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Träfflista för sökning "L773:0002 9262 srt2:(2015-2019)"

Search: L773:0002 9262 > (2015-2019)

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1.
  • Lu, Yunxia, et al. (author)
  • Metabolic predispositions and increased risk of colorectal adenocarcinoma by anatomical locations : a large population-based cohort study in Norway
  • 2015
  • In: American Journal of Epidemiology. - Stockholm : Karolinska Institutet, Dept of Molecular Medicine and Surgery. - 0002-9262 .- 1476-6256.
  • Journal article (peer-reviewed)abstract
    • Whether different definitions of metabolic syndrome (MetS) are differently associated with colorectal adenocarcinoma (CA) by anatomical location is unclear. A population-based cohort study, the Cohort of Norway (CONOR) Study, was conducted in Norway from 1995 to 2010. Anthropometric measurements, blood samples, and lifestyle data were collected at recruitment. CAs were identified through linkage to the Norwegian Cancer Register. A composite index of MetS as defined by the International Diabetes Federation (IDF) or/and the National Cholesterol Education Program's Adult Treatment Panel III (ATP III) and single components of MetS, including anthropometric factors, blood pressure, lipids, triglycerides, and glucose, were analyzed. Cox proportional hazards regression was performed to estimate hazard ratios and 95% confidence intervals. Significant associations between single MetS components and CA, except for reduced high-density lipoprotein cholesterol and nonfasting glucose levels, were observed. MetS defined by 2 criteria separately showed a similar association with CA in general, and MetS defined by both the IDF and ATP III showed consistent results. Stronger associations were observed in the proximal colon among men (IDF: hazard ratio (HR) = 1.51, 95% confidence interval (CI): 1.24, 1.84; ATP III: HR = 1.40, 95% CI: 1.15, 1.70) and in the rectum among women (IDF: HR = 1.42, 95% CI: 1.07, 1.89; ATP III: HR = 1.43, 95% CI: 1.08, 1.90).
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2.
  • Amirian, E. Susan, et al. (author)
  • The Glioma International Case-Control Study : A Report From the Genetic Epidemiology of Glioma International Consortium
  • 2016
  • In: American Journal of Epidemiology. - : Oxford University Press (OUP). - 0002-9262 .- 1476-6256. ; 183:2, s. 85-91
  • Journal article (peer-reviewed)abstract
    • Decades of research have established only a few etiological factors for glioma, which is a rare and highly fatal brain cancer. Common methodological challenges among glioma studies include small sample sizes, heterogeneity of tumor subtypes, and retrospective exposure assessment. Here, we briefly describe the Glioma International Case-Control (GICC) Study (recruitment, 2010-2013), a study being conducted by the Genetic Epidemiology of Glioma International Consortium that integrates data from multiple data collection sites, uses a common protocol and questionnaire, and includes biospecimen collection. To our knowledge, the GICC Study is the largest glioma study to date that includes collection of blood samples, which will allow for genetic analysis and interrogation of gene-environment interactions.
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3.
  • Andersson, Eva M., 1968, et al. (author)
  • Partial Mediation by Cadmium Exposure of the Association Between Tobacco Smoking and Atherosclerotic Plaques in the Carotid Artery
  • 2018
  • In: American Journal of Epidemiology. - : Oxford University Press (OUP). - 0002-9262 .- 1476-6256. ; 187:4, s. 806-816
  • Journal article (peer-reviewed)abstract
    • Exposure to cadmium confers increased cardiovascular risk. Tobacco smoke contains cadmium, which, hypothetically, may mediate parts of the tobacco-associated risk of developing atherosclerotic plaques. Baseline data from the Swedish Malmo Diet and Cancer cohort (1991-1996) were used to test this hypothesis. Mediation analysis was used to examine associations between smoking and blood cadmium levels and the prevalence of ultrasound-assessed carotid atherosclerotic plaques. The total association with smoking status (never smokers, 2 categories of former smokers, and current smokers) was split into direct and indirect association, and the proportion mediated was estimated. The adjusted estimated plaque prevalence was approximately 27% among never smokers. We identified both a direct and an indirect pathway between smoking and carotid plaques; the indirect association, through cadmium, was observed among current smokers and former smokers who had quit smoking less than 15 years before. For current smokers, the prevalence ratio for plaque was 1.5, with 60%-65% of the association with smoking being mediated through cadmium. Recent former smokers had a prevalence ratio of 1.3, and 40%-45% was mediated through cadmium. Long-time former smokers had a prevalence ratio of 1.2, but none of the association was mediated through cadmium. In conclusion, about two-thirds of the proatherosclerotic association with smoking was mediated by cadmium.
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5.
