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This can be a 3-in-1 reference booklet. It supplies an entire clinical dictionary overlaying hundreds of thousands of phrases and expressions on the subject of fibrosis. It additionally supplies broad lists of bibliographic citations. eventually, it offers details to clients on the way to replace their wisdom utilizing a number of net assets. The publication is designed for physicians, clinical scholars getting ready for Board examinations, scientific researchers, and sufferers who are looking to get to grips with study devoted to fibrosis. in the event that your time is efficacious, this publication is for you. First, you won't waste time looking the web whereas lacking loads of suitable details. moment, the booklet additionally saves you time indexing and defining entries. ultimately, you won't waste time and cash printing 1000's of web content.
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Additional info for Fibrosis - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References
Professor in Physiology, Pediatrics And; Cellular/Molecular Physiology; University of North Carolina Chapel Hill Office of Sponsored Research Chapel Hill, Nc 27599 Timing: Fiscal Year 2002; Project Start 01-SEP-1995; Project End 31-MAY-2007 Summary: (provided by applicant): Major objectives of this research are to gain a better understanding of positive and negative mediators of inflammation induced intestinal fibrosis, an incurable complication of Crohn's disease (CD). Findings in animal models of acute colitis and in patients with CD indicate benefits of growth hormone (GH) Studies 33 therapy in CD but the documented fibrogenic effects of GH and insulin-like growth factor-I (IGF-I) which is induced by GH, support a hypothesis that GH therapy may exacerbate fibrosis in CD.
During the previous funding period we proposed to test the hypothesis that 30 Fibrosis constitutive upregulation of collagen and other ECM genes in SSc is caused by different expression levels and modification patterns of transcription factors involved in collagen gene expression by SSc fibroblasts. Our recent findings significantly strengthen this hypothesis. We demonstrated that Ets family transcription factors, particularly Fli-1, are important regulators of collagen homeostasis in healthy skin fibroblasts and among the key contributors to the excessive collagen production by SSc fibroblasts.
During injury, cells are exposed to molecules such as interferon-gamma (IFN-gamma) and transforming growth factor-beta (TGFbeta), regulating production of matrix components. Clinical trials for interstitial pulmonary fibrosis (IPF) are ongoing. However, very little is understood concerning collagen repression by this mediator. This project focuses on establishing the mechanisms by which collagen transcription is repressed by IFN- gamma. We have recently described a regulatory factor for X-box (RFX) binding site at the collagen transcription start site.