Roben G. Gieling, Ahmed M. Elsharkawy, Jorge H. Caamaño, David E. Cowie, Matthew C. Wright, Mohammad R. Ebrahimkhani, Alastair D. Burt, Jelena Mann, Pradip Raychaudhuri, Hsiou‐Chi Liou, Fiona Oakley, Derek A. Mann – 19 October 2009 – In this study, we determined the role of the nuclear factor‐kappaB (NF‐κB) subunit c‐Rel in liver injury and regeneration.
Kumiko Isse, Susan M. Specht, John G. Lunz, Liang‐I Kang, Yoshiaki Mizuguchi, Anthony J. Demetris – 19 October 2009 – Females are more susceptible than males to several biliary tract diseases. Interleukin‐6 (IL‐6) is critical to triggering autoimmune reactions and contributes substantially to biliary epithelial cell (BEC) barrier function and wound repair, and estrogen differentially regulates IL‐6 expression in various cell types. We hypothesized that estrogen might stimulate BEC IL‐6 production.
William J. H. Griffiths, Roman Mayr, Ian McFarlane, Martin Hermann, David J. Halsall, Heinz Zoller, Timothy M. Cox – 19 October 2009 – Mutations in the SLC40A1 gene, which encodes ferroportin, are associated with autosomal dominant hemochromatosis. Ferroportin is inhibited directly by hepcidin, a key iron‐regulatory peptide, and functional consequences of SLC40A1 mutations account for observed phenotypic differences in patients with ferroportin disease.
Yujuan Xiong, Jian‐Hong Fang, Jing‐Ping Yun, Jine Yang, Ying Zhang, Wei‐Hua Jia, Shi‐Mei Zhuang – 19 October 2009 – Based on microarray data, we have previously shown a significant down‐regulation of miR‐29 in hepatocellular carcinoma (HCC) tissues. To date, the role of miR‐29 deregulation in hepatocarcinogenesis and the signaling pathways by which miR‐29 exerts its function and modulates the malignant phenotypes of HCC cells remain largely unknown.
Kojiro Taura, Kouichi Miura, Keiko Iwaisako, Christoph H. Österreicher, Yuzo Kodama, Melitta Penz‐Österreicher, David A. Brenner – 13 October 2009 – The origin of fibrogenic cells in liver fibrosis remains controversial. We assessed the emerging concept that hepatocytes contribute to production of extracellular matrix (ECM) in liver fibrosis through epithelial‐mesenchymal transition (EMT).
Soo Jung Park, Young‐Suk Lim, Shin Hwang, Nae Yun Heo, Han Chu Lee, Dong Jin Suh, Eunsil Yu, Sung Gyu Lee – 13 October 2009 – The outcomes of patients with acute liver failure (ALF) vary greatly according to etiology. Emergency adult‐to‐adult living‐donor liver transplantation (adult LDLT) would help address the shortage of available organs for patients with ALF, especially in hepatitis B virus (HBV)‐endemic areas. We analyzed a prospective database of 110 consecutive adult patients with ALF.
Paulette Bioulac‐Sage, Charles Balabaud, Jessica Zucman‐Rossi – 13 October 2009
Debbie L. Shawcross, Shabnam S. Shabbir, Nicholas J. Taylor, Robin D. Hughes – 13 October 2009 – Hepatic encephalopathy (HE) constitutes a neuropsychiatric syndrome which remains a major clinical problem in patients with cirrhosis. In the severest form of HE, cirrhotic patients may develop varying degrees of confusion and coma. Ammonia has been regarded as the key precipitating factor in HE, and astrocytes have been the most commonly affected cells neuropathologically.
Elizabeth B. Haagsma, Hubert G. M. Niesters, Arie P. van den Berg, Annelies Riezebos‐Brilman, Robert J. Porte, Harry Vennema, Johan H. J. Reimerink, Marion P. G. Koopmans – 29 September 2009 – Hepatitis E virus (HEV) infection is known to run a self‐limited course. Recently, chronic hepatitis E has been described in several immunosuppressed patients after solid organ transplantation. The prevalence of HEV infection after transplantation, however, is unknown.
Jacqueline G. O'Leary, Gary L. Davis – 29 September 2009 – Hyponatremia is associated with increased mortality in patients with end‐stage liver disease and a greater risk of perioperative mortality with liver transplantation. We performed a retrospective review of our experience with conivaptan as a means of acutely increasing serum sodium in end‐stage liver disease patients. The primary group consisted of 15 patients with end‐stage liver disease who remained hyponatremic despite discontinuation of diuretics and a 1‐L fluid restriction.