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Sökning: WFRF:(Bergmann Manuela) > (2005-2009) > (2009)

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1.
  • Newton-Cheh, Christopher, et al. (författare)
  • Genome-wide association study identifies eight loci associated with blood pressure
  • 2009
  • Ingår i: Nature Genetics. - Nature Publishing Group. - 1546-1718. ; 41:6, s. 666-676
  • Tidskriftsartikel (refereegranskat)abstract
    • Elevated blood pressure is a common, heritable cause of cardiovascular disease worldwide. To date, identification of common genetic variants influencing blood pressure has proven challenging. We tested 2.5 million genotyped and imputed SNPs for association with systolic and diastolic blood pressure in 34,433 subjects of European ancestry from the Global BPgen consortium and followed up findings with direct genotyping (N <= 71,225 European ancestry, N <= 12,889 Indian Asian ancestry) and in silico comparison (CHARGE consortium, N 29,136). We identified association between systolic or diastolic blood pressure and common variants in eight regions near the CYP17A1 (P = 7 x 10(-24)), CYP1A2 (P = 1 x 10(-23)), FGF5 (P = 1 x 10(-21)), SH2B3 (P = 3 x 10(-18)), MTHFR (P = 2 x 10(-13)), c10orf107 (P = 1 x 10(-9)), ZNF652 (P = 5 x 10(-9)) and PLCD3 (P = 1 x 10(-8)) genes. All variants associated with continuous blood pressure were associated with dichotomous hypertension. These associations between common variants and blood pressure and hypertension offer mechanistic insights into the regulation of blood pressure and may point to novel targets for interventions to prevent cardiovascular disease.
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2.
  • Rohrmann, Sabine, et al. (författare)
  • Ethanol intake and the risk of pancreatic cancer in the European prospective investigation into cancer and nutrition (EPIC)
  • 2009
  • Ingår i: Cancer Causes and Control. - Springer. - 1573-7225. ; 20:5, s. 785-794
  • Tidskriftsartikel (refereegranskat)abstract
    • To examine the association of baseline and lifetime ethanol intake with cancer of the pancreas in the European Prospective Investigation into Cancer and Nutrition (EPIC). Included in this analysis were 478,400 subjects, of whom detailed information on the intake of alcoholic beverages at baseline and over lifetime was collected between 1992 and 2000. During a median follow-up time of 8.9 years, 555 non-endocrine pancreatic cancer cases were observed. Multivariate Cox proportional hazard models were used to examine the association of ethanol intake at recruitment and average lifetime ethanol intake and pancreatic cancer adjusting for smoking, height, weight, and history of diabetes. Overall, neither ethanol intake at recruitment (relative risk (RR) = 0.94, 95% confidence interval (CI) 0.69-1.27 comparing 30+ g/d vs. 0.1-4.9 g/d) nor average lifetime ethanol intake (RR = 0.95, 95% CI 0.65-1.39) was associated with pancreatic cancer risk. High lifetime ethanol intake from spirits/liquor at recruitment tended to be associated with a higher risk (RR = 1.40, 95% CI 0.93-2.10 comparing 10+ g/d vs. 0.1-4.9 g/d), but no associations were observed for wine and beer consumption. These results suggest no association of alcohol consumption with the risk of pancreatic cancer.
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3.
