Mathieu Vinken, Tom Henkens, Evelien De Rop, Joanna Fraczek, Tamara Vanhaecke, Vera Rogiers – 26 February 2008 – The present review provides the state of the art of the current knowledge concerning gap junctional channels and their roles in liver functioning. In the first part, we summarize some relevant biochemical properties of hepatic gap junctional channels, including their structure and regulation. In the second part, we discuss the involvement of gap junctional channels in the occurrence of liver cell growth, liver cell differentiation, and liver cell death.

Zhen Fan Yang, Patricia Ngai, David W. Ho, Wan Ching Yu, Michael N.P. Ng, Chi Keung Lau, Mandy L. Y. Li, Ka Ho Tam, Chi Tat Lam, Ronnie T. P. Poon, Sheung Tat Fan – 26 February 2008 – Increasing evidence has revealed the importance of cancer stem cells (CSCs) in carcinogenesis. Although liver CSCs have been identified in hepatocellular carcinoma (HCC) cell lines, no data have shown the presence of these cells in human settings. The present study was designed to delineate CSCs serially from HCC cell lines, human liver cancer specimens to blood samples, using CD90 as a potential marker.

Diana Klein, Alexandra Demory, Francis Peyre, Jens Kroll, Hellmut G. Augustin, Wijnand Helfrich, Julia Kzhyshkowska, Kai Schledzewski, Bernd Arnold, Sergij Goerdt – 26 February 2008 – The mechanisms regulating the growth and differentiation of hepatic sinusoidal endothelial cells (HSECs) are not well defined. Because Wnt signaling has become increasingly important in developmental processes such as vascular and hepatic differentiation, we analyzed HSEC‐specific Wnt signaling in detail.

Go Anegawa, Hirofumi Kawanaka, Daisuke Yoshida, Kozo Konishi, Shohei Yamaguchi, Nao Kinjo, Akinobu Taketomi, Makoto Hashizume, Hiroaki Shimokawa, Yoshihiko Maehara – 26 February 2008 – In liver cirrhosis, down‐regulation of endothelial nitric oxide synthase (eNOS) has been implicated as a cause of increased intrahepatic resistance. We investigated whether Rho‐kinase activation is one of the molecular mechanisms involved in defective eNOS signaling in secondary biliary cirrhosis. Liver cirrhosis was induced by bile duct ligation (BDL).

Michael R. Beard, Karla J. Helbig – 26 February 2008

Keane K. Y. Lai, Deepak Kolippakkam, Laura Beretta – 26 February 2008 – We report a comprehensive and quantitative analysis of the mouse liver and plasma proteomes. The method used is based on extensive fractionation of intact proteins, further separation of proteins based on their abundance and size, and high‐accuracy mass spectrometry. This analysis reached a depth in proteomic profiling not reported to date for a mammalian tissue or a biological fluid, with 7099 and 4727 proteins identified with high confidence in the liver and in the corresponding plasma, respectively.

Song Hee Lee, Ran Song, Mi Nam Lee, Chon Saeng Kim, Hanna Lee, Young‐Yun Kong, Hoguen Kim, Sung Key Jang – 26 February 2008 – The hepatitis C virus (HCV) E2 protein has been shown to block apoptosis and has been suggested to facilitate persistent infection of the virus.

J. Eileen Hay – 26 February 2008 – Abnormal liver tests occur in 3%–5% of pregnancies, with many potential causes, including coincidental liver disease (most commonly viral hepatitis or gallstones) and underlying chronic liver disease. However, most liver dysfunction in pregnancy is pregnancy‐related and caused by 1 of the 5 liver diseases unique to the pregnant state: these fall into 2 main categories depending on their association with or without preeclampsia.

Robert Flisiak, Andrzej Horban, Philippe Gallay, Michael Bobardt, Suganya Selvarajah, Alicja Wiercinska‐Drapalo, Ewa Siwak, Iwona Cielniak, Jozef Higersberger, Jarek Kierkus, Christian Aeschlimann, Pierre Grosgurin, Valérie Nicolas‐Métral, Jean‐Maurice Dumont, Hervé Porchet, Raf Crabbé, Pietro Scalfaro – 26 February 2008 – Debio‐025 is an oral cyclophilin (Cyp) inhibitor with potent anti–hepatitis C virus activity in vitro. Its effect on viral load as well as its influence on intracellular Cyp levels was investigated in a randomized, double‐blind, placebo‐controlled study.

Ainhoa Iglesias Ara, Meng Xia, Komal Ramani, José M. Mato, Shelly C. Lu – 21 February 2008 – We previously showed that S‐adenosylmethionine (SAMe) and its metabolite methylthioadenosine (MTA) blocked lipopolysaccharide (LPS)‐induced tumor necrosis factor α (TNFα) expression in RAW (murine macrophage cell line) and Kupffer cells at the transcriptional level without affecting nuclear factor κ B nuclear binding. However, the exact molecular mechanism or mechanisms of the inhibitory effect were unclear. While SAMe is a methyl donor, MTA is an inhibitor of methylation.