Jim W. Burgess, Philip A. Sinclair, Christophe M. Chretien,'s Biochemistry of Atherosclerosis PDF

By Jim W. Burgess, Philip A. Sinclair, Christophe M. Chretien, Jonathon Boucher (auth.), Associate Professor Sukhinder Kaur Cheema (eds.)

ISBN-10: 0387312528

ISBN-13: 9780387312521

ISBN-10: 0387362797

ISBN-13: 9780387362793

About the Series:

Advances in Biochemistry in Heath and Disease provides state of the art discussions in state-of-the-art biochemical study, supplying interesting advancements that impression healthcare and sickness study. Volumes within the sequence specialise in cross-disciplinary biomedical examine and consider quite a few issues in biochemistry, phone biology, molecular biology, and biomedicine.

Biochemistry of Atherosclerosis

Sukhinder Kaur Cheema

Biochemistry of Atherosclerosis examines atherosclerosis in nice element, concentrating on the chance of atherosclerosis, and the biochemical pathways concerned. It offers a breadth of information in addition to new insights right into a number of subject matters with regards to atherosclerosis from top scientists all over the world who're on the vanguard of atherosclerosis learn. Biochemistry of Atherosclerosis is vital interpreting for biomedical and medical researchers.

Key topics:

    • Hyperlipidaemia and Atherosclerosis
    • Diabetes triggered Atherosclerosis
    • Hypertension caused Atherosclerosis
    • Homocysteine Metabolism and Atherosclerosis
    • Role of the Immune process in Atherosclerosis
    • Role of Infectious brokers in Atherogenesis
    • Dietary administration of Aherosclerosis

About the Editor:

Sukhinder Kaur Cheema is at present affiliate Professor of Biochemistry and a CIHR (Canadian Institutes of future health study) New Investigator on the Memorial collage of Newfoundland. knowledgeable in dietary biochemistry, lipid metabolism and heart problems, she is move appointed in school of drugs on the Memorial collage of Newfoundland.

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Extra resources for Biochemistry of Atherosclerosis

Sample text

68. 69. 19 lipoprotein-cholesteryl esters via the scavenger receptor B1. J Lipid Res 40: 1294–1303, 1999. Brundert M, Greten H, Rinninger F, Heeren J: Hepatic lipase mediates an increase in selective uptake of HDL-associated cholesteryl esters by cells in culture independent from SR-BI. J Lipid Res 44: 1020–1032, 2003. Connelly MA, Klein SM, Azhar S, Abumrad NA, Williams DL: Comparison of class B scavenger receptors, CD36 and scavenger receptor BI (SR-BI), shows that both receptors mediate high density lipoprotein-cholesteryl ester selective uptake but SR-BI exhibits a unique enhancement of cholesteryl ester uptake.

In this paradigm, one could envision a pool of HDL that would recycle between the smaller “metabolically active” form and the more mature form, and the cycle will continue to fuel the net movement of cell-derived cholesterol towards the liver for removal. LCAT is one of the several major modulators of the plasma HDL-C levels, the other being apoA-I, ABCA1, and CETP. In humans subjects with genetic deficiency of LCAT, those who are homozygous a functional LCAT gene mutation develop severe HDL deficiency and the ones heterozygous for a defective LCAT gene develop intermediate levels of HDL deficiency [10, 11].

30 Dominic S. NG LCAT knockout mice have been studied to explore the role of LCAT in atherosclerosis as well as to elucidate the possible mechanism for the paradoxical absence of accelerated atherosclerosis in LCAT deficient humans. A recent study by Lambert et al. [39] reported significant reductions in aortic atherosclerosis attributable to LCAT deficiency in a number of different dyslipidemic backgrounds, including wild type, LDL receptor knockout (LDLR−/−), and CETP transgenic mice, fed a cholate-containing, high cholesterol/high fat diet, and in apoE−/− background fed a chow diet.

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Biochemistry of Atherosclerosis by Jim W. Burgess, Philip A. Sinclair, Christophe M. Chretien, Jonathon Boucher (auth.), Associate Professor Sukhinder Kaur Cheema (eds.)


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