Tim Hon Man Chan, Leilei Chen, Ming Liu, Liang Hu, Bo‐jian Zheng, Vincent Kwok‐Man Poon, Pinzhu Huang, Yun‐Fei Yuan, Jian‐dong Huang, Jie Yang, George Sai‐wah Tsao, Xin‐Yuan Guan – 27 September 2011 – Emerging evidence implicates the chromodomain helicase/ATPase DNA binding protein 1–like gene (CHD1L) as a specific oncogene in human hepatocellular carcinoma (HCC).

Siobhán Q. Gregg, Verónica Gutiérrez, Andria Rasile Robinson, Tyler Woodell, Atsunori Nakao, Mark A. Ross, George K. Michalopoulos, Lora Rigatti, Carrie E. Rothermel, Irene Kamileri, George A. Garinis, Donna Beer Stolz, Laura J. Niedernhofer – 27 September 2011 – The liver changes with age, leading to an impaired ability to respond to hepatic insults and increased incidence of liver disease in the elderly. Therefore, there is critical need for rapid model systems to study aging‐related liver changes.

Kausik Das, Rajib Sarkar, Sk. Mahiuddin Ahmed, Asit R. Mridha, Partha S. Mukherjee, Kshaunish Das, Gopal K. Dhali, Amal Santra, Abhijit Chowdhury – 27 September 2011 – The liver stiffness measure (LSM) needs to be explored in ethnically and anthropometrically diverse healthy subjects (to derive an acceptable normal range) and also in patients with liver disease.

Kathleen E. Corey, Naga Chalasani – 27 September 2011

Philip Meuleman, Maria Teresa Catanese, Lieven Verhoye, Isabelle Desombere, Ali Farhoudi, Christopher T. Jones, Timothy Sheahan, Katarzyna Grzyb, Riccardo Cortese, Charles M. Rice, Geert Leroux‐Roels, Alfredo Nicosia – 27 September 2011 – Endstage liver disease caused by chronic hepatitis C virus (HCV) infection is the leading indication for liver transplantation in the Western world. However, immediate reinfection of the grafted donor liver by circulating virus is inevitable and liver disease progresses much faster than the original disease.

Kris V. Kowdley, Patricia Belt, Laura A. Wilson, Matthew M. Yeh, Brent A. Neuschwander‐Tetri, Naga Chalasani, Arun J. Sanyal, James E. Nelson, for the NASH Clinical Research Network. – 27 September 2011 – Serum ferritin (SF) levels are commonly elevated in patients with nonalcoholic fatty liver disease (NAFLD) because of systemic inflammation, increased iron stores, or both. The aim of this study was to examine the relationship between elevated SF and NAFLD severity.

Laurent Dollé, Jan Best, Christophe Empsen, Jie Mei, Elke Van Rossen, Philip Roelandt, Sarah Snykers, Mustapha Najimi, Feras Al Battah, Neil D. Theise, Konrad Streetz, Etienne Sokal, Isabelle A. Leclercq, Catherine Verfaillie, Vera Rogiers, Albert Geerts, Leo A. van Grunsven – 27 September 2011 – The role of progenitor cells in liver repair and fibrosis has been extensively described, but their purification remains a challenge, hampering their characterization and use in regenerative medicine.

Roja Barikbin, Daniel Neureiter, Jan Wirth, Annette Erhardt, Dorothee Schwinge, Johannes Kluwe, Christoph Schramm, Gisa Tiegs, Gabriele Sass – 27 September 2011 – Induction or overexpression of the heme‐degrading enzyme, heme oxygenase 1 (HO‐1), has been shown to protect mice from liver damage induced by acute inflammation. We have investigated the effects of HO‐1 induction in a mouse model of chronic liver inflammation and fibrogenesis with progression to hepatocellular carcinoma (HCC) (Mdr2ko; FVB.129P2‐Abcb4tm1Bor).

Yixin Chen, Philip P. Wong, Lucas Sjeklocha, Clifford J. Steer, M. Behnan Sahin – 27 September 2011 – Although there have been numerous reports describing the isolation of liver progenitor cells from the adult liver, their exact origin has not been clearly defined; and the role played by mature hepatocytes as direct contributors to the hepatic progenitor cell pool has remained largely unknown. Here, we report strong evidence that mature hepatocytes in culture have the capacity to dedifferentiate into a population of adult liver progenitors without genetic or epigenetic manipulations.

Robert S. Tacke, Hai‐Chon Lee, Celeste Goh, Jeremy Courtney, Stephen J. Polyak, Hugo R. Rosen, Young S. Hahn – 27 September 2011 – Impaired T‐cell responses in chronic hepatitis C virus (HCV) patients have been reported to be associated with the establishment of HCV persistent infection. However, the mechanism for HCV‐mediated T‐cell dysfunction is yet to be defined. Myeloid‐derived suppressor cells (MDSCs) play a pivotal role in suppressing T‐cell responses. In this study we examined the accumulation of MDSCs in human peripheral blood mononuclear cells (PBMCs) following HCV infection.