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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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Phenome-wide association analysis of LDL-cholesterol lowering genetic variants in PCSK9

Amand F. Schmidt, +182 more
TL;DR: Genetic variation at thePCSK9 locus recapitulates the effects of therapeutic inhibition of PCSK9 on major blood lipid fractions and MI, while indicating an increased risk of type 2 diabetes mellitus and no other possible safety concerns were shown.
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Effects of cigarette smoking on cardiovascular-related protein profiles in two community-based cohort studies

TL;DR: The findings of the present study suggest that cigarette smoking may interfere with several essential parts of the atherosclerosis process, as evidenced by associations with protein markers representing endothelial dysfunction, inflammation, neointimal formation, foam cell formation and plaque instability.

Protein-coding variants implicate novel genes related to lipid homeostasis contributing to body-fat distribution

Anne E. Justice, +287 more
TL;DR: A transancestral exome-wide association study for body-fat distribution identifies protein-coding variants that are significantly associated with waist-to-hip ratio adjusted for body mass index.
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Genome-Wide Association Studies of Estimated Fatty Acid Desaturase Activity in Serum and Adipose Tissue in Elderly Individuals: Associations with Insulin Sensitivity

TL;DR: The FADS cluster was the main genetic determinant of estimated FADS activity, however, fatty acid (FA) ratios in adipose tissue and cholesterol esters represent FADS activities in separate tissues and are thus influenced by different genetic factors with potential varying effects on IS.

Inference of the genetic architecture underlying BMI and height with the use of 20,240 sibling pairs

TL;DR: In this paper, the authors show that the distribution of the observed test statistics is consistent with both rare and common variants underlying a polygenic architecture and that previous reports of linkage signals in complex traits are probably a consequence of polygenicity rather than the segregation of variants with large effects.