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Pall T. Onundarson

Researcher at University of Iceland

Publications -  85
Citations -  2257

Pall T. Onundarson is an academic researcher from University of Iceland. The author has contributed to research in topics: Population & Medicine. The author has an hindex of 21, co-authored 68 publications receiving 1915 citations. Previous affiliations of Pall T. Onundarson include RMIT University & University of Rochester.

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Seventy-five genetic loci influencing the human red blood cell

Pim van der Harst, +194 more
- 20 Dec 2012 - 
TL;DR: A genome-wide association study of haemoglobin concentration and related parameters in up to 135,367 individuals identifies 75 independent genetic loci associated with one or more red blood cell phenotypes at P < 10−8, which together explain 4–9% of the phenotypic variance per trait.

Seventy-five genetic loci influencing the human red blood cell

Pim van der Harst, +194 more
TL;DR: In this article, the authors carried out a genome-wide association study of haemoglobin concentration and related parameters in up to 135,367 individuals and identified 75 independent genetic loci associated with one or more red blood cell phenotypes at P < 10−8, which together explain 4-9% of the phenotypic variance per trait.
Journal ArticleDOI

Genome-wide association study identifies a sequence variant within the DAB2IP gene conferring susceptibility to abdominal aortic aneurysm

Solveig Gretarsdottir, +103 more
- 01 Aug 2010 - 
TL;DR: It was found that rs7025486[A], located within DAB2IP, which encodes an inhibitor of cell growth and survival, is associated with early onset myocardial infarction, but not with intracranial aneurysm or ischemic stroke.
Journal ArticleDOI

Apolipoprotein(a) Genetic Sequence Variants Associated With Systemic Atherosclerosis and Coronary Atherosclerotic Burden But Not With Venous Thromboembolism.

Anna Helgadottir, +88 more
TL;DR: LPA sequence variants were associated with atherosclerotic burden, but not with primarily thrombotic phenotypes, and CAD cases carrying LPA risk variants had increased susceptibility to atherosclerosis manifestations outside of the coronary tree.