  • Gallo, Valentina, et al. (författare)
  • Smoking and risk for amyotrophic lateral sclerosis : analysis of the EPIC cohort
  • 2009
  • Ingår i: Annals of Neurology. - New York : J. Wiley & Sons. - 0364-5134 .- 1531-8249. ; 65:4, s. 378-385
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Objective: Cigarette smoking has been reported as "probable" risk factor for Amyotrophic Lateral Sclerosis (ALS), a poorly understood disease in terms of aetiology. The extensive longitudinal data of the European Prospective Investigation into Cancer and Nutrition (EPIC) were used to evaluate age-specific mortality rates from ALS and the role of cigarette smoking on the risk of dying from ALS.</p> <p>Methods: A total of 517,890 healthy subjects were included, resulting in 4,591,325 person-years. ALS cases were ascertained through death certificates. Cox hazard models were built to investigate the role of smoking on the risk of ALS, using packs/years and smoking duration to study dose-response.</p> <p>Results: A total of 118 subjects died from ALS, resulting in a crude mortality rate of 2.69 per 100,000/year. Current smokers at recruitment had an almost two-fold increased risk of dying from ALS compared to never smokers (HR = 1.89, 95% C.I. 1.14-3.14), while former smokers at the time of enrollment had a 50% increased risk (HR = 1.48, 95% C.I. 0.94-2.32). The number of years spent smoking increased the risk of ALS (p for trend = 0.002). Those who smoked more than 33 years had more than a two-fold increased risk of ALS compared with never smokers (HR = 2.16, 95% C.I. 1.33-3.53). Conversely, the number of years since quitting smoking was associated with a decreased risk of ALS compared with continuing smoking.</p> <p>Interpretation: These results strongly support the hypothesis of a role of cigarette smoking in aetiology of ALS. We hypothesize that this could occur through lipid peroxidation via formaldehyde exposure.</p>
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4.
  • Gallo, Valentina, et al. (författare)
  • Smoking and Risk for Amyotrophic Lateral Sclerosis: Analysis of the EPIC Cohort
  • 2009
  • Ingår i: Annals of Neurology. - John Wiley and Sons Inc.. - 1531-8249. ; 65:4, s. 378-385
  • Tidskriftsartikel (refereegranskat)abstract
    • Objective: Cigarette smoking has been reported as "probable" risk factor for Amyotrophic Lateral Sclerosis (ALS), a poorly understood disease in terms of aetiology. The extensive longitudinal data of the European Prospective Investigation into Cancer and Nutrition (EPIC) were used to evaluate age-specific mortality rates from ALS and the role of cigarette smoking on the risk of dying from ALS. Methods: A total of 517,890 healthy subjects were included, resulting in 4,591,325 person-years. ALS cases were ascertained through death certificates. Cox hazard models were built to investigate the role of smoking on the risk of ALS, using packs/years and smoking duration to study dose-response. Results: A total of 118 subjects died from ALS, resulting in a crude mortality rate of 2.69 per 100,000/year. Current smokers at recruitment had an almost two-fold increased risk of dying from ALS compared to never smokers (HR = 1.89, 95% C.I. 1.14-3.14), while former smokers at the time of enrolment had a 50% increased risk (HR = 1.48, 95% C.I. 0.94-2-32). The number of years spent smoking increased the risk of ALS (p for trend = 0.002). Those who smoked more than 33 years had more than a two-fold increased risk of ALS compared with never smokers (HR = 2.16, 95% C.I. 1.33-3.53). Conversely, the number of years since quitting smoking was associated with a decreased risk of ALS compared with continuing smoking. Interpretation: These results strongly support the hypothesis of a role of cigarette smoking in aetiology of ALS. We hypothesize that this could occur through lipid peroxidation via formaldehyde exposure. Ann Neurol 2009;65:378-385
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5.
