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Atheromatous deposit

Diseases. Liquid crystals have been impHcated in a number of disease conditions in the human body. A complex cholesterol—phosphoHpid—Hpoprotein Hquid crystal phase has been identified in the initiation and maintenance of atheromatous deposits on the aortic intima in dissected human and rabbit arteries (40). The paracrystalHne nature of this precursor to plaque buildup with the resultant loss of arterial elasticity... [Pg.202]

According to Loeper et al., who have studied the role of silicon in human and experimental atherosclerosis6 7 silicon has a protective function for the artery by decreasing the atheromatous deposits and by conserving the integrity of the elastic tissue and the connective tissue. [Pg.25]

Figure 2. Section of intimia of human artery showing early atheromatous deposit partly soluble in Sudan black... Figure 2. Section of intimia of human artery showing early atheromatous deposit partly soluble in Sudan black...
Figure 8. Atheromatous deposit from human artery (Figure 2) showing smectic mesophase with spherulitic structure... Figure 8. Atheromatous deposit from human artery (Figure 2) showing smectic mesophase with spherulitic structure...
Aeeording to a current medical dictionary antiatherosclerotics may be defined as a form of simple intimal arteriosclerosis with atheromatous deposits within and beneath the intima . [Pg.867]

The underl5ung cause of most cases of cardiovascular disease is atherosclerosis [3]. This term describes the stenotic type of atherosclerotic disease in which fatty ( atheromatous ) deposits are formed in the intimal layer of the larger elastic arteries and certain muscular arteries, and interfere with blood flow. Further consequences of this process are fibrosis and calcification of the subintimal and medial layers, and in the narrowed lumen, the growing possibility of thrombosis, leading to total occlusion. [Pg.219]

Figure 5.24 An illustration of arterial disease due to atheromatous deposits ... Figure 5.24 An illustration of arterial disease due to atheromatous deposits ...
The accumulation of apo(a) in the aorta wall and in saphenous vein bypass grafts in relation to Lp(a) levels was recently demonstrated (C14, R3). Subsequently, the preferential deposition of extracellular apo(a) in atherosclerotic lesions of aortic and coronary artery tissue, in conjunction with the intracellular localization of apo(a) in macrophage-derived foam cells, has been the focus of a number of studies (N6, P7, S34, S35, W17). These careful studies also demonstrated the avid binding of Lp(a) to extracellular matrix components and the colocalization of fibrin and apo(a) in atheromatous lesions (N8, W16). [Pg.95]

N6. Niendorf, A., Rath, M., Wolf, K., Peters, S., Arps, H., Beisiegel, U., and Dietel, M., Morphological detection and quantification of lipoprotein(a) deposition in atheromatous lesions. Virchows Arch. A Pathol. Anat. Histopathol. 417, 105-111 (1990). [Pg.127]

It occurs in the animal economy, normally in the bile, blood (especially that coming from the brain), nerve-tissue, brain,spleen, sebum, contents of the intestines, meconium, and faeces pathologically in biliary calculi, in the urine in diabetes and icterus, in the fluids of ascites, hydrocele, etc., in tubereular and cancerous deposits, in cataracts, in atheromatous degenerations, and sometimes in masses of considerable size, in cerebral tumors. It also exists in the vegetable world in peas, beans, olive-oil, wheat, etc. It is best obtained from biliary calculi, the lighter-colored varieties of which consist almost entirely of this substance. [Pg.433]

In older patients, and in those suffering from diabetes or chronic renal failure, microcalcifications in the wall of the cavernosal arteries are frequently detectable and are the expression of calcium deposits in atheromatous endothelial plaques (Fig. 6.2) or in the tunica media as observed in subjects on chronic hemodialysis (Fig. 6.3). [Pg.45]

It has been stated that the rate of deposition of cholesterol and desmosterol into atheromatous plaques is approximately the same [137]. Therefore, the therapeutic value of hypohpidemic agents that inhibit cholesterol bios5mthesis at the last stage of biosynthesis is questionable. In addition, triparanol exerted definite teratogenic action in the rat [138,139], showed high toxicity in the dog [140], and caused ichthyosis and loss of hair and cataracts in man [141, 142]. Due to these side effects this drug is no longer chnically available. [Pg.236]

A large fraction of the cholesterol present in lymph and blood plasma is found in the chylomicrons and about two-thirds of the plasma cholesterol is esterified with fatty acids giving cholesteryl esters. Cholesterol and its esters constitute a large fraction of the lipid present in the atheromatous plaques which are deposited in the intima of arteries in the condition of atherosclerosis (page 267). Cholesterol, which is insoluble in aqueous media, is also a major constituent of most gallstones. [Pg.265]

The major limitation to the use of roentgenography for atherosclerotic calcification as an atheroma assessment method is that calcium occurs principally in late lesions. Atheromatous calcification is a terminal process a deposit in dead or dying tissue. [Pg.122]

Several mechanisms have been suggested whereby an increase in plasma fibrinogen concentration may be linked to CHD. These include the involvement of fibrinogen and fibrin in the evolution of the atheromatous plaque through fibrin deposition and in... [Pg.165]


See other pages where Atheromatous deposit is mentioned: [Pg.152]    [Pg.154]    [Pg.187]    [Pg.531]    [Pg.152]    [Pg.154]    [Pg.187]    [Pg.531]    [Pg.37]    [Pg.437]    [Pg.198]    [Pg.1185]    [Pg.453]    [Pg.260]    [Pg.333]    [Pg.284]    [Pg.174]    [Pg.185]   
See also in sourсe #XX -- [ Pg.146 ]




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