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Smart WritingThe Structure of Biomedical ManuscriptTitleShort running titleAbstractKeywordsIntroductionMaterials and MethodsResultsTablesFiguresFigure legendDiscussionReferencesTITLEDo Not Underestimate the Importance of the Title!!! Shortest Abstract for Your Entire ManuscriptABSTRACTWhy?How?What?So?Keep in MindThere is a big difference between the abstracts ForManuscript and ConferenceWhy?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). How?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. What?Treatment with insulin resulted in 2.6-fold and 4.3-fold increases in Akt and eNOS phosphorylation, and a significant increase in NO production in ischemic/reperfused myocardial tissue. Phosphorylation of Akt and eNOS and increase of NO production by insulin were completely blocked by wortmannin, a PI3-kinase inhibitor. Pre-treatment with L-NAME, a non-selective NOS inhibitor, had no effect on Akt and eNOS phosphorylation, but significantly reduced NO production. Moreover, treatment with insulin markedly reduced myocardial apoptotic death (P0.01 vs. vehicle). Pre-treatment with wortmannin abolished the anti-apoptotic effect of insulin. Most importantly, pre-treatment with L-NAME also significantly reduced the anti-apoptotic effect of insulin (P0.01 vs. insulin). So? These results demonstrated that in vivo administration of insulin activated Akt through the PI3-kinase-dependent mechanism and reduced post-ischemic myocardial apoptotic death