Ken Shirabe, Masanori Yoshimatsu, Takashi Motomura, Kazuki Takeishi, Takeo Toshima, Jun Muto, Rumi Matono, Akinobu Taketomi, Hideaki Uchiyama, Yoshihiko Maehara – 3 May 2011 – The aim of this study was to investigate the effects of preoperative oral supplementation with branched‐chain amino acids (BCAAs) on postoperative bacteremia after living donor liver transplantation (LDLT) for chronic liver failure. Two hundred thirty‐six patients who underwent adult‐to‐adult LDLT were evaluated in this retrospective study.

Ting‐Jung Wu, Divya Dahiya, Ching‐Sung Lee, Chen‐Fang Lee, Hong‐Shiue Chou, Kun‐Ming Chan, Wei‐Chen Lee – 3 May 2011 – The aim of this study was to evaluate the effects of portal hemodynamics on indices of liver function and graft regeneration in patients after adult right lobe living donor liver transplantation (R‐LDLT). Sixty‐four patients who underwent R‐LDLT and had an uneventful postoperative course were enrolled in this study. The contribution of portal flow was greater to the recipient grafts versus the donor livers (90.74% versus 69.12%, P < 0.0001).

Ji‐Hua Shi, Henrik S. Huitfeldt, Zhen‐He Suo, Pål‐Dag Line – 3 May 2011 – Liver resection and liver transplantation are the treatment modalities with the greatest potential for curing hepatocellular carcinoma (HCC). Tumor recurrence after resection for HCC is, however, a major problem, and an increased rate of recurrence after living donor transplantation versus cadaveric whole liver transplantation has been suggested. Factors involved in liver regeneration may stimulate the growth of occult tumors.

Ruchi Bansal, Jai Prakash, Eduard Post, Leonie Beljaars, Detlef Schuppan, Klaas Poelstra – 29 April 2011 – Liver fibrogenesis is a process tightly controlled by endogenous anti‐ and pro‐fibrogenic factors. Interferon gamma (IFNγ) is a potent antifibrogenic cytokine in vitro and might therefore represent a powerful therapeutic entity. However, its poor pharmacokinetics and adverse effects, due to the presence of IFNγ receptors on nearly all cells, prevented its clinical application so far.

Tania M. Welzel, Barry I. Graubard, Stefan Zeuzem, Hashem B. El‐Serag, Jessica A. Davila, Katherine A. McGlynn – 29 April 2011 – Incidence rates of hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC) have increased in the United States. Metabolic syndrome is recognized as a risk factor for HCC and a postulated one for ICC. The magnitude of risk, however, has not been investigated on a population level in the United States. We therefore examined the association between metabolic syndrome and the development of these cancers.

Aijuan Qu, Matthew Taylor, Xiang Xue, Tsutomu Matsubara, Daniel Metzger, Pierre Chambon, Frank J. Gonzalez, Yatrik M. Shah – 29 April 2011 – Oxygen dynamics in the liver is a central signaling mediator controlling hepatic homeostasis, and dysregulation of cellular oxygen is associated with liver injury. Moreover, the transcription factor relaying changes in cellular oxygen levels, hypoxia‐inducible factor (HIF), is critical in liver metabolism, and sustained increase in HIF signaling can lead to spontaneous steatosis, inflammation, and liver tumorigenesis.

Gin‐Ho Lo – 29 April 2011

Mohsan Saeed, Masaaki Shiina, Tomoko Date, Daisuke Akazawa, Noriyuki Watanabe, Asako Murayama, Tetsuro Suzuki, Haruo Watanabe, Nobuhiko Hiraga, Michio Imamura, Kazuaki Chayama, Youkyung Choi, Krzysztof Krawczynski, T. Jake Liang, Takaji Wakita, Takanobu Kato – 29 April 2011 – Hepatitis C virus (HCV) employs various strategies to establish persistent infection that can cause chronic liver disease.

Lisa Franceschini, Stefano Realdon, Moira Marcolongo, Silvia Mirandola, Gladis Bortoletto, Alfredo Alberti – 29 April 2011 – Insulin resistance (IR) is common in chronic hepatitis C (CHC) and associates with reduced virological response to pegylated‐interferon (PEG‐IFN)/ribavirin therapy, but the underlying mechanisms are still unclear. We have previously shown that, in CHC patients, insulin plasma levels are inversely related to antiviral effect induced by PEG‐IFN.

Ayca Cinaroglu, Chuan Gao, Dru Imrie, Kirsten C. Sadler – 29 April 2011 – Many etiologies of fatty liver disease (FLD) are associated with the hyperactivation of one of the three pathways composing the unfolded protein response (UPR), which is a harbinger of endoplasmic reticulum (ER) stress. The UPR is mediated by pathways initiated by PRKR‐like endoplasmic reticulum kinase, inositol‐requiring 1A/X box binding protein 1, and activating transcription factor 6 (ATF6), and each of these pathways has been implicated to have a protective or pathological role in FLD.