Tenofovir for patients with lamivudine‐resistant hepatitis B virus (HBV) infection and high HBV DNA level during adefovir therapy

Florian van Bömmel, Bernhard Zöllner, Christoph Sarrazin, Ulrich Spengler, Dietrich Hüppe, Bernd Möller, Heinz‐Hubert Feucht, Bertram Wiedenmann, Thomas Berg – 26 July 2006 – Incomplete virological response to adefovir dipivoxil (ADV) has been observed in patients with lamivudine‐resistant hepatitis B virus (HBV) infection and may be associated with developing resistance and disease progression. We therefore investigated whether the efficacy of viral suppression could be improved by replacing ADV with tenofovir disoproxil fumarate (TDF).

Relationship of cosmetic procedures and drug use to hepatitis C and hepatitis B virus infections in a low‐risk population

Lu‐Yu Hwang, Jennifer R. Kramer, Catherine Troisi, Lara Bull, Carolyn Z. Grimes, Rob Lyerla, Miriam J. Alter – 26 July 2006 – We conducted an anonymous cross‐sectional seroprevalence study of a population with a low frequency of injection drug use to determine whether persons with a history of cosmetic procedures, such as tattooing and body piercing, or intranasal drug use were at increased risk for hepatitis C virus (HCV) or hepatitis B virus (HBV) infection. Students 18 years and older from eight college campuses in Houston, Texas, were invited to participate in the study.

Correlation between beta‐lipoprotein levels and outcome of hepatitis C treatment

Kavitha Gopal, Timothy C. Johnson, Saraswathi Gopal, Aaron Walfish, Christine T. Bang, Pauline Suwandhi, Helene N. Pena‐Sahdala, David J. Clain, Henry C. Bodenheimer, Albert D. Min – 26 July 2006 – The low‐density lipoprotein receptor (LDLR) has been proposed as a candidate receptor for the hepatitis C virus (HCV). Competitive inhibition of HCV binding to the LDLR by low‐density lipoprotein (LDL) has been shown in vitro.

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.

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.

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.

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.

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