美国杰斐逊大学马新亮教授在四医大的讲座报告之—医学论文写作技巧教程教案.ppt

Smart Writing;The Structure of Biomedical Manuscript;TITLE;Recent evidence from cultured endothelial cell studies suggests that phosphorylation of endothelial nitric oxide synthase (eNOS) via the PI3-kinase-Akt pathway increases NO production. The present study was designed to elucidate the signaling pathway involved in the anti-apoptotic effect of insulin in vivo and to test the hypothesis that phosphorylation of eNOS by insulin may participate in insulin’s cardioprotective effect following myocardial ischemia and reperfusion (MI/R). ;Male Sprague-Dawley rats were subjected to 30 min of MI and 4 hr of R. Rats were randomized to receive vehicle, insulin, insulin + wortmannin or insulin + L-NAME. ;;So?;Body of Manuscript;How to Be Logical?;How to Be Logical?;Body of Manuscript;INTRODUCTION;INTRODUCTION;INTRODUCTION; Metabolic modulation with glucose, insulin and potassium (GIK) in acute myocardial infarction (AMI) has a long and controversial history(1). A recent clinical trail has demonstrated that compared with patients receiving reperfusion therapy and placebo, those patients receiving GIK treatment prior to reperfusion had a remarkable 66% reduction in their relative in-hospital mortality risk. In contrast, in those patients receiving no reperfusion therapy, no significant difference was observed between patients receiving placebo or GIK. This landmark study suggested that GIK may attenuate myocardial reperfusion injury, and thus may exert significant cardioprotection in AMI patients receiving reperfusion(2). ; The mechanisms via which GIK exerts its cardioprotection remain largely speculative. It was hypothesized that metabolic modulations are likely the mechanisms of protection of GIK during the ischemic period(1;3). However, a recent study has demonstrated that GIK did not affect the pattern of myocardial substrate uptake or oxygen consumption during reperfusion, suggesting that metabolic manipulation is unlikely to be the major mechanism by which GIK exerts i