By Icon Health Publications

ISBN-10: 0597843384

ISBN-13: 9780597843389

ISBN-10: 141751258X

ISBN-13: 9781417512584

This can be a 3-in-1 reference publication. It supplies an entire scientific dictionary overlaying enormous quantities of phrases and expressions in relation to arteriosclerosis. It additionally provides wide lists of bibliographic citations. eventually, it offers details to clients on the best way to replace their wisdom utilizing numerous net assets. The publication is designed for physicians, scientific scholars getting ready for Board examinations, clinical researchers, and sufferers who are looking to get to grips with study devoted to arteriosclerosis. in case your time is effective, this ebook 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 money and time printing 1000s of web content.

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Extra info for Arteriosclerosis - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References

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The basic hypothesis of the ongoing and this proposed projects is that Hcy, at clinically relevant concentrations, selectively inhibits EC growth through a hypomethylation-related mechanism. The ongoing research is designed to investigate the role of Ras demethylation in Hcy-EC growth, to dissect the mechanism in Hcy signaling using cellular and animal models. Because damage to EC is a key feature of arteriosclerosis, Studies 31 the growth inhibition of EC may represent an important mechanism to explain Hcyinduced arteriosclerosis.

Then, we will determine whether hyperhomocysteinemia contributes to glomerular injury in Dahl S rats and whether decreases in plasma Hcys levels associated with a choline and vitamin B therapy regimen prevent the rapid progression of glomerular damages in these rats. We will also explore the renal mechanisms increasing plasma Hcys levels by characterizing the biochemical pathways responsible for the abnormal metabolism of Hcys in the kidney of Dahl S rats using the kinetic analysis of enzyme activities with HPLC techniques and by expression analysis of related genes.

While it has become clear that AGA is a multifactorial problem, the specific mechanisms leading to AGA remain unknown. Because of their pivotal role in the maintenance of vessel homeostasis, endothelial cells (EcS) are likely to represent prime targets in the pathogenesis of AGA. Project 1 is designed to provide in-depth characterization of the process that affects ECs in AGA, from extracellular factors to intracellular molecular pathways that transduce messages to the genome of ECs. By integrating our studies on ECs with other projects of this program, we intend to provide information that will be key to the development of specific strategies to suppress AGA.

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