Raphael B. Merriman, Linda D. Ferrell, Marco G. Patti, Shiobhan R. Weston, Mark S. Pabst, Bradley E. Aouizerat, Nathan M. Bass – 27 September 2006 – In the absence of surrogate markers, the evaluation of suspected nonalcoholic fatty liver disease (NAFLD) is highly dependent on histological examination. The extent of sampling variability affecting the reliability of a single liver biopsy in patients with suspected NAFLD is poorly characterized.

Rui Sun, Ogyi Park, Norio Horiguchi, Shailin Kulkarni, Won‐Il Jeong, Hao‐Yu Sun, Svetlana Radaeva, Bin Gao – 27 September 2006 – Increasing evidence suggests that liver regeneration is suppressed in patients with chronic HCV infection; however, the underlying mechanisms remain unclear. Previously, we demonstrated that injection of the synthetic double‐stranded RNA (dsRNA) poly I:C to mimic viral infection suppresses liver regeneration in the partial hepatectomy (PHx) model, whereby IFN‐γ contributes to the inhibition.

Mattias Ekstedt, Lennart E. Franzén, Ulrik L. Mathiesen, Lars Thorelius, Marika Holmqvist, Göran Bodemar, Stergios Kechagias – 27 September 2006 – Nonalcoholic fatty liver disease (NAFLD) is the most common cause of elevated liver enzymes in patients of developed countries. We determined the long‐term clinical and histological courses of such patients. In a cohort study, 129 consecutively enrolled patients diagnosed with biopsy‐proven NAFLD were reevaluated. Survival and causes of death were compared with a matched reference population.

27 September 2006

Hiroki Kawamura, Sugantha Govindarajan, Fred Aswad, Keigo Machida, Michael M.C. Lai, Vicky M.‐H. Sung, Gunther Dennert – 27 September 2006 – Hepatitis C virus (HCV) infection causes acute and chronic liver disease often leading to liver cirrhosis and hepatocellular carcinoma. Numerous studies have shown that despite induction of virus specific immunity, a curative response is often not attained; this has led to the hypothesis that HCV genes modulate immunity, thereby enabling chronic infections.

Marsha Y. Morgan, Angela M. Madden, Clare T. Soulsby, Richard W. Morris – 27 September 2006 – Accurate assessments of nutritional status are difficult to obtain in patients with cirrhosis. The aim of this study was to devise and validate a global nutritional assessment scheme for use in this patient population.

Heiner Wedemeyer, Markus Cornberg, Johannes Wiegand, Michael Manns – 27 September 2006

Udayan Apte, Gang Zeng, Peggy Muller, Xinping Tan, Amanda Micsenyi, Benjamin Cieply, Chunsun Dai, Youhua Liu, Klaus H. Kaestner, Satdarshan P. S. Monga – 27 September 2006 – Hepatocyte growth factor (HGF) and β‐catenin both play a crucial role in stimulating hepatocyte proliferation, but whether these 2 pathways cooperate in inducing hepatocyte proliferation is unclear. We have previously reported that β‐catenin forms a complex with c‐Met (HGF receptor) that undergoes dissociation because of β‐catenin tyrosine phosphorylation on stimulation by HGF.

Jacob Nattermann, Henning Zimmermann, Agathe Iwan, Marie von Lilienfeld‐Toal, Ludger Leifeld, Hans Dieter Nischalke, Bettina Langhans, Tilman Sauerbruch, Ulrich Spengler – 27 September 2006 – Dendritic cells (DC) are crucially involved in the induction of immune responses; however, reports on DC functions in chronic hepatitis C are controversial. Function of DC includes proper cell trafficking between sites of infection and lympho‐cellular compartments. Thus, we analyzed DC compartmentalization and changes in DC migration in hepatitis C virus (HCV)‐infected patients.

David A. Rudnick, Olga Shikapwashya, Keith Blomenkamp, Jeffrey H. Teckman – 27 September 2006 – Homozygous (PIZZ) alpha‐1‐antitrypsin (α1‐AT) deficiency is associated with the development of liver damage in children as well as chronic liver injury and hepatocellular carcinoma in adults. The α1‐AT mutant Z gene encodes a mutant protein that accumulates in the endoplasmic reticulum of hepatocytes rather than being secreted appropriately into serum. Liver injury is caused by the accumulation of α1‐AT mutant Z protein in hepatocytes, which triggers downstream intracellular injury pathways.