Kidney Failure - A Medical Dictionary, Bibliography, and by Icon Health Publications

By Icon Health Publications

This can be a 3-in-1 reference ebook. It provides an entire clinical dictionary protecting countless numbers of phrases and expressions on the subject of kidney failure. It additionally supplies huge lists of bibliographic citations. ultimately, it offers details to clients on how you can replace their wisdom utilizing a number of net assets. The publication is designed for physicians, scientific scholars getting ready for Board examinations, clinical researchers, and sufferers who are looking to familiarize yourself with examine devoted to kidney failure. in case your time is efficacious, this booklet is for you. First, you won't waste time looking out the net whereas lacking loads of proper details. moment, the e-book additionally saves you time indexing and defining entries. ultimately, you won't waste time and cash printing 1000s of websites.

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Pharmacology; Yale University 47 College Street, Suite 203 New Haven, Ct 065208047 Timing: Fiscal Year 2003; Project Start 01-JUN-2004 Summary: (provided by applicant): Autosomal dominant polycystic kidney disease (ADPKD) affects millions of people and it is the fourth leading cause of kidney failure in the United States. The two genes encoded in this disease are PKD1 and PKD2, and mutations in either gene are associated with the phoenotype seen in ADPKD. The longterm objective entails PKD2 gene product, polycystin-2, functions as a calcium permeable nonselective cation channel.

In Specific Aim 1, the effect on renal function of specific iNOS versus non-specific NOS inhibition during endotoxemia will be studied; the role of eNOS will be examined in eNOS knockout mice. In Specific Aim 2, the role of ET- 1 will be examined by assessment of renal function and capillary leak during early endotoxemia in ET-1 knockout mice and mice treated with an ET receptor antagonist. Specific Aim 3 will study the role of the interaction of the NO and ET-1 systems by examining the result of non-specific versus specific iNOS inhibition on ET-1 gene and protein expression.

This proposal will test the hypothesis that endotoxin- induced ARF is a consequence of renal neutrophil infiltration, renal cell apoptosis, and other forms of neurotic or sublytic injury by the direct action of TNF on renal tubular cells. The first specific aim seeks to characterize the time course of leukocyte accumulation in the kidney after endotoxin administration, to identify key adhesion molecules and chemokines mediating this process, and to evaluate their pathogenic role with the use of inhibitory antibodies and genetic "knockout" mice.

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