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Many cardiovascular risk factors such as diabetes mellitus, hypertension and hyperlipidemia are demonstrated to stimulate the interaction of Cav-1 and eNOS, reduce nitric oxide production resulting in endothelial dysfunction and subsequently the formation of atherosclerotic lesion 41,42,43
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Synthesis and glutathione S-transferase structure-affinity relationships of nonpeptide and peptidase-stable glutathione analogues
Hemolysis induced by infection
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