Hepatocyte nuclear factor 4α is implicated in endoplasmic reticulum stress–induced acute phase response by regulating expression of cyclic adenosine monophosphate responsive element binding protein H

Jennifer Luebke‐Wheeler, Kezhong Zhang, Michele Battle, Karim Si‐Tayeb, Wendy Garrison, Sodhi Chhinder, Jixuan Li, Randal J. Kaufman, Stephen A. Duncan – 26 September 2008 – Loss of the nuclear hormone receptor hepatocyte nuclear factor 4α (HNF4α) in hepatocytes results in a complex pleiotropic phenotype that includes a block in hepatocyte differentiation and a severe disruption to liver function. Recent analyses have shown that hepatic gene expression is severely affected by the absence of HNF4α, with expression of 567 genes reduced by ≥2.5‐fold (P ≤ 0.05) in Hnf4α−/− fetal livers.

Surveillance for hepatocellular carcinoma in patients with primary biliary cirrhosis

Marina G. Silveira, Ayako Suzuki, Keith D. Lindor – 26 September 2008 – Hepatocellular carcinoma (HCC) occurs with increased frequency in patients with primary biliary cirrhosis (PBC). Effectiveness of surveillance recommendations for HCC is controversial, and data are lacking in patients with PBC. In this study, we attempt to (1) establish the importance of surveillance for HCC in patients with PBC; (2) identify a target population of patients with PBC for HCC surveillance; and (3) propose surveillance recommendations for patients with PBC.

The critical role of toll‐like receptor (TLR) 4 in alcoholic liver disease is independent of the common TLR adapter MyD88

Istvan Hritz, Pranoti Mandrekar, Arumugam Velayudham, Donna Catalano, Angela Dolganiuc, Karen Kodys, Evelyn Kurt‐Jones, Gyongyi Szabo – 26 September 2008 – The Toll‐like receptor 4 (TLR4) that recognizes endotoxin, a trigger of inflammation in alcoholic liver disease (ALD), activates two signaling pathways utilizing different adapter molecules: the common TLR adapter, myeloid differentiation factor 88 (MyD88), or Toll/interleukin immune‐response–domain‐containing adaptor inducing interferon (IFN)‐β. The MyD88 pathway induces proinflammatory cytokine activation, a critical mediator of ALD.

Screening for Wilson disease in acute liver failure: A comparison of currently available diagnostic tests

Jessica D. Korman, Irene Volenberg, Jody Balko, Joe Webster, Frank V. Schiodt, Robert H. Squires, Robert J. Fontana, William M. Lee, Michael L. Schilsky, Pediatric and Adult Acute Liver Failure Study Groups – 26 September 2008 – Acute liver failure (ALF) due to Wilson disease (WD) is invariably fatal without emergency liver transplantation. Therefore, rapid diagnosis of WD should aid prompt transplant listing.

Calcium influx mechanisms underlying calcium oscillations in rat hepatocytes

Bertina F. Jones, Rebecca R. Boyles, Sung‐Yong Hwang, Gary S. Bird, James W. Putney – 26 September 2008 – The process of capacitative or store‐operated Ca2+ entry has been extensively investigated, and recently two major molecular players in this process have been described. Stromal interacting molecule (STIM) 1 acts as a sensor for the level of Ca2+ stored in the endoplasmic reticulum, and Orai proteins constitute pore‐forming subunits of the store‐operated channels.

Surface markers for the murine oval cell response

Craig Dorrell, Laura Erker, Kelsea M. Lanxon‐Cookson, Stephanie L. Abraham, Tristan Victoroff, Simon Ro, Pamela S. Canaday, Philip R. Streeter, Markus Grompe – 26 September 2008 – The biology of progenitor activation in the liver is of considerable medical and scientific interest. The powerful genetic tools available for the mouse make it an ideal model system to study this complex process involving many different cell types. However, reagents for the isolation and study of distinct hepatic subpopulations have been quite limited compared to those available for hematopoietic cells.

A mutation in the canalicular phospholipid transporter gene, ABCB4, is associated with cholestasis, ductopenia, and cirrhosis in adults

Daniel Gotthardt, Heiko Runz, Verena Keitel, Christine Fischer, Christa Flechtenmacher, Michael Wirtenberger, Karl Heinz Weiss, Sandra Imparato, Annika Braun, Kari Hemminki, Wolfgang Stremmel, Franz Rüschendorf, Adolf Stiehl, Ralf Kubitz, Barbara Burwinkel, Peter Schirmacher, A. S. Knisely, Johannes Zschocke, Peter Sauer – 26 September 2008 – Cholestatic liver disease (CLD) is a major cause of progressive liver damage and liver failure. Several forms of biliary cirrhosis are caused by mutations in specific genes.

Hepatitis C is a predictor of acute liver injury among hospitalizations for acetaminophen overdose in the United States: A nationwide analysis

Geoffrey C. Nguyen, Justina Sam, Paul J. Thuluvath – 26 September 2008 – Acute liver injury (ALI) following acetaminophen overdose (AO) occurs in less than 10% of cases, but that risk is increased among alcoholics and those with chronic alcoholic liver disease. We sought to assess whether coexistent hepatitis C virus (HCV) infection potentiated the hepatotoxic effects of acetaminophen. We queried the Nationwide Inpatient Sample (1998‐2005), a 20% sample of U.S.

Bone marrow–derived immune cells mediate sensitization to liver injury in a myeloid differentiation factor 88–dependent fashion

Istvan Hritz, Arumugam Velayudham, Angela Dolganiuc, Karen Kodys, Pranoti Mandrekar, Evelyn Kurt‐Jones, Gyongyi Szabo – 26 September 2008 – Toll‐like receptors (TLRs) expressed on both immune cells and hepatocytes recognize microbial danger signals and regulate immune responses. Previous studies showed that TLR9 and TLR2 mediate Propionibacterium acnes–induced sensitization to lipopolysaccharide‐triggered acute liver injury in mice. Ligand‐specific activation of TLR2 and TLR9 are dependent on the common TLR adaptor, myeloid differentiation factor 88 (MyD88).

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