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Atheromas cholesterol

Necrotic core (atheroma) cholesterol clefts, lipid, foam cells and necrotic debris... [Pg.96]

Wang N, Tabas I, Winchester R, Ravalli S, Rabbani LE, Tall A. Interleukin 8 is induced by cholesterol loading of macrophages and expressed by macrophage foam cells in human atheroma. J Biol Chem 1996 271(15) 8837-8842. [Pg.229]

Atherosclerosis is a wide-spread pathology, manifested chiefly by the deposition of cholesterol in arterial walls, which results in the formation of lipid plaques (atheromas). Lipid plaques are specific foreign bodies around which the connective tissue develops abnormally (this process is called sclerosis). This leads to the cal-cification of the impaired site of a blood vessel. The blood vessels become inelastic and compact, the blood supply through the vessels is impeded, and the plaques may develop into thrombi. [Pg.212]

Familial hypercholesterolemia is characterized by a selective elevation in plasma LDL and deposition of LDL-derived cholesterol in tendons (xanthomas) and arteries (atheromas). [Pg.112]

The data obtained with SERMs are more mixed. Tamoxifen attenuated atheroma development in apoE-null mice, an effect that correlated with changes in the lipoprotein profile and with elevated levels of transforming growth factor-/ (Reckless et al. 1997). The accumulation of cholesterol in atherosclerotic lesions (Bjarnason et al. 1997) in the aorta was limited by... [Pg.229]

Haines CJ, James AE, Panesar NS, Ngai TJ, Sahota DS, Jones RL, Chang AM (1999) The effect of percutaneous oestradiol on atheroma formation in ovariectomized cholesterol-fed rabbits. Atherosclerosis 143 369-375... [Pg.241]

A high plasma concentration of LDL (usually measured as LDL-cholesterol) is a risk factor for the development of atheroma whereas a high concentration of HDL is an anti-risk factor for cardiovascular disease (CVD). Fundamental discoveries relating to cholesterol metabolism and the importance of the LDL receptor made by Nobel laureates Joseph Goldstein and Michael Brown led to an understanding of the role of LDL in atherosclerosis. The impact of HDL in reducing CVD risk is often explained by the removal of excess cholesterol from tissues and its return to the liver, a process known as reverse cholesterol transport. However, evidence from research by Gillian Cockerill and others shows that HDL has a fundamental anti-inflammatory role to play in cardioprotection. [Pg.165]

According to our present knowledge, there are several ways to treat disorders (referred to as hypercholesterolemias or hyperlipoproteinemias) that enhance cholesterol-containing atheroma formation. The class of compounds referred to as statins dominates the treatment of these disorders. [Pg.318]

Our most common lethal disease is atherosclerosis, which causes constriction and blockage of arteries of the heart, brain, and other organs. In the United States, Europe, and Japan half of all deaths can be attributed to this ailment.a,b There seems to be a variety of causes. However, there is agreement that the disease begins with injury to the endothelial cells that form the inner lining of the arteries.3/C/d This is followed by the aggregation of blood platelets at the sites of injury and infiltration of smooth muscle cells, which may be attracted by 12-hydrox-yeicosotetraenoic acid and other chemoattractants formed by activated platelets.c "Foam cells" laden with cholesterol and other lipids appear, and the lesions enlarge to become the characteristic plaques (atheromas). [Pg.1249]

Zheng L, Settle M, Brubaker G, Schmitt D, Hazen SL, Smith JD, Kinter M (2005) Localization of Nitration and Chlorination Sites on Apolipoprotein A-I Catalyzed by Myeloperoxidase in Human Atheroma and Associated Oxidative Impairment in ABCA1-Dependent Cholesterol Efflux from Macrophages. J Biol Chem 280 38... [Pg.491]

Chronic diseases such as atherosclerosis are also propagated by oxidative stress (73). The sequence of events leading to arterial occlusion is complex and not fully understood. However, both platelet adhesion and macrophage activation participate in the formation of atherosclerotic plaques in the environment of elevated serum cholesterol (74). Oxidative chemistry can profoundly affect several steps in the formation of atheroma (75), including recruitment of immune cells such as macrophages, and as during ischemia-reperfusion, the antioxidant nature of NO can inhibit this process (76). [Pg.356]