  • Kolz, Melanie, et al. (författare)
  • Meta-analysis of 28,141 individuals identifies common variants within five new loci that influence uric acid concentrations
  • 2009
  • Ingår i: PLoS genetics. - 1553-7404. ; 5:6, s. e1000504
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Elevated serum uric acid levels cause gout and are a risk factor for cardiovascular disease and diabetes. To investigate the polygenetic basis of serum uric acid levels, we conducted a meta-analysis of genome-wide association scans from 14 studies totalling 28,141 participants of European descent, resulting in identification of 954 SNPs distributed across nine loci that exceeded the threshold of genome-wide significance, five of which are novel. Overall, the common variants associated with serum uric acid levels fall in the following nine regions: <em>SLC2A9</em> (p = 5.2×10<sup>−201</sup>), <em>ABCG2</em> (p = 3.1×10<sup>−26</sup>), <em>SLC17A1</em> (p = 3.0×10<sup>−14</sup>), <em>SLC22A11</em> (p = 6.7×10<sup>−14</sup>), <em>SLC22A12</em> (p = 2.0×10<sup>−9</sup>), <em>SLC16A9</em> (p = 1.1×10<sup>−8</sup>), <em>GCKR</em> (p = 1.4×10<sup>−9</sup>), <em>LRRC16A</em> (p = 8.5×10<sup>−9</sup>), and near <em>PDZK1</em> (p = 2.7×10<sup>−9</sup>). Identified variants were analyzed for gender differences. We found that the minor allele for rs734553 in <em>SLC2A9</em> has greater influence in lowering uric acid levels in women and the minor allele of rs2231142 in <em>ABCG2</em> elevates uric acid levels more strongly in men compared to women. To further characterize the identified variants, we analyzed their association with a panel of metabolites. rs12356193 within <em>SLC16A9</em> was associated with DL-carnitine (p = 4.0×10<sup>−26</sup>) and propionyl-L-carnitine (p = 5.0×10<sup>−8</sup>) concentrations, which in turn were associated with serum UA levels (p = 1.4×10<sup>−57</sup> and p = 8.1×10<sup>−54</sup>, respectively), forming a triangle between SNP, metabolites, and UA levels. Taken together, these associations highlight additional pathways that are important in the regulation of serum uric acid levels and point toward novel potential targets for pharmacological intervention to prevent or treat hyperuricemia. In addition, these findings strongly support the hypothesis that transport proteins are key in regulating serum uric acid levels.</p>
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6.
  • Menvielle, Gwenn, et al. (författare)
  • The role of smoking and diet in explaining educational inequalities in lung cancer incidence.
  • 2009
  • Ingår i: Journal of the National Cancer Institute. - 1460-2105. ; 101:5, s. 321-330
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>BACKGROUND: Studies in many countries have reported higher lung cancer incidence and mortality in individuals with lower socioeconomic status. METHODS: To investigate the role of smoking in these inequalities, we used data from 391,251 participants in the European Prospective Investigation into Cancer and Nutrition study, a cohort of individuals in 10 European countries. We collected information on smoking (history and quantity), fruit and vegetable consumption, and education through questionnaires at study entry and gathered data on lung cancer incidence for a mean of 8.4 years. Socioeconomic status was defined as the highest attained level of education, and participants were grouped by sex and region of residence (Northern Europe, Germany, or Southern Europe). Relative indices of inequality (RIIs) of lung cancer risk unadjusted and adjusted for smoking were estimated using Cox regression models. Additional analyses were performed by histological type. RESULTS: During the study period, 939 men and 692 women developed lung cancer. Inequalities in lung cancer risk (RII(men) = 3.62, 95% confidence interval [CI] = 2.77 to 4.73, 117 vs 52 per 100,000 person-years for lowest vs highest education level; RII(women) = 2.39, 95% CI = 1.77 to 3.21, 46 vs 25 per 100,000 person-years) decreased after adjustment for smoking but remained statistically significant (RII(men) = 2.29, 95% CI = 1.75 to 3.01; RII(women) = 1.59, 95% CI = 1.18 to 2.13). Large RIIs were observed among men and women in Northern European countries and among men in Germany, but inequalities in lung cancer risk were reverse (RIIs &lt; 1) among women in Southern European countries. Inequalities differed by histological type. Adjustment for smoking reduced inequalities similarly for all histological types and among men and women in all regions. In all analysis, further adjustment for fruit and vegetable consumption did not change the estimates. CONCLUSION: Self-reported smoking consistently explains approximately 50% of the inequalities in lung cancer risk due to differences in education.</p>
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7.
