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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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Exercise training increases electron and substrate shuttling proteins in muscle of overweight men and women with the metabolic syndrome.

TL;DR: It is proposed that training coordinately increases the levels of aspartate aminotransferase 1, lactate dehydrogenase B, and pyruvate dehydrogensase-alpha(1) subunit, increasing glucose metabolism in muscle by liberating pyruVate for oxidative metabolism and, therefore, limiting lactate efflux.
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A Novel Protein Glycan-Derived Inflammation Biomarker Independently Predicts Cardiovascular Disease and Modifies the Association of HDL Subclasses with Mortality.

TL;DR: Adding GlycA and smaller HDL subclasses into the GRACE and Framingham Heart Study Risk Scores improved mortality risk prediction, discrimination and reclassification and may increase precision for clinical risk assessment in secondary prevention populations.
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Genetic effects in the leukotriene biosynthesis pathway and association with atherosclerosis.

TL;DR: A modest role for the leukotriene pathway in Atherosclerosis pathogenesis is supported, important genomic interactions within the pathway are revealed, and the importance of using pathway-based modeling for evaluating the genomics of atherosclerosis susceptibility is suggested.
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Energy requirements in nonobese men and women: results from CALERIE

TL;DR: Estimates of TDEE from a 7-d physical activity recall and measured resting metabolic rate suggested that individuals significantly underreported physical activity and underreporting by overweight individuals was greater than that of normal-weight individuals.