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Jan Novak

Researcher at University of Alabama at Birmingham

Publications -  362
Citations -  19039

Jan Novak is an academic researcher from University of Alabama at Birmingham. The author has contributed to research in topics: Nephropathy & Medicine. The author has an hindex of 70, co-authored 320 publications receiving 16150 citations. Previous affiliations of Jan Novak include Masaryk University & Mahidol University.

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Glycosylation in health and disease.

TL;DR: The broad role of glycans in immunity, cancer, xenotransplantation and glomerular filtration and the potential of ‘glycomedicine’ are discussed.
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The Pathophysiology of IgA Nephropathy

TL;DR: Recent advances in understanding the biochemical, immunologic, and genetic pathogenesis of IgA nephropathy are discussed, and five distinct susceptibility loci are identified that potentially influence these processes and contain candidate mediators of disease.
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Genome-wide association study identifies susceptibility loci for IgA nephropathy

TL;DR: Three independent loci in the major histocompatibility complex, as well as a common deletion of CFHR1 and CFHR3 at chromosome 1q32 and a locus at chromosome 22q12 that each surpassed genome-wide significance, explain 4–7% of the disease variance and up to a tenfold variation in interindividual risk.
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Naturally Occurring Human Urinary Peptides for Use in Diagnosis of Chronic Kidney Disease

TL;DR: The establishment of a reproducible, high resolution method for peptidome analysis of naturally occurring human urinary peptides and proteins, ranging from 800 to 17,000 Da, using samples from 3,600 individuals analyzed by capillary electrophoresis coupled to MS is reported.
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Discovery of new risk loci for IgA nephropathy implicates genes involved in immunity against intestinal pathogens

Krzysztof Kiryluk, +91 more
- 01 Nov 2014 - 
TL;DR: A genome-wide association study of IgA nephropathy (IgAN), the most common form of glomerulonephritis, with discovery and follow-up in 20,612 individuals of European and East Asian ancestry is performed, suggesting a possible role for host–intestinal pathogen interactions in shaping the genetic landscape of IgAN.