TOXSCI ADVANCE ACCESS ORIGINALLY PUBLISHED ONLINE ON JANUARY 16, 2006 Toxicological Sciences 2006 90(2):569-585; doi:10.This Article All Versions of this take viagra who woman Article: 90/2/569 _most recent_ Services Search for citing articles in: Google Scholar PubMed UNIQUE GENE EXPRESSION AND HEPATOCELLULAR viagra message board INJURY IN THE LIPOPOLYSACCHARIDE-RANITIDINE DRUG IDIOSYNCRASY RAT MODEL:PARISON WITH FAMOTIDINE JAMES P.LOIS D.DAVID M.M.TIMOTHY P.BRUCE D.GLENN H.MADDOX, PATRICIA E.AND ROBERT A. Department of Pharmacology and Toxicology buy online purchase viagra , Center for Integrative Toxicology, National Food Safety and Toxicology Center, Michigan State University, East Lansing, Michigan 48824; Discovery Toxicology, Bristol-Myers Squibb, Princeton, New cyber pharmacy viagra Jersey; and Drug Safety Evaluation, Bristol-Myers Squibb, Syracuse, New York Received November 8, 2005; accepted January 10, 2006 Rats cotreated with download joke viagra lipopolysaccharide (LPS) and ranitidine (RAN) but not LPS and famotidine (FAM) develop hepatocellular injury online prescription viagra in an animal model of idiosyncratic drug reactions.Of liver gene expression in rats given LPS and/or RAN led to confirmation that the hemostatic system, hypoxia, and neutrophils (PMNs) are critical mediators in LPS/RAN-induced liver injury.Tested the hypothesis that unique gene expression changes distinguish LPS/RAN-treated rats from rats given LPS or RAN alone and from those cotreated with LPS/FAM.Were treated with a nonhepatotoxic dose of LPS (44.106 endotoxin units/kg, iv) or its vehicle.Hours thereafter they were given RAN (30 mg/kg, iv), FAM (either 6 mg/kg, a pharmacologically equi-efficacious dose, or 28.An equimolar dose, iv), or vehicle.Were killed 2 or 6 h after drug treatment for evaluation of hepatotoxicity (2 and 6 h) and liver gene expression (2 h only).A time before the onset of hepatocellular injury, hierarchical clustering distinguished rats treated with LPS/RAN from those given LPS alone.Probesets were expressed differentially to a greater or lesser degree only in LPS/RAN-treated ratspared to LPS/FAM or LPS alone, which did purchase viagra on line not develop liver injury.Included VEGF, EGLN3, MAPKAPK-2, BNIP3, MIP-2, COX-2, EGR-1, PAI-1, IFN-, and IL- by online viagra 6.Of these genes was confirmed by real-time PCR.Concentrations of MIP-2, PAI-1, IFN-, and IL-6 correlated with their respective gene expression patterns.The expression of several gene products capable of controlling requisite mediators of injury (i.Hemostasis, hypoxia, PMNs) in this model were enhanced in livers of LPS/RAN-treated rats.Enhanced expression of MAPKAPK-2 in RAN-treated rats and its target genes in LPS/RAN-treated rats suggests that p38/MAPKAPK-2 signaling is a regulation point for enhancement of LPS-induced gene expression by RAN._Key Words:_ inflammation; drug idiosyncrasy; gene array; lipopolysaccharide; hepatotoxicity.HAS BEEN CITED BY OTHER ARTICLES: F.Tukov, J.Luyendyk, P.Ganey, and R.Roth THE ROLE OF TUMOR NECROSIS FACTOR ALPHA IN LIPOPOLYSACCHARIDE/RANITIDINE-INDUCED INFLAMMATORY LIVER INJURY Toxicol.November 1, 2007; 100(1): 267 - 280.
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