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William E. Kraus

Researcher at Duke University

Publications -  625
Citations -  40583

William E. Kraus is an academic researcher from Duke University. The author has contributed to research in topics: Heart failure & Medicine. The author has an hindex of 93, co-authored 565 publications receiving 33692 citations. Previous affiliations of William E. Kraus include University of Texas Southwestern Medical Center & University of North Carolina at Chapel Hill.

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Exome sequencing identifies rare LDLR and APOA5 alleles conferring risk for myocardial infarction

Ron Do, +103 more
- 05 Feb 2015 - 
TL;DR: Kathiresan et al. as mentioned in this paper used exome sequencing of nearly 10,000 people to identify alleles associated with early-onset myocardial infarction; mutations in low-density lipoprotein receptor (LDLR) or apolipoprotein A-V (APOA5) were associated with disease risk.
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Population Approaches to Improve Diet, Physical Activity, and Smoking Habits: A Scientific Statement From the American Heart Association

TL;DR: In this article, the authors systematically reviewed and graded the current scientific evidence for effective population approaches to improve dietary habits, increase physical activity, and reduce tobacco use, including media and educational campaigns, labeling and consumer information, taxation, subsidies, and other economic incentives.
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Fatty acid homeostasis and induction of lipid regulatory genes in skeletal muscles of peroxisome proliferator-activated receptor (PPAR) alpha knock-out mice. Evidence for compensatory regulation by PPAR delta.

TL;DR: Results show redundancy in the functions of PPars α and δ as transcriptional regulators of fatty acid homeostasis and suggest that in skeletal muscle high levels of the δ-subtype can compensate for deficiency of PPARα.
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Relationships Between Circulating Metabolic Intermediates and Insulin Action in Overweight to Obese, Inactive Men and Women

TL;DR: Elevated concentrations of large, neutral amino acids were independently associated with insulin resistance and fatty acids were inversely related to the pancreatic response to glucose, suggesting that these metabolic intermediates might play a role in the progression to type 2 diabetes.