Chinnasamy Thirunavukkarasu, Simon C. Watkins, Chandrashekhar R. Gandhi – 26 July 2006 – Compelling experimental evidence indicates that the interactions between endotoxin and hepatic stellate cells (HSCs) can play a significant role in the pathogenesis of liver disease. Endotoxin‐induced release of a multifunctional mediator NO (via inducible NO synthase) and the proinflammatory cytokines tumor necrosis factor α (TNF‐α) and interleukin (IL)‐6 by HSCs could be an important mechanism of pathological changes in the liver.

Delphyne Descamps, Frédéric Vigant, Stéphanie Esselin, Elisabeth Connault, Paule Opolon, Michel Perricaudet, Karim Benihoud – 26 July 2006 – Fas and tumor necrosis factor receptor 1 (TNFR1) are death receptors involved in various diseases such as hepatitis, sepsis, or graft rejection. Neutralizing antibodies to death ligands or soluble death receptors can inhibit cell death; however, they induce side effects because of their systemic actions.

26 July 2006

Valerio Nobili, Matilde Marcellini, Rita Devito, Paolo Ciampalini, Fiorella Piemonte, Donatella Comparcola, Maria Rita Sartorelli, Paul Angulo – 26 July 2006 – Nonalcoholic fatty liver disease (NAFLD), a common cause of chronic liver disease in adults, is incompletely characterized in children. We conducted a prospective study to better characterize the clinical presentation of NAFLD in children and to determine the effect of lifestyle advice in the management of pediatric NAFLD.

Deborah L. Diamond, Sean C. Proll, Jon M. Jacobs, Eric Y. Chan, David G. Camp, Richard D. Smith, Michael G. Katze – 26 July 2006 – The wealth of human genome sequence information now available, coupled with technological advances in robotics, nanotechnology, mass spectrometry, and information systems, has given rise to a method of scientific inquiry known as functional genomics.

Yao‐Ming Wu, Brigid Joseph, Sanjeev Gupta – 26 July 2006 – Successful grafting of tissues or cells from mismatched donors requires systemic immunosuppression. It is yet to be determined whether immunosuppressive manipulations perturb transplanted cell engraftment or proliferation. We used syngeneic and allogeneic cell transplantation assays based on F344 recipient rats lacking dipeptidyl peptidase IV enzyme activity to identify transplanted hepatocytes.

Pallavi B. Limaye, Vishakha S. Bhave, Prajakta S. Palkar, Udayan M. Apte, Sharmilee P. Sawant, Songtao Yu, John R. Latendresse, Janardan K. Reddy, Harihara M. Mehendale – 26 July 2006 – Acute liver failure induced by hepatotoxic drugs results from rapid progression of injury. Substantial research has shown that timely liver regeneration can prevent progression of injury leading to a favorable prognosis. However, the mechanism by which compensatory regeneration prevents progression of injury is not known.

Hiroshi Uchinami, Ekihiro Seki, David A. Brenner, Jeanine D'Armiento – 26 July 2006 – Cholestasis occurs in a variety of clinical settings and often results in liver injury and secondary biliary fibrosis. Several matrix metalloproteinases (MMPs) are upregulated in the liver during cholestasis. The function of the major interstitial collagenase, MMP‐13, in the initial phase of liver fibrosis is unknown. The aim of this study was to evaluate the role of MMP‐13 during the development of cholestasis‐induced liver fibrosis by comparing wild‐type and MMP‐13‐deficient mice.

Jeffrey D. Browning, Jeannie Davis, M. Hossein Saboorian, Shawn C. Burgess – 26 July 2006

Jacques Bernuau, François Durand – 26 July 2006 – Monitoring of intracranial pressure (ICP) in acute liver failure (ALF) is controversial as a result of the reported complication risk (approximately 20%) and limited therapeutic options for intracranial hypertension. Using prospectively collected information from 332 patients with ALF and severe encephalopathy, we evaluated a recent experience with ICP monitoring in the 24 centers constituting the U.S. ALF Study Group.