Bacterial translocation during liver transplantation: A randomized trial comparing conventional with venovenous bypass vs. piggyback methods

Edson Abdala, Carlos Eduardo Sandoli Baía, Sérgio Mies, Paulo Celso Bosco Massarollo, Norma de Paula Cavalheiro, Vania Regina Mollo Baía, Conceição Aparecida Félix Inácio, Henry Corazza Sef, Antonio Alci Barone – 29 March 2007 – The aim of this study was to evaluate the bacterial translocation in liver transplantation (LT), comparing the conventional and the piggyback methods. A total of 32 patients were randomized into the 2 groups. Samples of blood were collected from the radial artery, portal vein (PV) and hepatic vein (HV), in up to 120 minutes postreperfusion.

Bile acid treatment alters hepatic disease and bile acid transport in peroxisome‐deficient PEX2 Zellweger mice

Megan H. Keane, Henk Overmars, Thomas M. Wikander, Sacha Ferdinandusse, Marinus Duran, Ronald J. A. Wanders, Phyllis L. Faust – 28 March 2007 – The marked deficiency of peroxisomal organelle assembly in the PEX2−/− mouse model for Zellweger syndrome provides a unique opportunity to developmentally and biochemically characterize hepatic disease progression and bile acid products. The postnatal survival of homozygous mutants enabled us to evaluate the response to bile acid replenishment in this disease state.

ERK2 but not ERK1 plays a key role in hepatocyte replication: An RNAi‐mediated ERK2 knockdown approach in wild‐type and ERK1 null hepatocytes

Christophe Frémin, Frédéric Ezan, Pierre Boisselier, Anne Bessard, Gilles Pagès, Jacques Pouysségur, Georges Baffet – 28 March 2007 – The mitogen‐activated protein kinases (MAPKs) ERK1 and ERK2 have been implicated in various physiological events, and specific targeting of these MAPKs could affect cell proliferation in many cell types. First, to evaluate the potential specific roles of these two MAPKs, we analyzed the mitogenic response in regenerating liver after partial hepatectomy (PH) and in primary culture of hepatocytes isolated from ERK1‐deficient mice.

Genome‐wide molecular profiles of HCV‐induced dysplasia and hepatocellular carcinoma

Elisa Wurmbach, Ying‐bei Chen, Greg Khitrov, Weijia Zhang, Sasan Roayaie, Myron Schwartz, Isabel Fiel, Swan Thung, Vincenzo Mazzaferro, Jordi Bruix, Erwin Bottinger, Scott Friedman, Samuel Waxman, Josep M. Llovet – 28 March 2007 – Although HCC is the third‐leading cause of cancer‐related deaths worldwide, there is only an elemental understanding of its molecular pathogenesis. In western countries, HCV infection is the main etiology underlying this cancer's accelerating incidence.

Management of hepatitis B: Summary of a clinical research workshop

Jay H. Hoofnagle, Edward Doo, T. Jake Liang, Russell Fleischer, Anna S.F. Lok – 28 March 2007 – Chronic hepatitis B is caused by persistent infection with the hepatitis B virus (HBV), a unique DNA virus that replicates through an RNA intermediate produced from a stable covalently closed circular DNA molecule. Viral persistence appears to be due to inadequate innate and adaptive immune responses. Chronic infection has a variable course after several decades resulting in cirrhosis in up to one‐third of patients and liver cancer in a proportion of those with cirrhosis.

Subscribe to