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Population perspectives on the prevention and treatment of obesity in minority populations buy discount lady era online menstrual nausea relief. Homocysteine and cardiovascular risk: In a recent meta-analysis order lady era from india women's health clinic coffs harbour, Boushey et al (3), concluded that homocysteine is an independent cardiovascular risk factor and that each 5 mol/L rise in homocysteine results in an increased odds ratio of 1. Plasma homocysteine levels are, in part, determined by plasma levels of vitamin B12, B6 and folate status and genetics. Homocysteine and vascular damage: Homocysteine may have a deleterious effect on the normal prothrombolytic and anticoagulant activities of endothelial cells. Elevated levels of homocysteine have been found to decrease protein C activation by decreasing the activity of thrombomodulin. Homo-cysteine has also been shown to increase the activity of tissue factors in endothelial cells (9), to modulate tissue plasminogen activator binding to endothelial cell receptors and to enhance the activity of coagulation factor Vin endothelial cells (10). Taken together, these data strongly suggest that elevated homocysteine levels are atherogenic by inducing a procoagulatory state. There is insufficient evidence to recommend measuring plasma homocysteine in the general population. Mutational analysis of the genes involved in homocysteine metabolism is not recommended in clinical practice. Empirical treatment of patients with vitamin supplementation, although unlikely to cause harm, cannot be recommended at this time. Plasma concentrations of Lp(a) are genetically determined and vary from 1 mg/dL to more than 100 mg/dL. Numerous cross-sectional and case control studies in subjects with coronary, carotid artery or peripheral vascular dis-ease have demonstrated that elevated Lp(a) concentrations are associated with premature atherosclerosis (17). The significance of these retrospective studies has been questioned, however, because it is difficult to ascertain whether increased Lp(a) levels were a cause or a consequence of disease. This is particularly relevant in the case of Lp(a), which has been identified as a positive acute phase reactant (18). The acute phase response that occurs with acute coronary syndromes or surgical revascularization procedures may, therefore, exaggerate the importance of raised Lp(a) levels. It has been proposed that different methods for measuring Lp(a), which have not been standardized, and the effects of variable length and temperature of sample storage may explain some of these different outcomes. The aforementioned epidemiological evidence implicating Lp(a) in the pathogenesis of atherosclerosis is supported by laboratory evidence showing that Lp(a) accumulates in atherosclerotic plaques (28); promotes thrombosis, due to its structural similarities with plasminogen (29); promotes foam cell formation by stimulating cellular cholesterol accumulation (30); stimulates smooth muscle cell proliferation (31); impairs endothelium- dependent vasodilation (32); and promotes monocyte chemoattractant activity in human vascular endothelial cells (33). Plasma Lp(a) levels correlate with reduced acetylcholine-mediated coronary vasodilation in human coronary arteries examined during diagnostic coronary angiography (35). The heritability index for Lp(a) in twin studies, sib-pair analysis and family studies is the highest for any of the known lipoprotein cardiovascular risk factors (36).

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