By Icon Health Publications
This can be a 3-in-1 reference e-book. It supplies a whole scientific dictionary overlaying hundreds and hundreds of phrases and expressions in terms of liver harm. It additionally supplies broad lists of bibliographic citations. eventually, it offers info to clients on easy methods to replace their wisdom utilizing a variety of web assets. The ebook is designed for physicians, clinical scholars getting ready for Board examinations, clinical researchers, and sufferers who are looking to get to grips with study devoted to liver harm. in the event that your time is efficacious, this publication is for you. First, you won't waste time looking out the web whereas lacking loads of correct info. moment, the booklet additionally saves you time indexing and defining entries. ultimately, you won't waste time and cash printing enormous quantities of web content.
Read or Download Liver Damage - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References PDF
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Additional info for Liver Damage - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References
Using transgenic mice that replicate HBV at high levels in the liver as recipients of HBV-specific CTLs, we have shown that the antiviral potential of the CTLs is primarily mediated by noricytolytic mechanisms that involve the intrahepatic production of type I inflammatory cytokines by these cells. This occurs after the CTLs specifically recognize viral antigens on the surface of the hepatocyte. Following antigen recognition, the CTLs also trigger the death of a small number of hepatocytes and this process leads to the recruitment of many hostderived lymphomononuclear and polymorphonuclear cells into the liver that contribute to the formation of necroinflaminatory foci histologically identical to classical viral hepatitis in man.
In addition to using new water soluble calpain inhibitors, we will block FAS and TNFalpha, well characterized extracellular pro-apoptotic mediators that may be active in the I/Rp-injured liver. A potential regulatory role for the Bcl-2 gene, whose product is inhibitory at various levels of the apoptotic process, will be investigated using transgenic mice overexpressing Bcl-2. Our whole-organ model is uniquely suited to these studies, since - if known precedents hold - signaling for apoptosis most likely involves complex interactions among several cell types.
Retinol deficiency can also cause many unwanted effects. Knockout technology avoids these potential problems. Tissue specific knockout further allows studying the function of the gene in a cell type specific manner without affecting the gene function systemically. We have established an animal model in that the RXRalpha gene is knocked out only in the hepatocyte. RXR-alpha is highly expressed in the liver and is required for almost all the nuclear receptor-mediated pathways. Therefore, hepatocyte RXR-alpha deficient mouse serves as an excellent model for studying retinoid signaling in alcoholic liver disease.