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 offers cutting-edge discussions in state-of-the-art biochemical examine, supplying interesting advancements that effect healthcare and sickness learn. Volumes within the sequence concentrate on cross-disciplinary biomedical examine and consider quite a few subject matters in biochemistry, cellphone biology, molecular biology, and biomedicine.

Biochemistry of Atherosclerosis

Sukhinder Kaur Cheema

Biochemistry of Atherosclerosis examines atherosclerosis in nice element, targeting the danger 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 when it comes to atherosclerosis from prime scientists all over the world who're on the vanguard of atherosclerosis learn. Biochemistry of Atherosclerosis is key interpreting for biomedical and medical researchers.

Key topics:

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

About the Editor:

Sukhinder Kaur Cheema is presently affiliate Professor of Biochemistry and a CIHR (Canadian Institutes of wellbeing and fitness learn) New Investigator on the Memorial college of Newfoundland. knowledgeable in dietary biochemistry, lipid metabolism and heart problems, she is pass appointed in college of medication on the Memorial collage of Newfoundland.

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Additional resources for Biochemistry of Atherosclerosis

Sample text

Putting it all together, data from families with genetic causes of LCAT deficiency suggest that FED mutations may confer higher risk of CAD than those with CLD. On the other hand, subjects homozygous for CLD mutations are generally not at risk of accelerated CAD but the heterozygotes with partial LCAT deficiency, appear to be more prone. , the proatherogenic potential of partial LCAT deficiency require confirmation as this would form the basis for LCAT being a potential therapeutic target. 28 Dominic S.

Unlike previous transgenic models, the short-term overexpression of the LCAT gene in this experiment, despite a 64% raise in the LCAT activity, did not result in any significant change in HDL-C, the plasma FC/CE ratio, or the ability of the plasma to increase efflux of cholesterol from cells [35]. Therefore, the observed reduction in atherosclerosis as a result of LCAT-gene transfer was attributed to LCAT playing a significant role in modulating the oxidative stress. Collectively, hepatic overproduction of LCAT in mouse models have resulted in mixed results in the context of its role in modulating atherogenicity.

Ann NY Acad Sci 902: 103–111, 2000. Pittman RC, Steinberg D: Sites and mechanisms of uptake and degradation of high density and low density lipoproteins. J Lipid Res 25: 1577–1585, 1984. Calvo D, Gomez-Coronado D, Lasuncion MA, Vega MA: CLA-1 is an 85-kD plasma membrane glycoprotein that acts as a high-affinity receptor for both native (HDL, LDL, and VLDL) and modified (OxLDL and AcLDL) lipoproteins. Arterioscler Thromb Vasc Biol 17: 2341–2349, 1997. Calvo D, Gomez-Coronado D, Suarez Y, Lasuncion MA, Vega MA: Human CD36 is a high affinity receptor for the native lipoproteins HDL, LDL, and VLDL.

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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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