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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Among the many, multifactorial etiologies of atherosclerosis is excessive filtration and deposition of lipids, particularly cholesterol esters, in arterial walls; furthermore, the monoclonal theory purports that the artheroma is an uncontrolled proliferation of cells similar to a benign tumor. These 2 aspects of atherosclerosis pathogenesis were studied in 5 healthy women on birth control pills by investigating the level of mononuclear cell cholesterol ester hydrolase (CEH). Control subjects underwent identical investigation. Mononuclear CEH activity was signficantly lower in women on oral contraceptives than in controls in 4 of the 5 test intervals and showed no signficant fluctuation in activity. Average value of CEH in 5 women on birth control pills was 927+ or -81 pmol/mg of protein/hour. In 5 men followed at 5-day intervals, no significant fluctuation of CEH activity was found. Mean average was 2373+ or -92. Total cholesterol and its ester in both plasma and mononuclear cells showed no signficant differences at the 5-day intervals between men and women. However, plasma cholesterol/cholesterol ester ratios were significantly higher in women than men at each of the 5-day intervals from Days 5-25. An additional link between female hormones and atherosclerosis is suggested by the finding that women on oral contracepitves, known to be predisposed to premature atherosclerosis, show reduced and nonfluctuating levels of mononuclear cell CEH.
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PMID:The effect of oral contraceptives on mononuclear cell cholesterol ester hydrolase activity in premenopausal women taking oral contraceptives: relevance to atherosclerosis. 75 88

Atherosclerosis, a leading cause of mortality in the developed world, has mainly been studied with respect to the pathogenic role of lipids. However, over the last few years, a new avenue of research has stemmed from Benditt's monoclonal theory which linkens the atheroma plaque to a benign tumor developed from a single smooth muscle cell. Investigations into mechanisms capable of initiating this monoclonal cell growth have included studies of protooncogene activation. Barrett and Benditt have reported increased expression of the sis oncogene in the atheroma plaque; the product of this oncogene is very similar to the beta chain of platelet-derived growth factor (PDGF) which may play a role in the development of the atheroma plaque. These recent studies focusing on the earliest step of formation of the atheroma plaque, ie, cell growth, complement the pathophysiologic theories studied until now.
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PMID:[Atherosclerosis and oncogenes]. 157 Jan 85

The multifactorial aetiology of atherosclerosis is nowadays well established. In parallel with confirmation of the lipidic hypothesis, a tumoral theory for this pathology was built up during the past decade. This theory considers atheroma a benign tumor. Among agents that can induce cell proliferation, oncogenic viruses seem to be the most efficient. In this review, we present several works suggesting viral involvement in atherosclerosis. The viral theory is based not only on clinical and epidemiologic data, but also on cell and molecular biology research. These three complementary approaches have established a relationship between herpes viruses and the atherogenic process. Cytomegalovirus (CMV) seems to be the suspect in human atherosclerosis. Several studies of the effects of CMV on cells involved in atheroma, especially smooth muscle cells and endothelial cells, are consistent with a possible role of this virus in atherosclerosis. This paper presents not only recent research developments in this increasingly explored field, but also questions that remain to be elucidated and the consequences of the viral theory of atherosclerosis.
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PMID:[Viral theory of atherosclerosis. Role of cytomegalovirus]. 821 7

Adrenal myelolipoma is an uncommon benign tumor usually discovered by chance in patients with hypertension, obesity, atherosclerosis, cancer or endocrine disorders. The association with adrenal endocrine dysfunctions appears to be the most frequent. Myelolipoma has been found in patients affected by Cushing's syndrome, hyperaldosteronism, Addison's disease, virilization. We report herein a case of association, based on clinical and radiological signs, between myelolipoma and adrenal adenoma in a patient with Conn's disease. The myelolipoma was localized in the opposite adrenal gland to that of adenoma, at difference with the other cases described.
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PMID:[Adrenal adenoma and myelolipoma in an elderly patient with Conn's syndrome]. 1076 42

Although no generalization can be made, it is of interest that cancer, cardiovascular diseases, and other chronic conditions often share common risk factors and common protective factors as well as common pathogenetic determinants, such as DNA damage, oxidative stress, and chronic inflammation. Atherosclerosis is the most important cause of vascular forms representing the major cause of death in the population of many geographical areas. A great deal of studies support the "response-to-injury" theory. A variety of experimental and epidemiological findings are also in favor of the somatic mutation theory, which maintains that the earliest event in the atherogenic process is represented by mutations in arterial smooth muscle cells, akin to formation of a benign tumor. These two theories can be harmonized, also taking into account the highly diversified nature of atherosclerotic lesions. Molecular epidemiology studies performed in our laboratory and other laboratories have shown that DNA adducts are systematically present in arterial smooth muscle cells, and their levels are correlated with atherogenic risk factors known from traditional epidemiology. Oxidative DNA damage was also consistently detected in these cells. The role of glutathione S-transferase polymorphisms on the frequency of the above molecular alterations and of arterial diseases is rather controversial. Prevention of both cancer and atherosclerosis is based on avoidance of exposure to risk factors and on fortification of the host defense mechanisms by means of dietary principles and chemopreventive drugs.
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PMID:Mutagenesis and cardiovascular diseases Molecular mechanisms, risk factors, and protective factors. 1738 89