  • Arokiasamy, Perianayagam, et al. (author)
  • Chronic Noncommunicable Diseases in 6 Low-and Middle-Income Countries : Findings From Wave 1 of the World Health Organization's Study on Global Ageing and Adult Health (SAGE)
  • 2017
  • In: American Journal of Epidemiology. - : Oxford University Press (OUP). - 0002-9262 .- 1476-6256. ; 185:6, s. 414-428
  • Journal article (peer-reviewed)abstract
    • In this paper, we examine patterns of self-reported diagnosis of noncommunicable diseases (NCDs) and prevalences of algorithm/measured test-based, undiagnosed, and untreated NCDs in China, Ghana, India, Mexico, Russia, and South Africa. Nationally representative samples of older adults aged >= 50 years were analyzed from wave 1 of the World Health Organization's Study on Global Ageing and Adult Health (2007-2010; n = 34,149). Analyses focused on 6 conditions: angina, arthritis, asthma, chronic lung disease, depression, and hypertension. Outcomes for these NCDs were: 1) self-reported disease, 2) algorithm/measured test-based disease, 3) undiagnosed disease, and 4) untreated disease. Algorithm/measured test-based prevalence of NCDs was much higher than self-reported prevalence in all 6 countries, indicating underestimation of NCD prevalence in low-and middle-income countries. Undiagnosed prevalence of NCDs was highest for hypertension, ranging from 19.7% (95% confidence interval (CI): 18.1, 21.3) in India to 49.6% (95% CI: 46.2, 53.0) in South Africa. The proportion untreated among all diseases was highest for depression, ranging from 69.5% (95% CI: 57.1, 81.9) in South Africa to 93.2% (95% CI: 90.1, 95.7) in India. Higher levels of education and wealth significantly reduced the odds of an undiagnosed condition and untreated morbidity. A high prevalence of undiagnosed NCDs and an even higher proportion of untreated NCDs highlights the inadequacies in diagnosis and management of NCDs in local health-care systems.
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6.
  • Baecklund, Fredrik, et al. (author)
  • Possible Interaction Between Cigarette Smoking and HLA-DRB1 Variation in the Risk of Follicular Lymphoma
  • 2017
  • In: American Journal of Epidemiology. - : OXFORD UNIV PRESS INC. - 0002-9262 .- 1476-6256. ; 185:8, s. 681-687
  • Journal article (peer-reviewed)abstract
    • Follicular lymphoma (FL) risk is strongly associated with germline genetic variation in human leukocyte antigen (HLA) class II. Cigarette smoking has been suggested to increase FL risk, primarily among women. We hypothesized that amino acids in HLA-antigen D-related beta 1 subunit (DRB1) interact with smoking in FL risk, as shown for rheumatoid arthritis. We analyzed 373 patients with FL and 818 controls from 2 population-based case-control studies in Sweden and Denmark (1999-2003). Haplotypes in HLA-DRB1 were imputed at amino acid positions 11, 13, 28, 30, and 70-74 (shared epitope). We estimated the relative risk of FL as odds ratios with 95% confidence intervals for different smoking status/haplotype combinations. Interaction was defined as departure from additivity of effects and quantified by the attributable proportion (AP). Relative to never-smokers carrying no shared epitope alleles, smoking was associated with the risk of FL among all subjects (for former smokers, odds ratio (OR) = 2.20, 95% confidence interval (CI): 1.10, 4.41; ORcurrent = 3.56, 95% CI: 1.60, 7.92) and women (ORformer = 2.95, 95% CI: 1.18, 7.37; ORcurrent = 5.63, 95% CI: 2.07, 15.3) carrying 2 shared epitope alleles but not among those carrying zero or 1 shared epitope allele. Smoking and shared epitope status interacted significantly as measured by AP (overall, AP = 0.6, 95% CI: 0.15, 1.0; for women, AP = 0.5, 95% CI: 0.005, 1.0). These results suggest a possible interaction between smoking and HLA-DRB1-associated antigen presentation in FL risk and provide a model to further unravel FL etiology.
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7.
  • Bellavia, Andrea, et al. (author)
  • Using Laplace Regression to Model and Predict Percentiles of Age at Death When Age Is the Primary Time Scale
  • 2015
  • In: American Journal of Epidemiology. - : OXFORD UNIV PRESS INC. - 0002-9262 .- 1476-6256. ; 182:3, s. 271-277
  • Journal article (peer-reviewed)abstract
    • Increasingly often in epidemiologic research, associations between survival time and predictors of interest are measured by differences between distribution functions rather than hazard functions. For example, differences in percentiles of survival time, expressed in absolute time units (e.g., weeks), may complement the popular risk ratios, which are unitless measures. When analyzing time to an event of interest (e.g., death) in prospective cohort studies, the time scale can be set to start at birth or at study entry. The advantages of one time origin over the other have been thoroughly explored for the estimation of risks but not for the estimation of survival percentiles. In this paper, we analyze the use of different time scales in the estimation of survival percentiles with Laplace regression. Using this regression method, investigators can estimate percentiles of survival time over levels of an exposure of interest while adjusting for potential confounders. Our findings may help to improve modeling strategies and ease interpretation in the estimation of survival percentiles in prospective cohort studies.
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9.
  • Bengtsson, Tommy, et al. (author)
  • Social Class and Excess Mortality in Sweden During the 1918 Influenza Pandemic
  • 2018
  • In: American Journal of Epidemiology. - : Oxford University Press (OUP). - 0002-9262 .- 1476-6256. ; 187:12, s. 2568-2576
  • Journal article (peer-reviewed)abstract
    • There is no consensus in the literature about the role of socioeconomic factors on influenza mortality during the 1918 pandemic. While some scholars have found that social factors were important, others have not. In this study, we analyzed differences in excess mortality by social class in Sweden during the 1918 pandemic. We analyzed individual-level mortality of the entire population aged 30–59, by combining information from death records with census data on occupation. Social class was measured by an occupation-based class scheme. Excess mortality during the pandemic was measured as mortality relative to the same month the year before. Social class differences in mortality were modeled using a complementary log-log model, adjusting for potential confounding at the family, the residential (urban/rural) and the county levels. Our findings indicated notable class differences in excess mortality but no perfect class gradient. Class differences were somewhat larger for men than for women.
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