By Jim W. Burgess, Philip A. Sinclair, Christophe M. Chretien, Jonathon Boucher (auth.), Associate Professor Sukhinder Kaur Cheema (eds.)
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.
- 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.
Read or Download Biochemistry of Atherosclerosis PDF
Similar biochemistry books
Biochemical research is a speedily increasing box and is a key part of smooth drug discovery and examine. equipment of Biochemical research presents a periodic and authoritative evaluation of the newest achievements in biochemical research. based in 1954 via Professor David Glick, equipment of Biochemical research offers a well timed assessment of the newest advancements within the box.
During this quantity, in vitro types for the research of lymphoid mobilephone features and strategies for the examine of lymphoid telephone receptors are awarded. Lymphocyte in vitro transformation is mentioned within the first part that describes tools for the in vitro stimulation of lymphocytes. a few specific media for the research of lymphocyte transformation also are mentioned.
- Inorganic chemical biology : principles, techniques and applications
- Enzyme Kinetics for Systems Biology
- Nucleotide Metabolism. An Introduction
- Carbonic Anhydrase: Its Inhibitors and Activators
- The Healing Factor: Vitamin C Against Disease
Extra resources for Biochemistry of Atherosclerosis
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.  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.
Biochemistry of Atherosclerosis by Jim W. Burgess, Philip A. Sinclair, Christophe M. Chretien, Jonathon Boucher (auth.), Associate Professor Sukhinder Kaur Cheema (eds.)