Scott T. Magness, Ramón Bataller, Liu Yang, David A. Brenner – 22 September 2004 – Activation of hepatic stellate cells (HSCs) and other resident mesenchymal cells into myofibroblasts expressing alpha smooth muscle actin (αSMA) and collagen I is a key event in liver fibrogenesis. However, the temporal expression profiles of αSMA and collagen I genes in these cells is unknown.
Martial Jaume, Sébastien Jacquet, Pierre Cavaillès, Gaëtane Macé, Lionel Stephan, Catherine Blanpied, Cécile Demur, Pierre Brousset, Gilles Dietrich – 22 September 2004 – Fas (CD95)‐induced hepatocyte apoptosis and cytotoxic activity of neutrophils infiltrating the injured liver are two major events leading to hepatitis. Because it has been reported that opioids, via a direct interaction, sensitize splenocytes to Fas‐mediated apoptosis by upregulating Fas messenger RNA (mRNA) and modulated neutrophil activity, we assumed that opioids may participate in the pathophysiology of hepatitis.
Christopher J. Parsons, Blair U. Bradford, Clark Q. Pan, Ellen Cheung, Michael Schauer, Andreas Knorr, Barbara Krebs, Sabine Kraft, Stefan Zahn, Bodo Brocks, Nikki Feirt, Baisong Mei, Myung‐Sam Cho, Roopa Ramamoorthi, Greg Roldan, Paul Ng, Peggy Lum, Claudia Hirth‐Dietrich, Adrian Tomkinson, David A. Brenner – 22 September 2004 – Liver fibrosis is characterized by increased synthesis, and decreased degradation, of extracellular matrix (ECM) within the injured tissue.
Shoshiro Oe, Eric R. Lemmer, Elizabeth A. Conner, Valentina M. Factor, Per Levéen, Jonas Larsson, Stefan Karlsson, Snorri S. Thorgeirsson – 22 September 2004 – Transforming growth factor β (TGF‐β) is a potent inhibitor of hepatocyte proliferation in vitro and is suggested to be a key negative regulator of liver growth.
Erick Edwards, Ann Harper – 21 September 2004 – Key Points 1Based on OPTN data, the ability of the model for end‐stage liver disease (MELD) to predict short‐term pretransplant and posttransplant outcomes was assessed.2Concordance with pretransplant mortality was excellent.3Concordance with pretransplant mortality was better for candidates listed for a primary transplant.4Of the MELD components, there were no statistically significant differences in the effects on pretransplant mortality between candidates listed for a primary or a repeat transplant.5Concordance with posttranplant outcomes w
Russell H. Wiesner – 21 September 2004 – Key Points 1Historical perspective of donor allocation to patients with fulminant hepatic failure (FHF).2Predicting prognosis in patients with FHF using the London and Clichy criteria.3Model for end‐stage liver disease (MELD) is a predictor of mortality in patients with FHF.4Outcomes of adults listed as Status 1 in the United States.5Outcomes of pediatric candidates listed as Status 1 in the United States.6Proposed redefinition for Status 1 in adult and pediatric candidates. (Liver Transpl 2004;10:S17–S22.)
Julie K. Heimbach, Michael G. Haddock, Steven R. Alberts, Scott L. Nyberg, Michael B. Ishitani, Charles B. Rosen, Gregory J.
Sue V. McDiarmid, Robert M. Merion, Dawn M. Dykstra, Ann M.
James R. Burton, Amnon Sonnenberg, Hugo R. Rosen – 21 September 2004 – Key Points 1Retransplantation (re‐LT) for hepatitis C virus (HCV) recurrence is controversial. Although re‐LT accounts for 10% of all liver transplants (LTs), the number of patients requiring re‐LT is expected to grow as primary LT recipients survive long enough to develop graft failure from recurrent disease.2Utility, as applied to the medical ethics of transplantation, refers to allocating organs to those individuals who will make the best use of them.