By Icon Health Publications
It is a 3-in-1 reference publication. It offers a whole scientific dictionary overlaying 1000s of phrases and expressions in relation to amyloidosis. It additionally supplies wide lists of bibliographic citations. ultimately, it presents info to clients on tips to replace their wisdom utilizing quite a few web assets. The booklet is designed for physicians, clinical scholars getting ready for Board examinations, scientific researchers, and sufferers who are looking to get to grips with examine devoted to amyloidosis. in the event that your time is efficacious, this booklet is for you. First, you won't waste time looking the web whereas lacking loads of appropriate details. moment, the e-book additionally saves you time indexing and defining entries. ultimately, you won't waste time and cash printing 1000's of websites.
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Additional info for Amyloidosis - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References
Professor; Medicine; Boston University Medical Campus 715 Albany St, 560 Boston, Ma 02118 Timing: Fiscal Year 2002; Project Start 12-APR-2002; Project End 31-MAR-2007 Summary: AL amyloidosis is a bone marrow plasma cell dyscrasia, related to multiple myeloma and other monoclonal gammopathies, in which a mutant immunoglobulin light-chain is over-expressed and deposits in many organs. It is the most common form of systemic amyloidosis in the Unite States, estimated to occur in more than 5-12 persons/million/year.
The amyloid-related vasculopathy will be defined as to regional distribution, vessel sizes and type. Fresh brain tissues will serve as a source of endothelial and smooth muscle cells for cultures and for ApoE isotyping. Vasculopathy with amyloid burden assessed histochemically, and immunocytochemically for Abeta peptide type, will be correlated with distribution of receptors such as gp330/megalin, a member of the LDL receptor family that binds Abeta/APO-J complex; RAGE, for Abeta binding; macrophage markers )CD11b, CD68); cell surface adhesion molecules (PECAM-1 and PAF receptors), and hemostasis markers (CPA, thrombomodulin).
The mice will sere as a whole animal model for testing hypotheses about AL amyloid pathogenesis; furthermore, in collaboration with Project 4, they will serve as a preclinical model for immunotherapy. ; Washington University Lindell and Skinker Blvd St. Louis, Mo 63130 Timing: Fiscal Year 2002 Summary: In Project 3, a neurotoxicological and behavioral studies are proposed to test the hypothesis that sensitivity to the effects results from suppression of N-methyl-Daspartate (NMDA) receptor function, referred to as NRHYPO, is increased in mice containing transgenes pertaining to the expression of human apolipoprotein E (apoE) and beta amyloid precursor protein (APP).