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Timothy H. Florin

Researcher at University of Queensland

Publications -  151
Citations -  14542

Timothy H. Florin is an academic researcher from University of Queensland. The author has contributed to research in topics: Inflammatory bowel disease & Colitis. The author has an hindex of 46, co-authored 143 publications receiving 12814 citations. Previous affiliations of Timothy H. Florin include Translational Research Institute & Royal Prince Alfred Hospital.

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Genome-wide meta-analysis increases to 71 the number of confirmed Crohn's disease susceptibility loci

Andre Franke, +97 more
- 01 Dec 2010 - 
TL;DR: A meta-analysis of six Crohn's disease genome-wide association studies and a series of in silico analyses highlighted particular genes within these loci implicated functionally interesting candidate genes including SMAD3, ERAP2, IL10, IL2RA, TYK2, FUT2, DNMT3A, DENND1B, BACH2 and TAGAP.
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Meta-analysis identifies 29 additional ulcerative colitis risk loci, increasing the number of confirmed associations to 47.

Carl A. Anderson, +113 more
- 01 Mar 2011 - 
TL;DR: A meta-analysis of six ulcerative colitis genome-wide association study datasets found many candidate genes that provide potentially important insights into disease pathogenesis, including IL1R2, IL8RA-IL8RB, IL7R, IL12B, DAP, PRDM1, JAK2, IRF5, GNA12 and LSP1.
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Mucin dynamics and enteric pathogens

TL;DR: The components of the secreted and cell surface mucosal barriers and the evidence that they form an effective barricade against potential pathogens are described and dynamic alterations in the mucin barrier are described driven by host innate and adaptive immune responses to infection.
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Mucolytic bacteria with increased prevalence in IBD mucosa augment in vitro utilization of mucin by other bacteria.

TL;DR: Increased total mucosa-associated bacteria 16S rRNA gene in macroscopically and histologically normal intestinal epithelium of both Crohn's disease and ulcerative colitis confirmed, which suggests the possibility of an increased source of digestible endogenous mucus substrate.
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Aberrant mucin assembly in mice causes endoplasmic reticulum stress and spontaneous inflammation resembling ulcerative colitis.

TL;DR: It is demonstrated that mucin misfolding and ER stress initiate colitis in mice, and that ER stress-related mucin depletion could be a fundamental component of the pathogenesis of human colitis and that clinical studies combining genetics, ER stressed pathology and relevant environmental epidemiology are warranted.