α1‐Antitrypsin mutations in NAFLD: High prevalence and association with altered iron metabolism but not with liver damage

Luca Valenti, Paola Dongiovanni, Alberto Piperno, Anna Ludovica Fracanzani, Marco Maggioni, Raffaela Rametta, Paola Loria, Maria Antonietta Casiraghi, Elda Suigo, Roberto Ceriani, Erica Remondini, Paola Trombini, Silvia Fargion – 27 September 2006 – Hyperferritinemia, a common feature of nonalcoholic fatty liver disease (NAFLD), has been associated with steatohepatitis and fibrosis. Heterozygosity for α1‐antitrypsin (AAT) mutations is a cofactor of liver damage, and AAT influences inflammation and iron metabolism.

Comparison of gene expression profiles between Opisthorchis viverrini and non‐Opisthorchis viverrini associated human intrahepatic cholangiocarcinoma

Natini Jinawath, Yaovalux Chamgramol, Yoichi Furukawa, Kazutaka Obama, Tatsuhiko Tsunoda, Banchob Sripa, Chawalit Pairojkul, Yusuke Nakamura – 27 September 2006 – Intrahepatic cholangiocarcinoma (ICC) is the second most common primary cancer in the liver, and its incidence is highest in the northeastern part of Thailand. ICCs in this region are known to be associated with infection with liver flukes, particularly Opisthorchis viverrini (OV), as well as nitrosamines from food.

Influence of hepatitis B virus genotypes on the intra‐ and extracellular expression of viral DNA and antigens

Masaya Sugiyama, Yasuhito Tanaka, Takanobu Kato, Etsuro Orito, Kiyoaki Ito, Subrat K. Acharya, Robert G. Gish, Anna Kramvis, Takashi Shimada, Namiki Izumi, Masahiko Kaito, Yuzo Miyakawa, Masashi Mizokami – 27 September 2006 – Various genotypes of the hepatitis B virus (HBV) induce liver disease of distinct severity, but the underlying virological differences are not well defined. Huh7 cells were transfected with plasmids carrying 1.24‐fold the HBV genome of different genotypes/subgenotypes (2 strains each for Aa/A1, Ae/A2, Ba/B2 and D; 3 each for Bj/B1 and C).

Coagulation disorders and hemostasis in liver disease: Pathophysiology and critical assessment of current management

Stephen H. Caldwell, Maureane Hoffman, Ton Lisman, B. Gail Macik, Patrick G. Northup, K. Rajender Reddy, Armando Tripodi, Arun J. Sanyal, Coagulation in Liver Disease Group – 27 September 2006 – Normal coagulation has classically been conceptualized as a Y‐shaped pathway, with distinct “intrinsic” and “extrinsic” components initiated by factor XII or factor VIIa/tissue factor, respectively, and converging in a “common” pathway at the level of the FXa/FVa (prothrombinase) complex.

Indomethacin increases liver damage in a murine model of liver injury from alpha‐1‐antitrypsin deficiency

David A. Rudnick, Olga Shikapwashya, Keith Blomenkamp, Jeffrey H. Teckman – 27 September 2006 – Homozygous (PIZZ) alpha‐1‐antitrypsin (α1‐AT) deficiency is associated with the development of liver damage in children as well as chronic liver injury and hepatocellular carcinoma in adults. The α1‐AT mutant Z gene encodes a mutant protein that accumulates in the endoplasmic reticulum of hepatocytes rather than being secreted appropriately into serum. Liver injury is caused by the accumulation of α1‐AT mutant Z protein in hepatocytes, which triggers downstream intracellular injury pathways.

Hepatitis C virus E2 and CD81 interaction may be associated with altered trafficking of dendritic cells in chronic hepatitis C

Jacob Nattermann, Henning Zimmermann, Agathe Iwan, Marie von Lilienfeld‐Toal, Ludger Leifeld, Hans Dieter Nischalke, Bettina Langhans, Tilman Sauerbruch, Ulrich Spengler – 27 September 2006 – Dendritic cells (DC) are crucially involved in the induction of immune responses; however, reports on DC functions in chronic hepatitis C are controversial. Function of DC includes proper cell trafficking between sites of infection and lympho‐cellular compartments. Thus, we analyzed DC compartmentalization and changes in DC migration in hepatitis C virus (HCV)‐infected patients.

Activation of Wnt/β‐catenin pathway during hepatocyte growth factor–induced hepatomegaly in mice

Udayan Apte, Gang Zeng, Peggy Muller, Xinping Tan, Amanda Micsenyi, Benjamin Cieply, Chunsun Dai, Youhua Liu, Klaus H. Kaestner, Satdarshan P. S. Monga – 27 September 2006 – Hepatocyte growth factor (HGF) and β‐catenin both play a crucial role in stimulating hepatocyte proliferation, but whether these 2 pathways cooperate in inducing hepatocyte proliferation is unclear. We have previously reported that β‐catenin forms a complex with c‐Met (HGF receptor) that undergoes dissociation because of β‐catenin tyrosine phosphorylation on stimulation by HGF.

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