Body iron level and iron depletion play an important role in the gender differences seen in death from cardiac disease. There is a better correlation with heart disease mortality in iron levels compared with levels of cholesterol (5). It was found that risk of coronary heart disease (6) and carotid atherosclerosis (7) is associated with increased iron stores. However, impaired endothelium-derived nitric oxide activity may be without overt atherosclerosis in patients with risk factors and may be associated with the presence of atherosclerosis (4). Thus, endothelial dysfunction related to iron activity not only may be an early marker for cardiovascular risk but also may contribute to the pathogenesis of atherosclerosis (2) by the stimulation of low-density lipoproteins (LDL) and membrane lipid peroxidation (I) and may be a key to the understanding of early mechanism in the development of atheroma (7,8). Nakayama et al. (9) showed the role of heme oxygenase induction in the modulation of macrophage activation in atherosclerosis. However, Howes et al. (10) concludes that at the moment, the available evidence on iron hypothesis remains circumstantial. Moreover, Kiechl et al. (7) showed that the adverse effect of iron is hypercholesterolemia, In patients... [Pg.241]

Atherosclerosis is characterized by cholesterol-rich arterial thickenings (atheromas) that narrow the arteries and cause blood clots to form. If these blood clots block the coronary arteries supplying the heart, the result is a myocardial infarction, or heart attack. [Pg.339]

This is an inherited disorder in which individuals have a lack of functional LDL receptors preventing cholesterol from being taken up by the tissues. The resulting high blood cholesterol level leads to an increase in the formation of atheromas and can cause death from myocardial infarction during childhood. [Pg.340]

Helianthus annuus (Asteraceae), Viciafaba (Fabaceae), Phoenix dactylifera (date palm) (Palmae), Rhodophyceae (marine red algae) animal membrane component hyperlipidaemia in many heart attack victims LDL carries cholesteryl esters f LDL -> cholesterol-rich arterial atheromas —> atherosclerosis -> blockage, clots — stroke myocardial infarction (heart attack)... [Pg.510]

Vital for membrane formation Preeursor of hormones too Bile salts from its oxidation Cholesterol is good for you Atheroma eareinoma ... [Pg.84]

GC-MS has been responsible for the identification of a variety of unusual lipids associated with diseased conditions. Hydroxyocta-decadienoic esters of cholesterol for example, have been isolated from aortal atheroma placques [277] and branched chain and odd numbered fatty acids identified in the glycerolipids of brain, spinal cord and sciatic nerve [278] from a patient with methylmalonic aciduria. The latter compounds are thought to arise by the replacement of malonyl CoA with methyl malonyl CoA, and acetyl CoA with propionyl CoA at certain stages of fatty acid synthesis. In these and other examples, the lipids need to be hydrolysed to permit the identification of the constituent fatty acids. As the class of lipids is usually known from the separation procedure used, the nature of the fatty acids may allow the characterisation of the complete molecule. However, volatilisation of the intact lipid into the mass spectrometer when possible would be preferable, particularly when it is present in a mixture and separation of the components is first made by GC. [Pg.54]

Choiesteroi oxygenated Atheroma formation arterial damage Atherosclerosis derivatives of cholesterol noncholesterol steroids... [Pg.473]

THD-341 - The tricyclic diterpenold THD-341 (11), at an oral dose of 3 mg/kg or as 0.001% of the diet, lowered serum lipids in cholesterol-cholate fed rats. At a dietary level of 0.01%, THD-341 prevented aortic atheroma formation in cholesterol-fed rabbits and inhibited the progression of established lesions in rabbits fed the cholesterol diet. ... [Pg.204]


See other pages where Atheromas cholesterol is mentioned: [Pg.157]    [Pg.157]    [Pg.130]    [Pg.131]    [Pg.227]    [Pg.16]    [Pg.192]    [Pg.206]    [Pg.154]    [Pg.160]    [Pg.73]    [Pg.312]    [Pg.92]    [Pg.444]    [Pg.317]    [Pg.318]    [Pg.592]    [Pg.246]    [Pg.247]    [Pg.164]    [Pg.295]    [Pg.342]    [Pg.342]    [Pg.288]    [Pg.153]    [Pg.227]    [Pg.55]    [Pg.1647]    [Pg.747]    [Pg.1725]    [Pg.270]    [Pg.1012]   
See also in sourсe #XX -- [ Pg.163 ]




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Atheromas

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