Impaired uptake of conjugated bile acids and hepatitis b virus pres1‐binding in na+‐taurocholate cotransporting polypeptide knockout mice

Davor Slijepcevic, Christina Kaufman, Catharina G.K. Wichers, Eduardo H. Gilglioni, Florian A. Lempp, Suzanne Duijst, Dirk R. de Waart, Ronald P.J. Oude Elferink, Walter Mier, Bruno Stieger, Ulrich Beuers, Stephan Urban, Stan F.J. van de Graaf – 10 January 2015 – The Na+‐taurocholate cotransporting polypeptide (NTCP) mediates uptake of conjugated bile acids (BAs) and is localized at the basolateral membrane of hepatocytes. It has recently been recognized as the receptor mediating hepatocyte‐specific entry of hepatitis B virus and hepatitis delta virus.

Altered hepatic gene expression in nonalcoholic fatty liver disease is associated with lower hepatic n‐3 and n‐6 polyunsaturated fatty acids

Bianca M. Arendt, Elena M. Comelli, David W.L. Ma, Wendy Lou, Anastasia Teterina, TaeHyung Kim, Scott K. Fung, David K.H. Wong, Ian McGilvray, Sandra E. Fischer, Johane P. Allard – 10 January 2015 – In nonalcoholic fatty liver disease, hepatic gene expression and fatty acid (FA) composition have been reported independently, but a comprehensive gene expression profiling in relation to FA composition is lacking. The aim was to assess this relationship.

Experimental transmission of equine hepacivirus in horses as a model for hepatitis C virus

Joshua D. Ramsay, Ryan Evanoff, Tom E. Wilkinson, Thomas J. Divers, Donald P. Knowles, Robert H. Mealey – 10 January 2015 – Equine hepacivirus (EHCV; nonprimate hepacivirus) is a hepatotropic member of the Flaviviridae family that infects horses. Although EHCV is the closest known relative to hepatitis C virus (HCV), its complete replication kinetics in vivo have not been described, and direct evidence that it causes hepatitis has been lacking. In this study, we detected EHCV in 2 horses that developed post‐transfusion hepatitis.

Adaptive remodeling of the biliary architecture underlies liver homeostasis

Kota Kaneko, Kenji Kamimoto, Atsushi Miyajima, Tohru Itoh – 8 January 2015 – Serving as the center for metabolism and detoxification, the liver is inherently susceptible to a wide variety of damage imposed by toxins or chemicals. Induction of cell populations with biliary epithelial phenotypes, which include progenitor‐like cells and are referred to as liver progenitor cells, is often observed in histopathological examination of various liver diseases in both human patients and animal models and has been implicated in regeneration.

Adaptive remodeling of the biliary architecture underlies liver homeostasis

Kota Kaneko, Kenji Kamimoto, Atsushi Miyajima, Tohru Itoh – 8 January 2015 – Serving as the center for metabolism and detoxification, the liver is inherently susceptible to a wide variety of damage imposed by toxins or chemicals. Induction of cell populations with biliary epithelial phenotypes, which include progenitor‐like cells and are referred to as liver progenitor cells, is often observed in histopathological examination of various liver diseases in both human patients and animal models and has been implicated in regeneration.

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