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Erik Ingelsson

Researcher at Stanford University

Publications -  546
Citations -  99427

Erik Ingelsson is an academic researcher from Stanford University. The author has contributed to research in topics: Genome-wide association study & Population. The author has an hindex of 124, co-authored 538 publications receiving 85407 citations. Previous affiliations of Erik Ingelsson include Karolinska Institutet & Cardiovascular Institute of the South.

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Birthweight, Type 2 Diabetes Mellitus, and Cardiovascular Disease: Addressing the Barker Hypothesis With Mendelian Randomization.

TL;DR: Lower birthweight, used as a proxy for intrauterine growth retardation, is causally related with increased susceptibility to coronary artery disease and T2D and positive causal association with body mass index but no associations with blood pressure.
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Risk Prediction Measures for Case-Cohort and Nested Case-Control Designs: An Application to Cardiovascular Disease

TL;DR: The authors have shown that case-cohort and nested case-control designs can be used in settings where the research aim is to evaluate the prediction ability of new markers and that matching strategies for nested case -control designs may lead to biased prediction measures.
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Myocardial Performance Index, a Doppler-Derived Index of Global Left Ventricular Function, Predicts Congestive Heart Failure in Elderly Men

TL;DR: MPI provides important prognostic information for the risk of future CHF, beyond other measurements of cardiac function and traditional heart failure risk factors in elderly men.
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Breastfeeding in infancy and adult cardiovascular disease risk factors.

TL;DR: Examination of the relations between maternal breastfeeding history and cardiovascular risk factors in Framingham Third Generation participants found that breastfeeding in infancy is inversely associated with adult BMI and positively associated with HDL cholesterol.
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Genetic Regulatory Mechanisms of Smooth Muscle Cells Map to Coronary Artery Disease Risk Loci

TL;DR: Tissue-specific and mechanistic insights are provided into the regulation of a critical vascular cell type associated with CAD in human populations through transcriptomic, epigenetic, and genetic regulatory mechanisms specific to HCASMCs.