Download Atherosclerosis - A Medical Dictionary, Bibliography, and by Health Publica Icon Health Publications PDF

By Health Publica Icon Health Publications

This can be a 3-in-1 reference ebook. It offers an entire clinical dictionary overlaying hundreds of thousands of phrases and expressions in terms of atherosclerosis. It additionally offers wide lists of bibliographic citations. eventually, it presents info to clients on the right way to replace their wisdom utilizing quite a few net 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 examine devoted to atherosclerosis. in case your time is effective, this booklet is for you. First, you won't waste time looking the net whereas lacking loads of correct details. moment, the ebook additionally saves you time indexing and defining entries. ultimately, you won't waste money and time printing 1000's of web content.

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Assistant Professor; Inst/Gene Therapy & Mol Med; Mount Sinai School of Medicine of Nyu of New York University New York, Ny 10029 Timing: Fiscal Year 2001; Project Start 30-SEP-2001; Project End 31-JUL-2005 Summary: (provided by applicant): During initiation of immune responses, dendritic cells migrate from sites of antigen capture to the T cell zones of lymphoid organs to activate antigen-specific T cells. It remains to be determined whether dendritic cells that enter or develop within atherosclerotic plaques migrate from the plaques, and if so, whether T dependent immune responses that may thereby develop against plaque antigens lead to progression of atherosclerosis.

The propensity to develop hyperlipidemia and atherosclerosis will be examined in transgenic mice that overexpress human PF4. These studies are designed to gain insight into a novel mechanism by which persistent platelet activation may promote the development of atherothrombotic disease. An understanding of the structural basis of the PF4-LDL-R interaction may identify a potential locus for therapeutic intervention. This research proposal is part of comprehensive training program designed to prepare the applicant for a career as an independent investigator in the field of vascular biology.

1). 2). 3). Aim 2: To characterize the region of p53 that interacts with fortilin and other molecules. 2) of p53 participates in fortilin binding, using deletion and point mutants, respectively. 3). Aim 3: To investigate the regulatory role of fortilin-p53 interaction in apoptosis. 3) THROUGH ITS DIRECT binding of p53. Knowledge gained I this proposal will enable us to have a solid foundation for the future intervention of human atherosclerosis. Generate_Screen • Project Title: CHEMOKINE RECEPTOR ANTAGONISTS IN INFLAMMATORY DISEASE Principal Investigator & Institution: Shahrara, Shiva; Medicine; Northwestern University Office of Sponsored Programs Chicago, Il 60611 Timing: Fiscal Year 2003; Project Start 01-FEB-2003; Project End 31-JAN-2008 Summary: (provided by applicant): There are many similarities in inflammatory responses observed in atherosclerosis and rheumatoid arthritis (RA).

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