Ributes the Lebensf Ability of Tofacitinib 540737-29-9 neural cells and an elongation of neurites in a down-regulation of p53 and upregulation of GSK 3b Ser9 P and Ser675 pb catenin, even in the presence of Ab1 40 Neurotoxizit t. Nevertheless, further studies are needed to determine whether cilostazol Wnt signaling pathway facilitated by the nucleic Re translocation of more b catenin activation by CK2a. Interestingly, Hashimoto, Ishima that the level of translation elongation factor EEF1A1 eukaryotic proteins were significantly increased by treatment with cilostazol Ht, but not by milrinone in PC12 cells in combination with nerve growth factor-induced increase in the number of cells with neurites mediated by activation of IP3 receptors and Ras / Raf / ERK / MAPK. Further studies are n IST to clarify whether eEF1A expression is obtained by treatment with cilostazol and milrinone in the absence of NGF in HT22 cells Ht, and if this expression is linked to the activation of CK2 neurite elongation. Taken together, these results show a fascinating pharmacological repertoire, cilostazol P p53, Bax and caspase 3 signaling and increased P GSK 3b and P b catenin D Coupled mediated mpft by activation of protein kinase cAMP is CK2a constructed and 40 Ab1-induced Neurotoxizit T and The Verl EXTENSIONS neurite improve. may be an alternative s new and more effective than aspirin for secondary rpr Convention of Schlaganf cases in Asian patients. The AHA guidelines are still not giving recommendations on the R Of cilostazol for the Pr Of secondary prevention Ren stroke. This article describes cilostazo mechanism of action as a platelet aggregation inhibitor, provides an overview of secondary Re Pr Prevention ish Endemic stroke trials, and compared with rates of bleeding cilostazol with other treatment options for the secondary Re Pr Prevention of Schlaganf Cases . Data Sources A literature search was MEDLINE and PubMed-related English-language journal articles and clinical studies to identify the use of Schlüsselw Rtern cilostazol, antiplatelet agents, aspirin, the acetylsalicylic Acid prevents secondary Rem stroke, accident ish Ischemic stroke, cerebral hemorrhage, intracranial, stroke and transient isch chemical attack. Reference citations of articles have been used to additionally Identify USEFUL literature as a reference. Data records Courts, and non-published shall clinical trials were also underway, he Rtert. Selection of articles on the pharmacology of platelet aggregation inhibitor concentrate, analyze the pathophysiology of atherosclerosis, stroke, clinical trials and safety. Mechanism of atherosclerotic plaques contain smooth muscle cells, macrophages and collagen in the heart of lipid. Plaque erosion, column and / or rupture due to shear stress exposing the subendothelial matrix, collagen and tissue factor in the lipid core. Each of these substrates is strongly Blutpl Ttchen formation.7 thrombus after rupture of unstable plaques, tissue factor and collagen-erh Ltlichen von HDAC antagonist Willebrand factor in the F Promotion of Blutpl Ttchen-Adh Sion and activation in the surface chemical the matrix sub-endothelial suspended. To activated platelets release adenosine and cyclooxygenase product thromboxane A2, mediators, vasoconstriction and platelet activation on f rdern. Thanks to the P2Y12 ADP receptor stimulates Blutpl Express ttchen of Gly.