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Cannabis Science Receives FDA Industry Guidelines For Mapping Out Its Initial Drugs Offerings For FDA Submission And Testing
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MU Public Health Program Receives Grant To Combat Human Trafficking
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GM, UAW Nearing Deal To Use Company Stock For Half Of VEBA Obligation, s Say
General Motors and the United Auto Workers are close to finalizing a deal that would reduce the automaker"s cash obligation to a retiree health care trust fund, according to people with knowledge of the matter, the Wall Street Journal reports. UAW in 2007 agreed to establish the voluntary employees" beneficiary association, totaling $35 billion, that would cover health care costs of retired GM workers and their spouses starting in 2010. GM has paid about $15 billion into the fund, but under the deal now being discussed, the remaining $20 billion obligation could be paid using about $10 billion in cash and a 39% equity stake in the restructured GM that will be formed under the Treasury Department"s "controlled bankruptcy" plan for the firm. The deal would be subject to approval by UAW"s 60,000 GM members, who likely would face "steep cuts" in pay and benefits as a result, as well as 20,000 additional layoffs, according to the Journal. Union officials also have expressed concern that the GM stock making up the equity stake is "illiquid and hard to value, posing a big risk for UAW members," the Journal reports. GM and UAW could agree to a final version of the deal "as early as next week," according to the Journal (Stoll, Wall Street Journal, 5/15). Chrysler
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Cystathionase Regulated By Farnesoid X Receptor

The expression and activity of Cystathionase is reduced in rodent models of liver injury, leading to hyper-homocysteinemia and impaired generation of hydrogen sulphide, two factors that contribute to endothelial dysfunction and increased intrahepatic resistance. In the present study the analysis of the human Cystathionase gene promoter demonstrates the presence of an inverted repeat sequence. Administration of an FXR ligand to carbon tetrachloride treated mice protected against down-regulation of Cystathionase expression, increased hydrogen sulphide generation, reduced portal pressure and attenuated the endothelial dysfunction of isolated and perfused livers. A research article published on May 7, 2009 in the World Journal of Gastroenterology refers. The research team led by Dr. Barbara Renga and her colleagues in the University of Perugia, Italy used luciferase transfection assay, Electrophoretic Mobility Shift Assay (EMSA), Chromatin Immunoprecipitation Assay and Real-Time PCR to confirm the role of FXR in the regulation of CSE transcription. The molecular mechanism of the CSE activation by FXR was revealed by identifying a sequence in the 5" flanking region of CSE gene containing a potential IR1 binding site. Co-transfection of HepG2 cells with luciferase reporter vector containing four copies of this putative IR1 resulted in transactivation of the CSE promoter in presence of an FXR ligand, while the mutation of the IR1 binding site abrogates this response. The functionality of this IR1 site was also confirmed by EMSA and CHIP assay. In the normal liver the CSE expression was significantly increased when mice were fed a chow diet supplemented with 5 mg/kg body weight of 6E-CDCA while the FXR ligand failed to up-regulate CSE mRNA expression in FXR knock-out mice. Contraction of presinusoidal myofibroblasts has relevance in regulating intrahepatic resistance and short term administration of 6E-CDCA regulates CSE expression in normal mice, therefore the authors have investigated whether acute administration of an FXR ligand effectively modulates CSE expression in CCl4 treated mice. The author demonstrated that CSE liver expression was down-regulated in an animal model of liver damage induced by CCl4 and that treatment with 6E-CDCA resulted in a robust induction of CSE expression only in FXR +/+ mice The reduction of CSE expression in the cirrhotic liver contributes to the development of increased intrahepatic resistance and portal hypertension. The authors therefore investigated whether in vivo administration of an FXR ligand modulates hepatic resistance in cirrhotic rats. In conclusion, they have shown that CSE is an FXR-regulated gene. By linking the deficiency of CSE to the FXR activity the present study provides a new molecular explanation to the pathophysiology of portal hypertension. It also proposes the concept that FXR agonists might correct for the altered generation of endogenous hepatic vasodilators that takes place in chronic liver diseases. Reference: Renga B, Mencarelli A, Migliorati M, Distrutti E, Fiorucci S. Bile-acid-activated farnesoid X receptor regulates hydrogen sulfide production and hepatic microcirculation. World J Gastroenterol 2009; 15(17): 2097-2108 http://www.wjgnet.com/1007-9327/15/2097.asp Correspondence to: Barbara Renga, Department of Clinical and Experimental Medicine University of Perugia, Via E dal Pozzo, 06122 Perugia, Italy. Lin Tian World Journal of Gastroenterology


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