HepatoProteomics: Applying proteomic technologies to the study of liver function and disease

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.

NAFLD in children: A prospective clinical‐pathological study and effect of lifestyle advice

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.

Expression of non‐signaling membrane‐anchored death receptors protects murine livers in different models of hepatitis

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.

Mechanisms of endotoxin‐induced NO, IL‐6, and TNF‐α production in activated rat hepatic stellate cells: Role of p38 MAPK

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.

Aspartyl‐asparagyl β hydroxylase over‐expression in human hepatoma is linked to activation of insulin‐like growth factor and notch signaling mechanisms

M. Chiara Cantarini, Suzanne M. de la Monte, Maoyin Pang, Ming Tong, Antonia D'Errico, Franco Trevisani, Jack R. Wands – 26 July 2006 – Aspartyl‐(Asparagyl)‐β‐hydroxylase (AAH) is overexpressed in various malignant neoplasms, including hepatocellular carcinomas (HCCs). The upstream regulation of AAH and its functional role in Notch‐mediated signaling and motility in HCC cells was accessed.

Induction of murine liver damage by overexpression of CD40 ligand provides an experimental model to study fulminant hepatic failure

Volker Schmitz, Frank Dombrowski, Jesús Prieto, Cheng Qian, Linda Diehl, Percy Knolle, Tilman Sauerbruch, Wolfgang H. Caselmann, Ulrich Spengler, Ludger Leifeld – 26 July 2006 – Previously, we demonstrated that intrahepatic upregulation of the immunoactivating molecules CD40 and CD40 ligand (CD40L) are early mechanisms for liver cell damage in human and murine fulminant hepatic failure (FHF). In the present study, we investigated the functional effects of intrahepatic overexpression of CD40L by adenoviral‐mediated gene transfer (AdCD40L) in mice.

Subscribe to