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Titlebook: Lipoprotein Metabolism and Atherogenesis; Toru Kita (Professor),Masayuki Yokode (Assistant P Conference proceedings 2000 Springer-Verlag T

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书目名称Lipoprotein Metabolism and Atherogenesis
编辑Toru Kita (Professor),Masayuki Yokode (Assistant P
视频videohttp://file.papertrans.cn/587/586905/586905.mp4
概述Presenting the exciting results of research in the areas of the molecular basis of lipoprotein metabolism,.the link between lipoprotein metabolism disorder and atherogenesis, and the molecular approac
图书封面Titlebook: Lipoprotein Metabolism and Atherogenesis;  Toru Kita (Professor),Masayuki Yokode (Assistant P Conference proceedings 2000 Springer-Verlag T
描述Atherosclerosis leading to coronary heart disease and to cerebrovascular disorders is the number one cause of death in industrialized societies. For the last two decades, great ad­ vances have been made in understanding the pathogenesis of those disorders. Recent studies have revealed that the earliest event in atherogenesis is the adhesion of circulating leukocytes to the vascular endothelial cells and their migration into the subendothelial space. These cells are known to playa central role in the formation of a fatty streak consist­ ing of lipid-laden foam cells. As pathological events continue, the lesion is converted to a more fibrous lesion associated with vascular smooth muscle cells. To solve the enigma of this complicated process, intensive studies in molecular biology have disclosed the genes involved in those events. Some of the genes have been verified by creation of novel animal models, which have led to novel therapeutic strategies for subjects with atherosclerosis. This volume contains papers presented at the International Symposium on Lipoprotein Metabolism and Atherogenesis held in Kyoto December 5-8, 1998, supported in part by the Japan Intractable Diseases Resear
出版日期Conference proceedings 2000
关键词Atherogenesis; Atherosclerosis; Insulin; Lipoprotein Metabolism; Risk Factors; Vascular Endothelial Cells
版次1
doihttps://doi.org/10.1007/978-4-431-68424-4
isbn_softcover978-4-431-68426-8
isbn_ebook978-4-431-68424-4
copyrightSpringer-Verlag Tokyo 2000
The information of publication is updating

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Role Of Lipid Concentrations and Apolipoproteins In Altering ApoB Metabolism and Promoting Coronary inked to coronary events are HDL cholesterol and triglycerides. Baseline triglycerides predict coronary risk in the major statin trials. In CARE and 4S, the triglyceride concentrations during treatment with pravastatin or simvastatin were associated with coronary events. Additional lipid mechanisms
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Long-term Effect of LDL-Apheresis on Familial Hypercholesterolemia Homozygotest in South Africa showed atorvastatin being capable of suppressing cholesterol synthesis and useful in reducing the rebound in patients with homozygous FH under apheresis treatment. Another clinical trial carried out in Japan also showed the efficacy of the statin in such patients, suggesting that t
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Diabetes and Atherosclerosis (5.2±0.1 and 3.2±0.6 ng/mg cell protein, respectively; p<0.02). The amount of oxidized LDL associated to cells grown in 400 mg/dl of glucose was markedly increased compared with the cells grown in 200 mg/dl of glucose. Our results suggesetd that an suitable glucose concentration (400 mg/dl) associa
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Molecular Analysis of Apolipoprotein A-I and E Mutants in Japann of apoE gene is etiologically related to LPG. However, our cases indicate that other genetic or environmental factors seem to be necessary for the development of LPG. Identification of naturally occurring apolipoprotein variants allows understanding the role of apolipoproteins and the mechanism of
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Novel mutations of the LDL Receptor Gene in Familial Hypercholesterolemia Pedigrees in Hokkaido stretch at 1774-8 (codons 571-572), causing a frameshift, in six members of family D; (5) a one-base deletion of T at nucleotide 1963-4 (codon 634), causing a frameshift, in three members of family E. Through the molecular genetic approach a total of 28 individuals were diagnosed unequivocally as h
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Preheparin Lipoprotein Lipase Mass Might Reflect the Amount of Working Lipoprotein Lipase in the Whos augmented, and was also enhanced in the situations in which insulin is functioning well. Then, it might be concluded that preheparin LPL mass can be a noble indicator for the amount of LPL functioning in a whole body, even though indirectly.
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Evidence of linkage in familial combined hyperlipidemia to chromosome 1q21-q23y avoid problems associated with each of the analysis methods alone. No evidence for linkage existed between FCHL and intragenic markers of the candidate genes studied. However, one flanking marker for the apolipoprotein A-II (apoA2) gene resulted in a statistically significant lod score of 3.50 on
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Effect of troglitazone on plasma lipid metabolism and lipoprotein lipaseplasma glucose and glycohemoglobin Alc were 216 ± 34, 160±84, 57± 19, 145±30 mg/dl and 7.8 ± 1.6 %. Four weeks after treatment, those levels were 209 ±36, 105 ±27 ( p=0.004 ), 63 ± 19 ( p=0.02 ) mmol/l, 139±41 mg/dl and 7.3 ±0.6 % ( p=0.01), respectively. The postheparin plasma LPL mass increased fr
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