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Ranjan Deka

Researcher at University of Cincinnati

Publications -  197
Citations -  10628

Ranjan Deka is an academic researcher from University of Cincinnati. The author has contributed to research in topics: Population & Allele. The author has an hindex of 52, co-authored 178 publications receiving 9856 citations. Previous affiliations of Ranjan Deka include University of Texas Health Science Center at Houston & Boston Children's Hospital.

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Type 2 Diabetes and Three Calpain-10 Gene Polymorphisms in Samoans: No Evidence of Association

TL;DR: This study failed to detect any association between case subjects and control subjects in allele frequencies, haplotype frequencies, or haplotype combinations of UCSNP43, -19, and -63, and showed no evidence of linkage, among 201 affected sib pairs, in the region of chromosome 2 that contains these SNPs.
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Persistence of lung CD8 T cell oligoclonal expansions upon smoking cessation in a mouse model of cigarette smoke-induced emphysema.

TL;DR: It is demonstrated that chronic cigarette smoke exposure, alone, causes a persistent adaptive T cell immune response, which has important implications for therapeutic approaches in the treatment of COPD, and provides insight into potential mechanisms involved in disease pathogenesis.
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A population genetic study of six VNTR loci in three ethnically defined populations.

TL;DR: Lack of fit of all VNTR loci to one particular model of mutational change, either the Infinite Allele Model or the Stepwise Mutation Model, suggests more than one mechanism for production of new VnTR alleles.
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Intra‐ and inter‐population diversity at short tandem repeat loci in diverse populations of the world

TL;DR: This study dispels some of the concerns regarding the applicability of DNA typing data for forensic use and observes a reciprocal relationship between gene diversity and FST levels.
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Toward the evaluation of function in genetic variability: characterizing human SNP frequencies and establishing BAC-transgenic mice carrying the human CYP1A1_CYP1A2 locus.

TL;DR: Function in human CYP1A1_CYP1A2 locus variability will be evaluated, with regard to toxicity and cancer caused by combustion products.