Industrialization of the Soviet Far East
In: Far Eastern survey, Band 4, S. 49-53
ISSN: 0362-8949
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In: Far Eastern survey, Band 4, S. 49-53
ISSN: 0362-8949
In: Pacific affairs: an international review of Asia and the Pacific, Band 7, Heft 4, S. 395
ISSN: 1715-3379
In: Pacific affairs, Band 7, Heft 4, S. 395
ISSN: 0030-851X
In: Pacific affairs, Band 7, S. 395-405
ISSN: 0030-851X
In: Pacific affairs: an international review of Asia and the Pacific, Band 11, Heft 2, S. 274
ISSN: 1715-3379
In: Pacific affairs: an international review of Asia and the Pacific, Band 8, Heft 2, S. 254
ISSN: 1715-3379
In: Far Eastern survey, Band 7, Heft 5, S. 47-53
In: Far Eastern survey, Band 7, S. 47-53
ISSN: 0362-8949
In: Pacific affairs: an international review of Asia and the Pacific, Band 10, Heft 4, S. 490
ISSN: 1715-3379
In: The women's review of books, Band 8, Heft 6, S. 9
In: Pacific affairs: an international review of Asia and the Pacific, Band 9, Heft 2, S. 294
ISSN: 1715-3379
In: International affairs, Band 19, Heft 1, S. 62
ISSN: 1468-2346
In: Pacific affairs: an international review of Asia and the Pacific, Band 13, Heft 1, S. 92
ISSN: 1715-3379
In: Pacific affairs: an international review of Asia and the Pacific, Band 13, Heft 3, S. 354
ISSN: 1715-3379
Platelet aggregation at the site of atherosclerotic vascular injury is the underlying pathophysiology of myocardial infarction and stroke. To build upon prior GWAS, here we report on 16 loci identified through a whole genome sequencing (WGS) approach in 3,855 NHLBI Trans-Omics for Precision Medicine (TOPMed) participants deeply phenotyped for platelet aggregation. We identify the RGS18 locus, which encodes a myeloerythroid lineage-specific regulator of G-protein signaling that co-localizes with expression quantitative trait loci (eQTL) signatures for RGS18 expression in platelets. Gene-based approaches implicate the SVEP1 gene, a known contributor of coronary artery disease risk. Sentinel variants at RGS18 and PEAR1 are associated with thrombosis risk and increased gastrointestinal bleeding risk, respectively. Our WGS findings add to previously identified GWAS loci, provide insights regarding the mechanism(s) by which genetics may influence cardiovascular disease risk, and underscore the importance of rare variant and regulatory approaches to identifying loci contributing to complex phenotypes. © 2021, This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply. ; National Institutes of Health ; https://doi.org/10.1038/s41467-021-23470-9
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