Current epidemiology of hepatitis E virus infection in the United States: Low seroprevalence in the National Health and Nutrition Evaluation Survey

Ivo Ditah, Fausta Ditah, Pardha Devaki, Calistus Ditah, Patrick S. Kamath, Michael Charlton – 13 May 2014 – Analysis of the National Health and Nutrition Evaluation Survey (NHANES) 1988‐1994 dataset found a relatively high seroprevalence (21%) of hepatitis E virus (HEV) infection in the U.S. general population. Using data obtained within the NHANES 2009‐2010 survey, where a high performance assay for HEV was used, we estimated the weighted seroprevalence of HEV infection among U.S. individuals 6 years and older. We also evaluated factors associated with HEV seropositivity.

Overexpression of far upstream element (FUSE) binding protein (FBP)‐interacting repressor (FIR) supports growth of hepatocellular carcinoma

Mona Malz, Michael Bovet, Jana Samarin, Uta Rabenhorst, Carsten Sticht, Michaela Bissinger, Stephanie Roessler, Justo Lorenzo Bermejo, Marcus Renner, Diego Francesco Calvisi, Stephan Singer, Matthias Ganzinger, Achim Weber, Norbert Gretz, Martin Zörnig, Peter Schirmacher, Kai Breuhahn – 13 May 2014 – The far upstream element binding protein (FBP) and the FBP‐interacting repressor (FIR) represent molecular tools for transcriptional fine tuning of target genes.

Retinoblastoma protein potentiates the innate immune response in hepatocytes: Significance for hepatocellular carcinoma

Jack Hutcheson, Ryan J. Bourgo, Uthra Balaji, Adam Ertel, Agnieszka K. Witkiewicz, Erik S. Knudsen – 13 May 2014 – Cancers mediated by viral etiology must exhibit deregulated cellular proliferation and evade immune recognition. The role of the retinoblastoma tumor suppressor (RB) pathway, which is lost at relatively high frequency in hepatocellular carcinoma (HCC), has recently been expanded to include the regulation of innate immune responsiveness. In this study we investigated the coordinate impact of RB‐loss on cell cycle control and immune function in the liver.

Predictors of donor follow‐up after living donor liver transplantation

Robert S. Brown, Abigail R. Smith, Mary Amanda Dew, Brenda W. Gillespie, Peg Hill‐Callahan, Daniela P. Ladner – 13 May 2014 – Donor safety in living liver donation is of paramount importance; however, information on long‐term outcomes is limited by incomplete follow‐up. We sought to ascertain factors that predicted postdonation follow‐up in 456 living liver donors in the Adult‐to‐Adult Living Donor Liver Transplantation Cohort Study. Completed donor follow‐up was defined as physical, phone, or laboratory contact at a given time point.

Hepatic DNA deposition drives drug‐induced liver injury and inflammation in mice

Pedro Elias Marques, André Gustavo Oliveira, Rafaela Vaz Pereira, Bruna Araújo David, Lindisley Ferreira Gomides, Adriana Machado Saraiva, Daniele Araújo Pires, Júlia Tosta Novaes, Daniel O. Patricio, Daniel Cisalpino, Zélia Menezes‐Garcia, W. Matthew Leevy, Sarah Ellen Chapman, GermánArturo Mahecha, Rafael Elias Marques, Rodrigo Guabiraba, Vicente Paulo Martins, Danielle Gloria Souza, Daniel Santos Mansur, Mauro Martins Teixeira, M.

Risk factors and surgical management of anastomotic biliary complications after pediatric liver transplantation

Tom Darius, Jairo Rivera, Fabio Fusaro, Quirino Lai, Catherine de Magnée, Christophe Bourdeaux, Magdalena Janssen, Philippe Clapuyt, Raymond Reding – 9 May 2014 – Biliary complications (BCs) still remain the Achilles heel of liver transplantation (LT) with an overall incidence of 10% to 35% in pediatric series.

Cognitive impairment and electroencephalographic alterations before and after liver transplantation: What is reversible?

Francesca Campagna, Sara Montagnese, Sami Schiff, Anna Biancardi, Daniela Mapelli, Paolo Angeli, Carlo Poci, Umberto Cillo, Carlo Merkel, Angelo Gatta, Piero Amodio – 9 May 2014 – The influence of liver transplantation (LT) on mental performance is debated, as is the role of pretransplant overt hepatic encephalopathy (OHE). The aim of this study was to evaluate the time course of the neuropsychological and electroencephalogram (EEG) features of patients with cirrhosis before and after LT with respect to prior OHE.

Cylindromatosis gene CYLD regulates hepatocyte growth factor expression in hepatic stellate cells through interaction with histone deacetylase 7

Rajeswara R. Pannem, Christoph Dorn, Claus Hellerbrand, Ramin Massoumi – 9 May 2014 – Hepatic fibrosis is considered as a physiological wound‐healing response to liver injury. The process involves several factors, such as hepatocyte growth factor (HGF), which restrains hepatic injury and facilitates reversibility of fibrotic reaction in response to an acute insult. Chronic liver injury and sustained inflammation cause progressive fibrosis and, ultimately, organ dysfunction. The mechanisms tipping the balance from restoration to progressive liver tissue scarring are not well understood.

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