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Hypercholesterolemia, Hypocholesterolemia, Hypertriglyceridemia, in Vivo Kinetics (Paperback, Softcover reprint of the original 1st ed. 1991)
Loot Price: R1,584
Discovery Miles 15 840
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Hypercholesterolemia, Hypocholesterolemia, Hypertriglyceridemia, in Vivo Kinetics (Paperback, Softcover reprint of the original 1st ed. 1991)
Series: Advances in Experimental Medicine and Biology, 285
Expected to ship within 15 - 20 working days
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The past two decades have seen steady progress in our understanding
of the pathogenesis of atherosclerosis. The role of low density
lipoprotein (LOL) increase and of LOL receptor deficiency or
malfunctions in familial hypercholesterolemia has been largely
enlightened by the works of Brown and Goldstein. These authors
postulated also that modification of LOL to a form recognized by
the scavenger or acetyl-LOL receptor may be required for lipid
loading of macrophage-derived foam cells in the lesions. A growing
body of evidence suggests that oxidative modification of LOL could
enhance its atherogenicity by its implication as a factor in the
generation of foam cells. Thus, if the role of LOL in the
pathogenesis of hypercholesterolemia was well established a great
deal of information appears currently on new approaches such as the
mechanisms leading to the accumulation of foam cells, the impact of
LOL structural alterations, notably oxidation and the role of gene
mutations of apolipoprotein Band/or LOL receptor The opening topic
is devoted to these new avenues outlined in the field of
hypercholesterolemia. The first part concerns the genetic aspects
of atherosclerosis: mainly the genetics of apo 1 ipoprote ins ,
their transcriptional regulation, the amino acid mutations of the
apo B gene and of the LOL receptor gene, the structural domains and
the acylation sites of apoprotein B.
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