Graft rotation and late portal vein complications in pediatric living donor liver transplantation using left‐sided grafts: Long‐term computed tomography observations

Suk‐Bae Moon, Ju‐Ik Moon, Choon‐Hyuk David Kwon, Sung‐Joo Kim, Jeong‐Meen Seo, Jae‐Won Joh, Suk‐Koo Lee – 14 January 2011 – Right‐side rotation of the graft is an uncommon event after pediatric living donor liver transplantation (LDLT) with a left‐sided graft. However, graft rotation might lead to gradual portal vein (PV) stretching and late portal vein complications (PVCs). The goal of this study was to quantify the degree of graft rotation (R) by computed tomography (CT) and to determine the effect of graft rotation on the development of late PVCs.

Human hepatic stem cell and maturational liver lineage biology

Rachael Turner, Oswaldo Lozoya, Yunfang Wang, Vincenzo Cardinale, Eugenio Gaudio, Gianfranco Alpini, Gemma Mendel, Eliane Wauthier, Claire Barbier, Domenico Alvaro, Lola M. Reid – 12 January 2011 – Livers are comprised of maturational lineages of cells beginning extrahepatically in the hepato‐pancreatic common duct near the duodenum and intrahepatically in zone 1 by the portal triads.

Controlling autophagy: A new concept for clearing liver disease

Frank Tacke, Christian Trautwein – 12 January 2011 – In the classical form of alpha1‐antitrypsin (AT) deficiency, a point mutation in AT alters the folding of a liver‐derived secretory glycoprotein and renders it aggregation‐prone. In addition to decreased serum concentrations of AT, the disorder is characterized by accumulation of the mutant alpha1‐antitrypsin Z (ATZ) variant inside cells, causing hepatic fibrosis and/or carcinogenesis by a gain‐of‐toxic function mechanism. The proteasomal and autophagic pathways are known to mediate degradation of ATZ.

Activation of v‐Myb avian myeloblastosis viral oncogene homolog‐like2 (MYBL2)‐LIN9 complex contributes to human hepatocarcinogenesis and identifies a subset of hepatocellular carcinoma with mutant p53

Diego F. Calvisi, Maria M. Simile, Sara Ladu, Maddalena Frau, Matthias Evert, Maria L. Tomasi, Maria I. Demartis, Lucia Daino, Maria A. Seddaiu, Stefania Brozzetti, Francesco Feo, Rosa M. Pascale – 12 January 2011 – Up‐regulation of the v‐Myb avian myeloblastosis viral oncogene homolog‐like2 B‐Myb (MYBL2) gene occurs in human hepatocellular carcinoma (HCC) and is associated with faster progression of rodent hepatocarcinogenesis.

Evidence for distinct pathways of hepcidin regulation by acute and chronic iron loading in mice

Emilio Ramos, Léon Kautz, Richard Rodriguez, Michael Hansen, Victoria Gabayan, Yelena Ginzburg, Marie‐Paule Roth, Elizabeta Nemeth, Tomas Ganz – 12 January 2011 – In response to iron loading, hepcidin synthesis is homeostatically increased to limit further absorption of dietary iron and its release from stores. Mutations in HFE, transferrin receptor 2 (Tfr2), hemojuvelin (HJV), or bone morphogenetic protein 6 (BMP6) prevent appropriate hepcidin response to iron, allowing increased absorption of dietary iron, and eventually iron overload.

Constitutional telomerase mutations are genetic risk factors for cirrhosis

Rodrigo T. Calado, Jennifer Brudno, Paulomi Mehta, Joseph J. Kovacs, Colin Wu, Marco A. Zago, Stephen J. Chanock, Thomas D. Boyer, Neal S. Young – 12 January 2011 – Some patients with liver disease progress to cirrhosis, but the risk factors for cirrhosis development are unknown. Dyskeratosis congenita, an inherited bone marrow failure syndrome associated with mucocutaneous anomalies, pulmonary fibrosis, and cirrhosis, is caused by germline mutations of genes in the telomerase complex. We examined whether telomerase mutations also occurred in sporadic cirrhosis.

IL28B genetic variation and treatment response in patients with hepatitis C virus genotype 3 infection

Amir Moghaddam, Espen Melum, Nils Reinton, Helmer Ring‐Larsen, Hans Verbaan, Kristian Bjøro, Olav Dalgard – 12 January 2011 – Polymorphisms near the IL28B gene, which code for interferon (IFN)‐λ3, predict response to pegylated interferon‐α (PEG‐IFN) and ribavirin treatment in hepatitis C virus (HCV) genotype 1 infected patients. Follow‐up studies of the effect of IL28B gene in HCV non–genotype 1 infected patients have almost always used predominantly HCV genotype 2–infected or mixed genotype 2/3–infected cohorts with results partly conflicting with HCV genotype 1.

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