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Tae Hwi Schwantes-An

Researcher at National Institutes of Health

Publications -  8
Citations -  396

Tae Hwi Schwantes-An is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Population & Genome-wide association study. The author has an hindex of 7, co-authored 7 publications receiving 350 citations. Previous affiliations of Tae Hwi Schwantes-An include Washington University in St. Louis & Indiana University.

Papers
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Meta-analysis of gene–environment-wide association scans accounting for education level identifies additional loci for refractive error

Qiao Fan, +172 more
TL;DR: Six novel loci (FAM150B-ACP1, LINC00340, FBN1, DIS3L-MAP2K1, ARID2-SNAT1 and SLC14A2) associated with refractive error are identified and represent an important advance in understanding how gene and environment interactions contribute to the heterogeneity of myopia.
Journal ArticleDOI

Association of the OPRM1 Variant rs1799971 (A118G) with Non-Specific Liability to Substance Dependence in a Collaborative de novo Meta-Analysis of European-Ancestry Cohorts

Tae Hwi Schwantes-An, +120 more
- 01 Mar 2016 - 
TL;DR: In this article, the non-synonymous variant of the mu1 opioid receptor gene (A118G, Asn40Asp) has been extensively studied, yet its role in addiction has remained unclear, with conflicting association findings.
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Smoking and Genetic Risk Variation Across Populations of European, Asian, and African American Ancestry—A Meta‐Analysis of Chromosome 15q25

Li-Shiun Chen, +64 more
- 01 May 2012 - 
TL;DR: In this paper, the observed consistent association of rs16969968 with heavy smoking across multiple populations, combined with its known biological significance, suggests it is most likely a functional variant that alters risk for heavy smoking.
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Increased Genetic Vulnerability to Smoking at CHRNA5 in Early-Onset Smokers

Sarah M. Hartz, +156 more
TL;DR: In this article, the association between rs16969968 and smoking is modified by age at onset of regular smoking, which highlights an increased genetic vulnerability to smoking in early-onset smokers.