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

Atherosclerosis is a systemic disease responsible for strokes, myocardial infarction, renal hypertension, and intermittent claudication. Acute coronary syndromes (unstable angina, acute myocardial infarction, and sudden cardiac death) are the major causes of morbidity and mortality in developed countries. These acute manifestations of heart disease share a common pathophysiologic phenomenon: coronary thrombosis. Two principal mechanisms are responsible for coronary thrombosis: plaque disruption (75%) and plaque erosion (25%). Disrupted plaques exhibit a large lipid content, increased macrophages, and a thin fibrous cap. Hypercholesterolemia and diabetes are associated with plaque disruption. Eroded plaques are smooth muscle-cell rich with an intact fibrous cap. Cigarette smoking is associated with plaque erosion, most frequently in women with sudden death when they are younger than 50 years of age. Systemic inflammation is a novel, robust marker for future cardiovascular events, not only in patients with established atherosclerotic disease but also in apparently healthy individuals. Local inflammation at the plaque disruption site is documented by increased macrophage infiltration. Macrophages are responsible for plaque disruption, neovascularization, smooth muscle cell apoptosis, and plaque thrombogenicity. Experimental studies have identified the lipid core as the most thrombogenic substrate of the atherosclerotic plaque. Tissue factor, a cell membrane-bound protein, is crucial in thrombus formation. Tissue factor is expressed in apoptotic macrophages, suggesting that macrophages are not only responsible for plaque disruption but also pivotal in thrombus generation, the most important mechanism of acute coronary syndromes.
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PMID:Pathophysiology of plaque disruption and thrombosis in acute ischemic syndromes. 1790 43

Many studies, both national and international, have shown that tea has protective effects on many chronic diseases and their risk factors. In cancer prevention, our studies indicated that tea drinking could inhibit the carcinogenicity of various chemical carcinogens, including oral tumors induced by 7,12-dimethylbenz[a]anthracene (DMBA) in Golden hamsters, esophageal tumors in rats by blocking in vivo synthesis of N-Nitroso-methylbenzylamine (NMBzA), esophageal cancer induced by NMBzA in rats, precancerous liver lesions (r-GT and GST-P) induced by diethylnitrosamine (DENA) in rats, intestinal preneoplastic lesion (ACF) and intestinal tumors induced by 1,2-dimethyl-hydrazine (DMH) in rats, lung carcinoma induced by nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone(NNK) in A/J mice. Our studies have also shown that the protective effects of tea against cancer is a combined effects of various tea ingredients, among which the major ones are polyphenols and tea pigments. Based on animal studies, antioxidant properties, protection against DNA damage and modulation of immune functions were found to be the main mechanisms of anticancer effects of tea. In human trials, tea drinking showed protective effects against oxidative damage and DNA damage caused by cigarette smoking. Mixed tea drinking significantly blocked lesion progress in patients with oral mucosa leukoplakia, therefore, demonstrated its protective effects on oral cancer. Our studies have also shown effects of tea on prevention of cardiovascular diseases (CVD). For example, tea pigments was found to significantly inhibit LDL oxidation induced by Cu2+, Fe2+ in in vitro studies. In vivo studies showed that tea could prevent blood coagulation, facilitate fibrinogen dissolution, inhibit platelet aggregation, lower endothelin levels, enhance GSH-Px activities, protect against oxidated LDL-induced damage in endothelium cells, and prevent atherosclerosis of coronary arteries. The mechanisms of these protective effects of tea are possibly related to its antioxidant properties or its inhibition of lipid oxidation. Green tea and pigments was also found to inhibit cardiac hypertrophy induced by renal hypertension in rat models, whose mechanisms might, at least partly, involve its modulation on nitric oxide, angiotensin II and endothelin-1. Clinical intervention trials have indicated that tea and tea extracts decreased blood lipid, improved blood flow of coronary artery, and played an important role in atherosis inhibition and prevention. Our studies also showed that tea drinking has protective effects on diabetes. White tea drinking could significantly relieve symptoms including polyuria, polydipsia, polyphagia and weight loss in diabetic mice, decrease fasting plasma glucose level and improve glucose tolerance. In human trial, continuous white tea drinking could significantly improve symptoms of diabetic patients, such as relieve polydipsia, decrease plasma glucose levels, both fasting and 2 hours after meal, and increase insulin secretion. The effective rate for glucose lowering is 48% in clinical study.
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PMID:[Studies on tea and health]. 2227 81


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