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Nilesh J. Samani

Researcher at University of Leicester

Publications -  836
Citations -  127518

Nilesh J. Samani is an academic researcher from University of Leicester. The author has contributed to research in topics: Genome-wide association study & Population. The author has an hindex of 149, co-authored 779 publications receiving 113545 citations. Previous affiliations of Nilesh J. Samani include University Hospitals of Leicester NHS Trust & Glenfield Hospital.

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Insertion/deletion polymorphism in the angiotensin-converting enzyme gene and risk of restenosis after coronary angioplasty

TL;DR: It is concluded that, in patients undergoing elective PTCA, the I/D polymorphism in the ACE gene does not influence the extent of restenosis, and typing for the polymorphism will not be a useful predictor of risk before the procedure.
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Whole-genome sequencing identifies rare genotypes in COMP and CHADL associated with high risk of hip osteoarthritis.

TL;DR: A genome-wide association study of total hip replacements, based on variants identified through whole-genome sequencing, shows that the full-length CHADL transcript is expressed in cartilage and discovers two rare signals that strongly associate with osteoarthritis total hip replacement.
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Analysis of predicted loss-of-function variants in UK Biobank identifies variants protective for disease

Connor A. Emdin, +55 more
TL;DR: In this paper, the authors found that less than 3% of protein-coding genetic variants are predicted to result in loss of protein function through the introduction of a stop codon, frameshift, or the disruption of an essential splice site; however, such predicted loss-of-function (pLOF) variants provide insight into effector transcript and direction of biological effect.
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Leukocyte telomere length and coronary artery calcification

TL;DR: In this paper, the authors examined the association of telomere length with coronary artery calcification in middle aged adults and found that the relation of length is negatively associated with the presence of coronary atherosclerosis.