  • Menvielle, Gwenn, et al. (författare)
  • The Role of Smoking and Diet in Explaining Educational Inequalities in Lung Cancer Incidence.
  • 2009
  • Ingår i: Journal of the National Cancer Institute. - Oxford University Press. - 1460-2105. ; 101:5, s. 321-330
  • Tidskriftsartikel (refereegranskat)abstract
    • Background Studies in many countries have reported higher lung cancer incidence and mortality in individuals with lower socioeconomic status. Methods To investigate the role of smoking in these inequalities, we used data from 391 251 participants in the European Prospective Investigation into Cancer and Nutrition study, a cohort of individuals in 10 European countries. We collected information on smoking (history and quantity), fruit and vegetable consumption, and education through questionnaires at study entry and gathered data on lung cancer incidence for a mean of 8.4 years. Socioeconomic status was defined as the highest attained level of education, and participants were grouped by sex and region of residence (Northern Europe, Germany, or Southern Europe). Relative indices of inequality (RIIs) of lung cancer risk unadjusted and adjusted for smoking were estimated using Cox regression models. Additional analyses were performed by histological type. Results During the study period, 939 men and 692 women developed lung cancer. Inequalities in lung cancer risk (RII(men) = 3.62, 95% confidence interval [CI] = 2.77 to 4.73, 117 vs 52 per 100 000 person-years for lowest vs highest education level; RII(women) = 2.39, 95% CI = 1.77 to 3.21, 46 vs 25 per 100 000 person-years) decreased after adjustment for smoking but remained statistically significant (RII(men) = 2.29, 95% CI = 1.75 to 3.01; RII(women) = 1.59, 95% CI = 1.18 to 2.13). Large RIIs were observed among men and women in Northern European countries and among men in Germany, but inequalities in lung cancer risk were reverse (RIIs < 1) among women in Southern European countries. Inequalities differed by histological type. Adjustment for smoking reduced inequalities similarly for all histological types and among men and women in all regions. In all analysis, further adjustment for fruit and vegetable consumption did not change the estimates. Conclusion Self-reported smoking consistently explains approximately 50% of the inequalities in lung cancer risk due to differences in education.
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8.
  • Newton-Cheh, Christopher, et al. (författare)
  • Genome-wide association study identifies eight loci associated with blood pressure
  • 2009
  • Ingår i: Nature Genetics. - 1061-4036 .- 1546-1718. ; 41:6, s. 666-676
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Elevated blood pressure is a common, heritable cause of cardiovascular disease worldwide. To date, identification of common genetic variants influencing blood pressure has proven challenging. We tested 2.5 million genotyped and imputed SNPs for association with systolic and diastolic blood pressure in 34,433 subjects of European ancestry from the Global BPgen consortium and followed up findings with direct genotyping (<em>N</em> ≤ 71,225 European ancestry, <em>N</em> ≤ 12,889 Indian Asian ancestry) and <em>in silico</em> comparison (CHARGE consortium, <em>N</em> = 29,136). We identified association between systolic or diastolic blood pressure and common variants in eight regions near the <em>CYP17A1</em> (<em>P</em> = 7 × 10<sup>−24</sup>), <em>CYP1A2</em> (<em>P</em> = 1 × 10<sup>−23</sup>), <em>FGF5</em> (<em>P</em> = 1 × 10<sup>−21</sup>), <em>SH2B3</em> (<em>P</em> = 3 × 10<sup>−18</sup>), <em>MTHFR</em> (<em>P</em> = 2 × 10<sup>−13</sup>), <em>c10orf107</em> (<em>P</em> = 1 × 10<sup>−9</sup>), <em>ZNF652</em> (<em>P</em> = 5 × 10<sup>−9</sup>) and <em>PLCD3</em> (<em>P</em> = 1 × 10<sup>−8</sup>) genes. All variants associated with continuous blood pressure were associated with dichotomous hypertension. These associations between common variants and blood pressure and hypertension offer mechanistic insights into the regulation of blood pressure and may point to novel targets for interventions to prevent cardiovascular disease.</p>
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9.
