4,499 research outputs found
Yc-1 Prevents Sodium Nitroprusside-Mediated Apoptosis in Vascular Smooth Muscle Cells
No full textObjective: Nitric oxide signaling pathways are of central importance in both the maintenance of vascular homeostasis and the progression of vascular disease. Since smooth muscle cell apoptosis is associated with numerous vascular disorders, the authors investigated whether YC-1, a soluble guanylyl cyclase (sGC) activator, regulates apoptosis in vascular smooth muscle cells (VSMC). Methods and results: Sodium nitroprusside (SNP ) (1 mM) induced cGMP (guanosine 3' :5'-cyclic monophosphate)-independent apoptosis in rat vascular smooth muscle cells using MTT assay and TUNEL- reaction techniques. Furthermore, sodium nitroprusside induced apoptosis via Bcl-2 down-regulation, cytochrome c release reaction, and caspase-3 activation by Western blotting analysis and enzymatic assay methods. YC-1 abolished these apoptotic signaling cascades and prevented apoptosis through a cGMP-involved pathway, and phosphatidylinositol (PI) 3-kinase behaved a downstream event in this pathway. Conclusions: These results suggest that YC-1 inhibits sodium nitroprusside-induced vascular smooth muscle cells apoptosis via a cGMP- and phosphatidylinositol 3-kinase- involved inhibition on Bcl-2 down-regulation/cytochrome c release/ caspase -3 activation cascades. The ability of YC-1 to prevent smooth muscle cell apoptosis may play an important role in blocking lesion formation at sites of vascular injury. (C) 2003 European Society of Cardiology. Published by Elsevier B.V. All rights reserved
Video-assisted thoracoscopic excision of intradiaphragmatic bronchogenic cysts: two cases.
No full textVideo-assisted thoracoscopic surgery for the diagnosis of patients with hilar and mediastinal lymphadenopathy.
No full textThymic carcinoma associated with Sjogren’s syndrome and syndrome of inappropriate antidiuretic hormone.
No full textA Potential Role of Yc-1 on the Inhibition of Cytokine Release in Peripheral Blood Mononuclear Leukocytes and Endotoxemic Mouse Models
No full textTo evaluate the anti-sepsis potential of YC-1,we have examined the effect of YC-1 on the regulation of cytokine production in human leukocytes and endotoxemic mice. The data demonstrated thatYC-1 showed a preferential inhibition on proinflammatory cytokine production without inhibition of cell growth or induction of cytotoxicity in human leukocytes. On the other hand, in the septic mouse model, treatment with an intraperitoneal application of LPS caused a cumulative death within 27 hours.The post- treatment administration of YC-1 significantly increased the survival rate in endotoxemic mice. Furthermore, several mediators were detected and the data showed thatYC-1 profoundly blocked LPS-induced NO as well asTNF-α production, and prevented lung damage by histological examination. Samples from the animal model showed that LPS-induced NF- κ B/DNA binding activity and consequent up-regulation of iNOS expression in tissues were abolished by post-administration of YC-1.Furthermore,YC-1,by itself,did not modify cGMP content while significantly inhibit LPS-induced cGMP formation, suggesting thatYC-1-mediated effect was not through a cGMP- elevating pathway.Taken together, it is evident that the post-treatment administration of YC-1 after LPS application significantly inhibits NF- κ B activation, iNOS expression, NO over-production, and cytokine release reaction resulting in an improved survival rate in endotoxemic mice. It is suggested thatYC-1 may be a potential agent for the therapeutic treatment of sepsis
The evolution of the diagnosis and understanding of lung cancer pathology: living through an epoch.
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