User:Patelurology2/Pprbt

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 * http://www.webmd.com/cancer/news/20120531/diabetes-drug-actos-again-linked-to-bladder-cancer Diabetes Drug Actos Again Linked to Bladder Cancer: Study: Use of Actos for More Than 2 Years Doubles Bladder Cancer RiskIn an editorial accompanying the study, Dominique Hillaire-Buys and Jean-Luc Faillie from the Department of Medical Pharmacology and Toxicology in Montpellier, France, write: "It can confidently be assumed that [Actos] increases the risk of bladder cancer. It also seems that this association could have been predicted earlier."
 * http://www.scopus.com/record/display.url?eid=2-s2.0-0033206336&origin=inward&txGid=vYy_jaWUux47CoNA2roe4Y9%3a2 Expression of Peroxisome Proliferator-Activated Receptor γ (PPARγ) in Human Transitional Bladder Cancer and its Role in Inducing Cell Death: The present study examined the expression and role of the thiazolidinedione (TZD)-activated transcription factor, peroxisome proliferator-activated receptor γ (PPARγ), in human bladder cancers. In situ hybridization shows that PPARγ mRNA is highly expressed in all human transitional epithelial cell cancers (TCCa's) studied (n=11). PPARγ was also expressed in five TCCa cell lines as determined by RNase protection assays and immunoblot. Retinoid X receptor α (RXRα), a 9-cis-retinoic acid stimulated (9-cis-RA) heterodimeric partner of PPARγ, was also co-expressed in all TCCa tissues and cell lines. Treatment of the T24 bladder cancer cells with the TZD PPARγ agonist troglitazone, dramatically inhibited 3H-thymidine incorporation and induced cell death. Addition of the RXRα ligands, 9-cis-RA or LG100268, sensitized T24 bladder cancer cells to the lethal effect of troglitazone and two other PPARγ activators, ciglitazone and 15-deoxy-Δ12,14-PGJ2 (15dPGJ2). Troglitazone treatment increased expression of two cyclin-dependent kinase inhibitors, P21WAF1/CIP1 and p16INK4, and reduced cyclin D1 expression, consistent with G1 arrest. Troglitazone also induced an endogenous PPARγ target gene in T24 cells, adipocyte-type fatty acid binding protein (A-FABP), the expression of which correlates with bladder cancer differentiation. In situ hybridization shows that A-FABP expression is localized to normal uroepithelial cells as well as some TCCa's. Taken together, these results demonstrate that PPARγ is expressed in human TCCa where it may play a role in regulating TCCa differentiation and survival, thereby providing a potential target for therapy of uroepithelial cancers.
 * http://www.ncbi.nlm.nih.gov/pubmed/19229877 Rosiglitazone and PPAR-gamma overexpression protect mitochondrial membrane potential and prevent apoptosis by upregulating anti-apoptotic Bcl-2 family proteins.
 * http://www.ncbi.nlm.nih.gov/pubmed/20219857 Ischaemic preconditioning-regulated miR-21 protects heart against ischaemia/reperfusion injury via anti-apoptosis through its target PDCD4.
 * http://www.ncbi.nlm.nih.gov/pubmed/19287816 Protection of the ischaemic heart: investigations into the phenomenon of ischaemic preconditioning.
 * http://www.ncbi.nlm.nih.gov/pubmed/18182064 The paradigm of postconditioning to protect the heart.: Ischaemic preconditioning limits the damage induced by subsequent ischaemia/reperfusion (I/R). However, preconditioning is of little practical use as the onset of an infarction is usually unpredictable
 * http://www.ncbi.nlm.nih.gov/pubmed/19248760 Cardioprotection: a radical view Free radicals in pre and postconditioning.: A series of brief (a few minutes) ischemia/reperfusion cycles (ischemic preconditioning, IP) limits myocardial injury produced by a subsequent prolonged period of coronary artery occlusion and reperfusion. Postconditioning (PostC), which is a series of brief (a few seconds) reperfusion/ischemia cycles at reperfusion onset, attenuates also ischemia/reperfusion injury. In recent years the main idea has been that reactive oxygen species (ROS) play an essential, though double-edged, role in cardioprotection: they may participate in reperfusion injury or may play a role as signaling elements of protection in the pre-ischemic phase.
 * http://www.ncbi.nlm.nih.gov/pubmed/19641507 BAD: undertaker by night, candyman by day.: By executing its 'day' and 'night' jobs in metabolism and apoptosis, respectively, BAD helps coordinate mitochondrial fuel metabolism and the apoptotic machinery.
 * http://www.ncbi.nlm.nih.gov/pubmed/20127524 Anti-apoptotic actions of PPAR-gamma against ischemic stroke.