Model for end‐stage liver disease (MELD) exception small‐for‐size syndrome
Patricia Sheiner, Jacques Belghiti, Robert G. Gish, Charles Miller – 22 November 2006
Model for end‐stage liver disease (MELD) exception for cholangiocarcinoma or biliary dysplasia
Gregory J. Gores, Robert G. Gish, Debra Sudan, Charles B. Rosen – 22 November 2006
Model for end‐stage liver disease (MELD) exception for cystic fibrosis
Simon Horslen, Stuart Sweet, Robert G. Gish, Ross Shepherd – 22 November 2006
Model for end‐stage liver disease (MELD) exception for hepatic encephalopathy
John Ham, Robert G. Gish, Kevin Mullen – 22 November 2006
Model for end‐stage liver disease (MELD) exception for unusual metabolic liver diseases
Sue McDiarmid, Robert G. Gish, Simon Horslen, George V. Mazariegos – 22 November 2006
Model for end‐stage liver disease (MELD) exception for primary hyperoxaluria
Simon Horslen, Robert G. Gish, Ruth McDonald – 22 November 2006
Human UDP‐glucuronosyltransferase (UGT)1A3 enzyme conjugates chenodeoxycholic acid in the liver
Jocelyn Trottier, Mélanie Verreault, Susan Grepper, Didier Monté, Julie Bélanger, Jenny Kaeding, Patrick Caron, Ted T. Inaba, Olivier Barbier – 20 October 2006 – Chenodeoxycholic acid (CDCA) is a liver‐formed detergent and plays an important role in the control of cholesterol homeostasis. During cholestasis, toxic bile acids (BA) accumulate in hepatocytes causing damage and consequent impairment of their function. Glucuronidation, a conjugation reaction catalyzed by UDP‐glucuronosyltransferase (UGT) enzymes, is considered an important metabolic pathway for hepatic BA.
The half‐life of hepatitis B virions
John M. Murray, Robert H. Purcell, Stefan F. Wieland – 20 October 2006 – The virion half‐life of hepatitis B virus (HBV) is currently estimated at approximately 1 day. This estimate has been obtained from drug perturbation experiments with reverse transcriptase inhibitors. However, the analyses of those experiments have not considered the export of virions produced from preformed mature DNA‐containing HBV capsids in infected cells.
Inactivation of oxidized and S‐nitrosylated mitochondrial proteins in alcoholic fatty liver of rats
Kwan‐Hoon Moon, Brian L. Hood, Bong‐Jo Kim, James P. Hardwick, Thomas P. Conrads, Timothy D. Veenstra, Byoung J. Song – 20 October 2006 – Increased oxidative/nitrosative stress is a major contributing factor to alcohol‐mediated mitochondrial dysfunction. However, which mitochondrial proteins are oxidatively modified under alcohol‐induced oxidative/nitrosative stress is poorly understood.
Randomized controlled study of tenofovir and adefovir in chronic hepatitis B virus and HIV infection: ACTG A5127
Marion G. Peters, Janet Andersen, Patrick Lynch, Tun Liu, Beverly Alston‐Smith, Carol L. Brosgart, Jeffrey M. Jacobson, Victoria A. Johnson, Richard B. Pollard, James F. Rooney, Kenneth E. Sherman, Susan Swindells, Bruce Polsky, ACTG Protocol A5127 Team – 20 October 2006 – Chronic hepatitis B virus (HBV) infection is an important cause of morbidity and mortality in subjects coinfected with HIV. Tenofovir disoproxil fumarate (TDF) and adefovir dipivoxil (ADV) are licensed for the treatment of HIV‐1 and HBV infection, respectively, but both have in vivo and in vitro activity against HBV.