Kinji Asahina, Shirley Y. Tsai, Peng Li, Mamoru Ishii, Robert E. Maxson, Henry M. Sucov, Hidekazu Tsukamoto – 24 February 2009 – The knowledge concerning fetal hepatic stellate cells (HSCs) is scarce, and their cell lineage and functions are largely unknown. The current study isolated fetal liver mesenchymal cells from a mouse expressing β‐galactosidase under the control of Msx2 promoter by fluorescence‐activated cell sorting (FACS) and surveyed marker genes by microarray analysis.

Sara D. Sackett, Zhaodong Li, Reginald Hurtt, Yan Gao, Rebecca G. Wells, Karrie Brondell, Klaus H. Kaestner, Linda E. Greenbaum – 24 February 2009 – The liver contains a population of small bipotential facultative progenitor cells that reconstitute liver function when mature hepatocytes or cholangiocytes are unable to proliferate. Mesenchymal markers, including members of the forkhead transcription factor gene family, have been detected in hepatic progenitor cells.

Timo H.‐W. Lüdtke, Vincent M. Christoffels, Marianne Petry, Andreas Kispert – 24 February 2009 – After specification of the hepatic endoderm, mammalian liver organogenesis progresses through a series of morphological stages that culminate in the migration of hepatocytes into the underlying mesenchyme to populate the hepatic lobes. Here, we show that in the mouse the transcriptional repressor Tbx3, a member of the T‐box protein family, is required for the transition from a hepatic diverticulum with a pseudo‐stratified epithelium to a cell‐emergent liver bud.

Jinsheng Guo, Johnny Loke, Feng Zheng, Feng Hong, Steven Yea, Masayuki Fukata, Mirko Tarocchi, Olivia T. Abar, Hongjin Huang, John J. Sninsky, Scott L. Friedman – 24 February 2009 – In a recent study, a single nucleotide polymorphism (SNP) of the Toll‐like receptor 4 (TLR4) gene (c.1196C>T [rs4986791, p.T399I]) emerged as conferring protection from fibrosis progression compared to a major, wild‐type (WT) CC allele (p.T399).

Hua Huang, Shizuo Akira, Manuela M. Santos – 24 February 2009 – Under normal conditions, iron is taken up by the cells through the transferrin‐mediated pathway. However, in hereditary hemochromatosis, a common iron‐overloading disorder associated with mutations in the HFE gene, iron in plasma exceeds transferrin‐binding capacity, and non–transferrin‐bound iron (NTBI) appears in the circulation of patients with iron overload. NTBI can be taken up by hepatocytes through a transferrin‐independent pathway.

Norman M. Kneteman, Anita Y. M. Howe, Tiejun Gao, Jamie Lewis, Dan Pevear, Gary Lund, Donna Douglas, David F. Mercer, D. Lorne J. Tyrrell, Frederick Immermann, Inder Chaudhary, John Speth, Stephen A. Villano, John O'Connell, Marc Collett – 24 February 2009 – Anti‐hepatitis C virus (HCV) drug development has been challenged by a lack of experience with inhibitors inclusive of in vitro, animal model, and clinical study.

Hermann E. Wasmuth, Carmen G. Tag, Eddie Van de Leur, Claus Hellerbrand, Tobias Mueller, Thomas Berg, Gero Puhl, Peter Neuhaus, Didier Samuel, Christian Trautwein, Sandip M. Kanse, Ralf Weiskirchen – 24 February 2009 – Genetic risk factors play an important role for the progression of liver fibrosis in chronic hepatitis C virus (HCV) infection, but functional data on specific alleles and their related proteins are limited.

Don C. Rockey, Stephen H. Caldwell, Zachary D. Goodman, Rendon C. Nelson, Alastair D. Smith – 24 February 2009

Ibrahim Dagher, Tuan Huy Nguyen, Marie‐Thérèse Groyer‐Picard, Panagiotis Lainas, Sylvie Mainot, Catherine Guettier, Danièle Pariente, Dominique Franco, Anne Weber – 24 February 2009 – The feasibility of ex vivo gene therapy as an alternative to liver transplantation for the treatment of liver metabolic diseases needs to be analyzed in large animal models. This approach requires appropriate gene transfer vectors and effective hepatocyte engraftment.

Ana Lleo, Carlo Selmi, Pietro Invernizzi, Mauro Podda, Ross L. Coppel, Ian R. Mackay, Gregory J. Gores, Aftab A. Ansari, Judy Van de Water, M. Eric Gershwin – 24 February 2009 – Primary biliary cirrhosis (PBC) is characterized by antimitochondrial antibodies (AMAs), directed to the E2 component of the pyruvate dehydrogenase complex (PDC‐E2). Notwithstanding the presence of mitochondria in virtually all nucleated cells, the destruction in PBC is limited to small intrahepatic bile ducts.