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

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Role of Apolipoprotein A-IV in Reverse Cholesterol Transportis of apo A-IV, the intestinal induction of this apoprotein has been studied in more detail. In primary cultures of nonproliferating rat hepatocytes dexamethasone and insulin increased apo A-IV mRNA substantially and could be shown to act synergistically when applied simultaneously [13].

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https://doi.org/10.1007/978-3-662-09700-7 and specific amphipathic proteins (see [1] for review). The latter, the apolipoproteins, not only are responsible for maintaining the structure of the particle but also act as recognition signals for cell membrane receptors which trigger lipoprotein endocytosis [2]. The “classical” lipoprotein rece

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Analyse der Automatisierungsaufgabe,abolized by a complex process that is regulated by a number of different factors [1]. These include the assembly and secretion of triglyceride-rich apo B containing lipoprotein particles, intravascular lipolysis of the triglycerides, exchange of lipids and proteins between lipoprotein particles, and

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https://doi.org/10.1007/978-3-642-52219-2 lipoproteins which are then internalized by the cells. Insofar as lipoprotein receptors affect the concentration of lipoproteins in the plasma and may play a role in lipoprotein accumulation in arterial cells, they have both a direct and an indirect influence on the progression of atherosclerosis.

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Situation der Arbeitsplatzgestaltung,FCHL) was first used by Joseph Goldstein and associates at the University of Washington to designate families exhibiting multiple lipoprotein phenotypes. At the same time, similar families were described by Esko Nikkilä in Helsinki and Herbert Rose in New York. Affected members of families with FCHL

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Hans-Friedrich Peters,Rudolf Kollerurveys conducted in many countries over the past 30 years have uniformly shown that atherosclerosis becomes more severe as the mean level of low-density lipoprotein (LDL) cholesterol rises in a population [2, 3]. Especially in patients with familial hypercholesterolemia (FH), there are elevations of

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,Gestaltänderung technischer Gebilde,ata in some cases, and increased risk of myocardial infarction [5]. The genetic basis of FH was analysed by Brown and Goldstein et al. in 1983, who demonstrated that FH is caused by mutation in the LDL receptor gene, and that the defective gene is inherited as an autosomal dominant disorder [6]. The

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https://doi.org/10.1007/978-3-642-81905-6 to be associated with a specific lipoprotein fraction that is now commonly termed Lp(a) (for recent review see [2]). This lipoprotein has pre-β-mobility on zone electrophoresis as opposed to the β-mobility of LDL, and it has a higher hydrated density of 1.06–1.12 g/ml.

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https://doi.org/10.1007/978-3-322-87681-2e early atherosclerotic lesion [1]. Monocytes/macrophages invade the aortic wall through an intact endothelial layer early after induction of a hypercholesterolemic state in humans and various experimental animal systems [2–4]. The underlying mechanisms stimulating the cell migration are still unkno