Primary biliary cirrhosis: Report of a focus study group
Nora V. Bergasa, Andrew Mason, Annarosa Floreani, Jenny Heathcote, Mark G. Swain, David E. J. Jones, Keith M. Lindor, Margaret F. Bassendine, Howard J. Worman – 7 March 2007
Nora V. Bergasa, Andrew Mason, Annarosa Floreani, Jenny Heathcote, Mark G. Swain, David E. J. Jones, Keith M. Lindor, Margaret F. Bassendine, Howard J. Worman – 7 March 2007
Zhenyuan Song, Zhanxiang Zhou, Silvia Uriarte, Lipeng Wang, Y. James Kang, Theresa Chen, Shirish Barve, Craig J. McClain – 7 March 2007 – In alcoholic liver disease, tumor necrosis factor‐α (TNFα) is a critical effector molecule, and abnormal methionine metabolism is a fundamental acquired metabolic abnormality. Although hepatocytes are resistant to TNFα‐induced killing under normal circumstances, previous studies have shown that primary hepatocytes from rats chronically fed alcohol have increased TNFα cytotoxicity.
7 March 2007
7 March 2007
7 March 2007
Juan Córdoba, Nuria Raguer, Montserrat Flavià, Víctor Vargas, Carlos Jacas, Juli Alonso, Alex Rovira – 7 March 2007 – Magnetic resonance has shown T2 hyperintensity along the cortico‐spinal tract in the brain of cirrhotic patients. This abnormality, which is reversible after liver transplantation, appears to correspond to mild edema. Because astrocytic edema present in hepatic encephalopathy may be responsible for neuronal dysfunction, we studied whether T2 hyperintensity along the cortico‐spinal tract may relate to functional abnormalities.
Peter F. Whitington – 7 March 2007
Richard B. Freeman – 7 March 2007
Maryline Mancini‐Bourgine, Hélène Fontaine, Daniel Scott‐Algara, Stanislas Pol, Christian Bréchot, Marie‐Louise Michel – 7 March 2007 – Despite the availability of effective hepatitis B vaccines for many years, over 370 million people remain persistently infected with hepatitis B virus (HBV). Viral persistence is thought to be related to poor HBV‐specific T‐cell responses. A phase I clinical trial was performed in chronic HBV carriers to investigate whether HBV DNA vaccination could restore T‐cell responsiveness.