Therefore, the optimal duration of DAPT after coronary stent implantation is still controversial

otic and anti-necrotic actions in other systems, includingthe brain,kidneys, and the liver, in which EPO acts against the apoptosis and necrosis caused by I/R. EPO, pre-treatment was able to attenuate the renal dysfunction and injury associated with I/R.Administration of EPO in rat model of type II collageninduced arthritis tissue injury resulted in decreased proinflammatory cytokines in the circulation. Additionally, during chronic hypoxia EPO exerts PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/19672638 significant beneficial effects when administered 18 hours post-cecal ligation and puncture . Short-term low-dose’ EPO improved cardiac function and infarct size without any clinical adverse effects, but it did not prevent neointimal hyperplasia in percutaneous coronary intervention treated acute myocardial infarction patients. Evidence suggests, EPO treatments protected adult rat cardiomyocytes in-vitro and in-vivo in a rat model of myocardial infarction. EPO also prevents motor neuron apoptosis and neurological disability in spinal cord injury. The neuroprotective effect of EPO is conferred by attenuating the production of ROS and reducing the basilar artery vasoconstriction on neural vascular endothelium. EPO pretreatments GFT505 site showed a protective effect by decreasingcaspase-3 activity, and the mechanism of inhibition is inferred to be through the modulation of pro-survival signaling pathway Akt. Evidence of this mechanism was illustrated by blocking the Akt pathway by Wortmannin inhibitor and an increase in caspase-3 activity was observed compared PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/1967325 to the control.Accordingly, protectionfrom apoptosis and necrosiswas abolished in cells solely treated with Wortmannin, thus confirming that the effect is primarily due to phosphorylation of Akt, the major survival pathway. In conclusion, this study illustrates a novel finding thatshows the protective effect of EPO against apoptosis and necrosis in H9C2 cells subjected to H/R injury. It was found that the treatment with EPO protects cardiomyocytes by phosphorylation of Akt. This treatment also attenuates both the increase in activity of caspase-3, intracellular ROS induced by H/R and stabilizes DYm and intracellular Ca2+ homeostasis. Together these findings support mechanistic evidence for the protective effect of EPO in cardiomyocytes to prevent H/R-induced cell death and possibly create new avenues for effective cardioprotective therapeutics. Micro-RNAs are small non-coding RNAs with important roles in post-transcriptional gene expression regulation. More than a hundred miRNAs are expressed in the skin. MiRNAs were found to be essential for skin development in a conditional knock-out mouse model of Dicer, a cardinal enzyme for miRNA processing. Loss of Dicer in keratinocyte produced several distinct defects in the skin. Our knowledge on the role of miRNAs in skin development stems mainly from studies on miRNA expression in skin disorders. We and others explored the differential expression of miRNAs in normal skin, psoriatic lesions, un-involved skin from psoriatic patients. Others also compared psoriasis patient’s skin to miRNA expression from skin of patients with atopic eczema. Experimental systems of human KC revealed that miRNAs can target major components in KC development. MiR-203 was found to target p63 and miR-125b was found to target KGFR. Both proteins are well known to be involved in skin differentiation and in epithelial repair processes. We found that miR-99a targets IGF-1R, a major player in KC proliferation and differentiation. De