  • Romaguera, Dora, et al. (författare)
  • Adherence to the Mediterranean Diet Is Associated with Lower Abdominal Adiposity in European Men and Women
  • 2009
  • Ingår i: Journal of Nutrition. - American Society for Nutrition. - 1541-6100. ; 139:9, s. 1728-1737
  • Tidskriftsartikel (refereegranskat)abstract
    • Given the lack of consistent evidence of the relationship between Mediterranean dietary patterns and body fat, we assessed the cross-sectional association between adherence to a modified Mediterranean diet, BMI, and waist circumference (WC). A total of 497,308 individuals (70.7% women) aged 25-70 y from 10 European countries participated in this study. Diet was assessed at baseline using detailed validated country-specific questionnaires, and anthropometrical measurements were collected using standardized procedures. The association between the degree of adherence to the modified-Mediterranean Diet Score (mMDS) (including high consumption of vegetables, legumes, fruits and nuts, cereals, fish and seafood, and unsaturated: saturated fatty acids ratio; moderate alcohol intake; and low consumption of meat and meat products and dairy products) and BMI (kg.m(-2)) or WC (cm was modeled through mixed-effects linear regression, controlling for potential confounders. Overall, the mMDS was not significantly associated with BMI. Higher adherence to the Mediterranean diet was significantly associated with lower WC, for a given BMI, in both men (-0.09; 95% CI -0.14 to -0.04) and women (-0.06; 95% CI -0.10 to -0.01). The association was stronger in men (-0.20; 95% CI -0.23 to -0.17) and women (-0.17; 95% CI -0.21 to -0.13) from Northern European countries. Despite the observed heterogeneity among regions, results of this study suggest that adherence to a modified Mediterranean diet, high in foods of vegetable origin and unsaturated fatty acids, is associated with lower abdominal adiposity measured by WC in European men and women. J. Nutr. 139: 1728-1737, 2009.
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10.
  • Romaguera, Dora, et al. (författare)
  • Adherence to the Mediterranean diet is associated with lower abdominal adiposity in European men and women.
  • 2009
  • Ingår i: Journal of Nutrition. - 0022-3166 .- 1541-6100. ; 139:9, s. 1728-1737
  • Tidskriftsartikel (refereegranskat)abstract
    • <p>Given the lack of consistent evidence of the relationship between Mediterranean dietary patterns and body fat, we assessed the cross-sectional association between adherence to a modified Mediterranean diet, BMI, and waist circumference (WC). A total of 497,308 individuals (70.7% women) aged 25-70 y from 10 European countries participated in this study. Diet was assessed at baseline using detailed validated country-specific questionnaires, and anthropometrical measurements were collected using standardized procedures. The association between the degree of adherence to the modified-Mediterranean Diet Score (mMDS) (including high consumption of vegetables, legumes, fruits and nuts, cereals, fish and seafood, and unsaturated:saturated fatty acids ratio; moderate alcohol intake; and low consumption of meat and meat products and dairy products) and BMI (kg.m(-2)) or WC (cm) was modeled through mixed-effects linear regression, controlling for potential confounders. Overall, the mMDS was not significantly associated with BMI. Higher adherence to the Mediterranean diet was significantly associated with lower WC, for a given BMI, in both men (-0.09; 95% CI -0.14 to -0.04) and women (-0.06; 95% CI -0.10 to -0.01). The association was stronger in men (-0.20; 95% CI -0.23 to -0.17) and women (-0.17; 95% CI -0.21 to -0.13) from Northern European countries. Despite the observed heterogeneity among regions, results of this study suggest that adherence to a modified Mediterranean diet, high in foods of vegetable origin and unsaturated fatty acids, is associated with lower abdominal adiposity measured by WC in European men and women.</p>
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