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Titlebook: Cholesterol Transport Systems and Their Relation to Atherosclerosis; Armin Steinmetz,Hans Kaffarnik,Jürgen Schneider Conference proceeding

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樓主: Spouse
41#
發(fā)表于 2025-3-28 15:16:47 | 只看該作者
https://doi.org/10.1007/978-3-322-87681-2vel must either decrease the rate of LDL formation or speed up the rate of its clearance from the plasma. The latter can be effected by increasing the specific LDL (or apo B, E) receptor activity in the liver, as is actually brought about by administration of bile acid sequestrants [3] and/or compac
42#
發(fā)表于 2025-3-28 20:36:56 | 只看該作者
43#
發(fā)表于 2025-3-28 23:30:20 | 只看該作者
Verfahrensbeschreibung Tiefziehen,own that half of apo A-I is associated with apo A-II while the rest occurs in lipoproteins which contain no apo A-II [1, 2]. These two types of lipoprotein particles, present in vivo, were described by numerous authors and have been suggested to represent metabolically distinct entities [1–6]. Both
44#
發(fā)表于 2025-3-29 06:30:46 | 只看該作者
45#
發(fā)表于 2025-3-29 10:23:34 | 只看該作者
https://doi.org/10.1007/978-3-642-75092-2ir capacity to donate cholesteryl ester (CE) to other lipoproteins [1]. These two processes are fundamental to the uptake of cholesterol by tissues and to the removal of cholesterol from tissues. Various plasma proteins are involved in these processes firstly, lecithin cholesterol acyltransferase (L
46#
發(fā)表于 2025-3-29 12:57:28 | 只看該作者
47#
發(fā)表于 2025-3-29 17:33:24 | 只看該作者
Cholesterol Transport Systems and Their Relation to Atherosclerosis978-3-642-83665-7Series ISSN 1431-7567
48#
發(fā)表于 2025-3-29 20:48:20 | 只看該作者
49#
發(fā)表于 2025-3-30 03:29:28 | 只看該作者
https://doi.org/10.1007/978-3-322-87681-2vel must either decrease the rate of LDL formation or speed up the rate of its clearance from the plasma. The latter can be effected by increasing the specific LDL (or apo B, E) receptor activity in the liver, as is actually brought about by administration of bile acid sequestrants [3] and/or compactin or mevinolin [4].
50#
發(fā)表于 2025-3-30 06:40:43 | 只看該作者
https://doi.org/10.1007/978-3-642-83665-7Lipoprotein; atherosclerosis; heart; high-density lipoprotein (HDL); homeostasis; metabolism; protein; meta
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