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Articles by D Gu
Total Records ( 3 ) for D Gu
  A Moran , D Gu , D Zhao , P Coxson , Y. C Wang , C. S Chen , J Liu , J Cheng , K Bibbins Domingo , Y. M Shen , J He and L. Goldman
 

Background— The relative effects of individual and combined risk factor trends on future cardiovascular disease in China have not been quantified in detail.

Methods and Results— Future risk factor trends in China were projected based on prior trends. Cardiovascular disease (coronary heart disease and stroke) in adults ages 35 to 84 years was projected from 2010 to 2030 using the Coronary Heart Disease Policy Model–China, a Markov computer simulation model. With risk factor levels held constant, projected annual cardiovascular events increased by >50% between 2010 and 2030 based on population aging and growth alone. Projected trends in blood pressure, total cholesterol, diabetes (increases), and active smoking (decline) would increase annual cardiovascular disease events by an additional 23%, an increase of approximately 21.3 million cardiovascular events and 7.7 million cardiovascular deaths over 2010 to 2030. Aggressively reducing active smoking in Chinese men to 20% prevalence in 2020 and 10% prevalence in 2030 or reducing mean systolic blood pressure by 3.8 mm Hg in men and women would counteract adverse trends in other risk factors by preventing cardiovascular events and 2.9 to 5.7 million total deaths over 2 decades.

Conclusions— Aging and population growth will increase cardiovascular disease by more than a half over the coming 20 years, and projected unfavorable trends in blood pressure, total cholesterol, diabetes, and body mass index may accelerate the epidemic. National policy aimed at controlling blood pressure, smoking, and other risk factors would counteract the expected future cardiovascular disease epidemic in China.

  D Gu , M Wang , Z Zhang and J. Chen
 

Published data regarding the association between the apurinic/apyrimidinic endonuclease 1 (APE1) T1349G (Asp148Glu) polymorphism and cancer risk show inconclusive results. To derive a more precise estimation of the relationship, we performed a meta-analysis of 27 published studies that included 12 432 cancer cases and 17 349 controls. We used odds ratios (ORs) and 95% confidence intervals (CIs) to evaluate the strength of the associations. The overall results suggested that the variant genotypes were associated with a moderately increased risk of all cancer types (OR = 1.09, 95% CI = 1.01–1.18 for TG versus TT; OR = 1.08, 95% CI = 1.00–1.18 for GG/TG versus TT). In the stratified analyses, the risk remained for studies of colorectal cancer, European populations and population-based studies. Although some modest bias could not be eliminated, this meta-analysis supported that the APE1 T1349G polymorphism is a low-penetrance risk factor for cancer development.

  H Chu , M Wang , D Gu , D Wu , Z Zhang , J Tang and Z. Zhang
 

Myeloperoxidase (MPO) is an endogenous oxidant enzyme that generates reactive oxygen species and plays an important role in the aetiology of cancer. The MPO –463G>A polymorphism influences MPO transcription and has been implicated in cancer risk. However, results from published studies on the association between the MPO –463G>A polymorphism and risk of cancer are conflicting. To derive a more precise estimation of association between the MPO –463G>A polymorphism and risk of cancer, we performed a meta-analysis based on 43 case–control studies, including a total of 14 171 cancer cases and 17 319 controls. We used odds ratios (ORs) with 95% confidence intervals (CIs) to assess the strength of the association. Overall, individuals with the –463A allele had a 0.93-fold lower cancer risk in a dominant model (OR = 0.93, 95% CI = 0.87–1.00). In the stratified analyses, we observed a similar association in European populations (heterozygote comparison: OR = 0.90, 95% CI = 0.82–0.99) and hospital-based studies (dominant model: OR = 0.88, 95% CI = 0.79–0.99). When stratified by cancer type, however, no significant association was found. The results suggested that the MPO –463A allele does not contribute to the development of cancer. Additional well-designed large studies are required to validate these findings in different populations.

 
 
 
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