a poor prognosis; approximately one third of the patients will die within 3 years. 相似文献
7.
N K Sharova I Kubinova G K Vorkunova B Tumova A G Bukrinskaia 《Voprosy virusologii》1989,34(5):573-575
Cross reactions among paramyxoviruses were determined by the immunoblot method. Human parainfluenza viruses, types 1-3, avian parainfluenza virus type 4, mumps, Sendai, and measles viruses were used. Antisera to human parainfluenza viruses were shown to cross-interact with proteins NP and M of other types, and all antisera to the members of Paramyxovirus genus cross-reacted with M proteins of other paramyxoviruses. No cross reactions with measles virus proteins were observed. It is concluded that M protein is the most conservative protein of paramyxoviruses. 相似文献
8.
STUDY OBJECTIVES: COPD is a systemic disorder that is associated with increases of inflammatory proteins in systemic circulation. However, no data on the potential role of systemic inflammation in pulmonary hypertension secondary to COPD are available. Therefore, our aim was to investigate the degree of systemic inflammation reflected by circulatory levels of C-reactive protein (CRP), tumor-necrosis factor (TNF)-alpha, and interleukin (IL)-6 in COPD patients with and without pulmonary hypertension. DESIGN: Cross-sectional study. SETTING: University hospital, tertiary referral setting. PATIENTS AND MEASUREMENTS: In 43 consecutive patients with COPD (mean [+/- SD] age, 65.0 +/- 10.5 years; mean FEV(1), 46.2 +/- 18.1% predicted), lung function was assessed using body plethysmography; pulmonary artery pressure (Ppa) levels were measured by echocardiography. Serum TNF-alpha and IL-6 levels were assessed by enzyme-linked immunosorbent assay, and high-sensitivity serum CRP levels were measured by chemiluminescent immunoassay. RESULTS: Pulmonary hypertension was present in 19 patients and was absent in 24 patients. In patients with pulmonary hypertension, serum CRP and TNF-alpha levels were significantly higher than in those patients without hypertension (median, 3.6 mg/L [25th to 75th percentile, 1.4 to 13.0 mg/L] vs 1.8 mg/L [25th to 75th percentile, 0.8 to 2.8 mg/L; p = 0.034]; and median, 4.2 pg/mL [25th to 75th percentile, 3.4 to 10.9 pg/mL] vs 3.1 pg/mL [25th to 75th percentile, 2.1 to 4.2 pg/mL]; p = 0.042, respectively). No differences were seen in serum IL-6 (median, 10.4 pg/mL [25th to 75th percentile, 8.8 to 12.2 pg/mL] vs 10.5 pg/mL [25th to 75th percentile, 9.4 to 39.1 pg/mL]; p = 0.651) between the groups. In multiple linear regression analysis, the following two variables were independent predictors of systolic Ppa (R(2) = 0.373): Pao(2) (p = 0.011); and log-transformed serum CRP level (p = 0.044). CONCLUSION: We conclude that increases in Ppa in patients with COPD are associated with higher serum levels of CRP and TNF-alpha, raising the possibility of a pathogenetic role for low-grade systemic inflammation in the pathogenesis of pulmonary hypertension in COPD patients. 相似文献
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Zidzik J Slabá E Joppa P Kluchová Z Dorková Z Skyba P Habalová V Salagovic J Tkácová R 《Croatian medical journal》2008,49(2):182-191