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Articles by A. B Miller
Total Records ( 2 ) for A. B Miller
  J. E Lee , S Mannisto , D Spiegelman , D. J Hunter , L Bernstein , P. A van den Brandt , J. E Buring , E Cho , D. R English , A Flood , J. L Freudenheim , G. G Giles , E Giovannucci , N Hakansson , P. L Horn Ross , E. J Jacobs , M. F Leitzmann , J. R Marshall , M. L McCullough , A. B Miller , T. E Rohan , J. A Ross , A Schatzkin , L. J Schouten , J Virtamo , A Wolk , S. M Zhang and S. A. Smith Warner
 

Fruit and vegetable consumption has been hypothesized to reduce the risk of renal cell cancer. We conducted a pooled analysis of 13 prospective studies, including 1,478 incident cases of renal cell cancer (709 women and 769 men) among 530,469 women and 244,483 men followed for up to 7 to 20 years. Participants completed a validated food-frequency questionnaire at baseline. Using the primary data from each study, the study-specific relative risks (RR) were calculated using the Cox proportional hazards model and then pooled using a random effects model. We found that fruit and vegetable consumption was associated with a reduced risk of renal cell cancer. Compared with <200 g/d of fruit and vegetable intake, the pooled multivariate RR for ≥600 g/d was 0.68 [95% confidence interval (95% CI) = 0.54-0.87; P for between-studies heterogeneity = 0.86; P for trend = 0.001]. Compared with <100 g/d, the pooled multivariate RRs (95% CI) for ≥400 g/d were 0.79 (0.63-0.99; P for trend = 0.03) for total fruit and 0.72 (0.48-1.08; P for trend = 0.07) for total vegetables. For specific carotenoids, the pooled multivariate RRs (95% CIs) comparing the highest and lowest quintiles were 0.87 (0.73-1.03) for -carotene, 0.82 (0.69-0.98) for β-carotene, 0.86 (0.73-1.01) for β-cryptoxanthin, 0.82 (0.64-1.06) for lutein/zeaxanthin, and 1.13 (0.95-1.34) for lycopene. In conclusion, increasing fruit and vegetable consumption is associated with decreasing risk of renal cell cancer; carotenoids present in fruit and vegetables may partly contribute to this protection. (Cancer Epidemiol Biomarkers Prev 2009;18(6):1730–9)

  M. R Zile , W. H Gaasch , I. S Anand , M Haass , W. C Little , A. B Miller , J Lopez Sendon , J. R Teerlink , M White , J. J McMurray , M Komajda , R McKelvie , A Ptaszynska , S. J Hetzel , B. M Massie , P. E Carson and for the I Preserve Investigators
 

Background— The mode of death has been well characterized in patients with heart failure and a reduced ejection fraction; however, less is known about the mode of death in patients with heart failure and a preserved ejection fraction (HFPEF). The purpose of this study was to examine the mode of death in patients with HFPEF enrolled in the Irbesartan in Heart Failure With Preserved Ejection Fraction Study (I-Preserve) trial and to determine whether irbesartan altered the distribution of mode of death in HFPEF.

Methods and Results— All deaths were reviewed by a clinical end-point committee, and the mode of death was assigned by consensus of the members. The annual mortality rate was 5.2% in the I-Preserve trial. There were no significant differences in mortality rate between the placebo and irbesartan groups. The mode of death was cardiovascular in 60% (including 26% sudden, 14% heart failure, 5% myocardial infarction, and 9% stroke), noncardiovascular in 30%, and unknown in 10%. There were no differences in the distribution of mode-specific mortality rates between placebo and irbesartan.

Conclusions— Sixty percent of the deaths in patients with HFPEF were cardiovascular, with sudden death and heart failure death being the most common. Treatment with irbesartan did not affect overall mortality or the distribution of mode-specific mortality rates.

Clinical Trial Registration— URL: http://www.clinicaltrials.gov. Unique identifier: NCT00095238.

 
 
 
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