Samuele Minicis, Chiara Rychlicki, Laura Agostinelli, Stefania Saccomanno, Cinzia Candelaresi, Luciano Trozzi, Eleonora Mingarelli, Bruna Facinelli, Gloria Magi, Claudio Palmieri, Marco Marzioni, Antonio Benedetti, Gianluca Svegliati‐Baroni – 19 August 2013 – Nonalcoholic fatty liver disease (NAFLD) may lead to hepatic fibrosis. Dietary habits affect gut microbiota composition, whereas endotoxins produced by Gram‐negative bacteria stimulate hepatic fibrogenesis. However, the mechanisms of action and the potential effect of microbiota in the liver are still unknown.

Toshana L. Foster, Gary S. Thompson, Arnout P. Kalverda, Jayakanth Kankanala, Matthew Bentham, Laura F. Wetherill, Joseph Thompson, Amy M. Barker, Dean Clarke, Marko Noerenberg, Arwen R. Pearson, David J. Rowlands, Steven W. Homans, Mark Harris, Richard Foster, Stephen Griffin – 12 August 2013 – Current interferon‐based therapy for hepatitis C virus (HCV) infection is inadequate, prompting a shift toward combinations of direct‐acting antivirals (DAA) with the first protease‐targeted drugs licensed in 2012.

Dalbir S. Sandhu, Esha Baichoo, Lewis R. Roberts – 12 August 2013 – Fibroblast growth factors, or FGFs, are a large family of polypeptide cytokines exhibiting a pleiotropy of functions, from cell growth to angiogenesis, wound healing, and tissue repair. This review broadly covers the genetics and protein expression of the FGF family members and the signaling pathways involved in FGF‐mediated growth regulation. We emphasize the role of FGFs in the pathogenesis of hepatocellular carcinoma (HCC), including their effects on regulation of the tumor microenvironment and angiogenesis.

Dalbir S. Sandhu, Esha Baichoo, Lewis R. Roberts – 12 August 2013 – Fibroblast growth factors, or FGFs, are a large family of polypeptide cytokines exhibiting a pleiotropy of functions, from cell growth to angiogenesis, wound healing, and tissue repair. This review broadly covers the genetics and protein expression of the FGF family members and the signaling pathways involved in FGF‐mediated growth regulation. We emphasize the role of FGFs in the pathogenesis of hepatocellular carcinoma (HCC), including their effects on regulation of the tumor microenvironment and angiogenesis.

John F. Renz – 12 August 2013

Dan Yin, Vasu Kulhalli, Ann P. Walker – 12 August 2013 – Hyperferritinemia and bilateral cataracts are features of the rare hereditary hyperferritinemia cataract syndrome (HHCS; OMIM #600886). HHCS is an autosomal dominant condition caused by mutations which increase expression of the ferritin light polypeptide (FTL) gene. We report a patient with HHCS who was misdiagnosed and treated as having hemochromatosis, in whom a heterozygous c.‐160A>G mutation was identified in the iron responsive element (IRE) of FTL, causing ferritin synthesis in the absence of iron overload.

Jung‐Hwan Kim, Aijuan Qu, Janardan K. Reddy, Bin Gao, Frank J. Gonzalez – 12 August 2013 – Growth arrest and DNA damage‐inducible beta (GADD45b) plays an important role in many intracellular events, such as cell cycle arrest, DNA repair, cell survival, apoptosis, and senescence. However, its mechanism of transcriptional regulation remains unclear. In this study the mechanism of peroxisome proliferator‐activated receptor α (PPARα) ligand induction of the Gadd45b gene in mouse liver was investigated.

Kathryn M. Kitrinos, Amoreena Corsa, Yang Liu, John Flaherty, Andrea Snow‐Lampart, Patrick Marcellin, Katyna Borroto‐Esoda, Michael D. Miller – 12 August 2013 – One major challenge in the treatment of chronic hepatitis B is to maintain long‐term viral suppression without promoting the selection of drug‐resistant mutations. We analyzed data from 347 hepatitis B e antigen‐negative and 238 hepatitis B e antigen‐positive patients receiving tenofovir disoproxil fumarate (TDF) in an open‐label, long‐term extension of two phase 3 studies.

Dan Yin, Vasu Kulhalli, Ann P. Walker – 12 August 2013 – Hyperferritinemia and bilateral cataracts are features of the rare hereditary hyperferritinemia cataract syndrome (HHCS; OMIM #600886). HHCS is an autosomal dominant condition caused by mutations which increase expression of the ferritin light polypeptide (FTL) gene. We report a patient with HHCS who was misdiagnosed and treated as having hemochromatosis, in whom a heterozygous c.‐160A>G mutation was identified in the iron responsive element (IRE) of FTL, causing ferritin synthesis in the absence of iron overload.

M. Eric Gershwin, Edward L. Krawitt – 12 August 2013