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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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G Protein–Coupled Receptor Kinase 5 Gene Polymorphisms Are Associated With Postoperative Atrial Fibrillation After Coronary Artery Bypass Grafting in Patients Receiving β-Blockers

TL;DR: In this paper, genetic variations in the adrenergic signaling pathway and cytochrome P450 2D6 enzyme were associated with new-onset atrial fibrillation (AF) in patients who underwent coronary artery bypass grafting and were treated with perioperative β-blockers (BBs).
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A Putatively Functional Polymorphism in the HTR2C Gene is Associated with Depressive Symptoms in White Females Reporting Significant Life Stress

TL;DR: The findings support prior work that suggests a functional SNP on the HTR2C gene may confer an increased risk for depressive symptoms in White women with a history of significant life stress and support the moderation hypothesis.
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Assessing risk for coronary heart disease: Beyond Framingham

TL;DR: Cohn et al. as discussed by the authors proposed a method for risk assessment that focuses on measurements of early vasculardysfunction and disease markers rather than standard risk factors, and compared risk assessments to disease outcomes over time.
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Gene Expression Profiles Link Respiratory Viral Infection, Platelet Response to Aspirin, and Acute Myocardial Infarction.

TL;DR: A viral GES of non-specific, respiratory viral infection was associated with acute MI; 18% of the top 49 genes in the viral G ES are involved with hemostasis and/or platelet aggregation.
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Longevity-related molecular pathways are subject to midlife "switch" in humans.

TL;DR: The present observations link, for the first time, model organism longevity programs with the endogenous but temporary genome‐wide responses to aging in humans, revealing a pattern that may ultimately underpin personalized rates of health span.