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Examining ERBB2 as a candidate gene for susceptibility to leprosy (Hansen's disease) in Brazil

This study examines whether polymorphisms in the ERBB2 gene were associated with leprosy in primary and replication cohorts from northeastern Brazil.

A Genome-Wide Search for Type 2 Diabetes Susceptibility Genes in an Extended Arab Family

We performed a discovery GWAS in an extended UAE family (N = 178; 66 diabetic; 112 healthy) genotyped on the Illumina Human 660 Quad Beadchip, with...

Genetic and epigenetic susceptibility to early life infection

To date there have been relatively few studies on genetic determinants of susceptibility to neonatal infection and many of these have methodological...

Alternative Recruitment Strategies Influence Saliva Sample Return Rates in Community-Based Genetic Association Studies

Using data from three large-scale genetic association studies we compared recruitment strategy and sample return rates.

A "Candidate-Interactome" Aggregate Analysis of Genome-Wide Association Data in Multiple Sclerosis

The interaction between genotype and Epstein Barr virus emerges as relevant for multiple sclerosis etiology.

Association of a NOD2 gene polymorphism and T-helper 17 cells with presumed ocular toxoplasmosis

We assessed 30 sibships and 89 parent/case trios of presumed ocular toxoplasmosis (POT) to evaluate associations with polymorphisms in the NOD2 gene.

New findings in the pathogenesis of otitis media

This study was the first to concurrently identify middle ear pathogens in both bacterial biofilm and intracellularly in the middle ear mucosa of children and to identify extensive DNA stranding in the MEF from children with AOM

Common and Rare Genetic Variants That Could Contribute to Severe Otitis Media in an Australian Aboriginal Population

Our goal was to identify genetic risk factors for severe otitis media (OM) in Aboriginal Australians.

Reduced socs1 expression in lung fibroblasts from patients with ipf is not mediated by promoter methylation or mir155

The interleukin (IL)-6 family of cytokines and exaggerated signal transducer and activator of transcription (STAT)3 signaling is implicated in idiopathic pulmonary fibrosis (IPF) pathogenesis, but the mechanisms regulating STAT3 expression and function are unknown. Suppressor of cytokine signaling (SOCS)1 and SOCS3 block STAT3, and low SOCS1 levels have been reported in IPF fibroblasts and shown to facilitate collagen production. Fibroblasts and lung tissue from IPF patients and controls were used to examine the mechanisms underlying SOCS1 down-regulation in IPF.