Hepatitis B virus precore protein augments genetic immunizations of the truncated hepatitis C virus core in BALB/c mice

Guoyang Liao, Yue Wang, Jinhai Chang, Tao Bian, Wenjie Tan, Mingbo Sun, Weidong Li, Huijuan Yang, Junying Chen, Xinwen Zhang, Shengli Bi, Masao Omata, Shude Jiang – 26 December 2007 – DNA immunization has been used to induce either humoral or cellular immune responses against many antigens, including hepatitis C virus (HCV). In addition, DNA immunizations can be enhanced or modulated at the nucleotide level.

Present status of ABO‐incompatible living donor liver transplantation in Japan

Hiroto Egawa, Satoshi Teramukai, Hironori Haga, Minoru Tanabe, Masanori Fukushima, Motohide Shimazu – 26 December 2007 – ABO‐incompatible (ABO‐I) living donor liver transplantation (LDLT) has been performed in Japan to overcome the organ shortage. Reported herein are the results of this approach through March 2006 in the National Registry of the Japan Study Group for ABO‐incompatible transplantation. The questionnaires consisted of patient characteristics, operative data, and strategies for preventing antibody‐mediated rejection (AMR).

Stabilization of β‐catenin affects mouse embryonic liver growth and hepatoblast fate

Thomas Decaens, Cécile Godard, Aurélien de Reyniès, David S. Rickman, François Tronche, Jean‐Pierre Couty, Christine Perret, Sabine Colnot – 26 December 2007 – During hepatogenesis, after the liver has budded out of the endoderm, the hepatoblasts quickly expand and differentiate into either hepatocytes or biliary cells, the latter of which arise only within the ductal plate surrounding the portal vein.

A polymorphism of the alpha1‐antitrypsin gene represents a risk factor for liver disease

Sally Chappell, Nedim Hadzic, Robert Stockley, Tamar Guetta‐Baranes, Kevin Morgan, Noor Kalsheker – 26 December 2007 – Alpha1‐antitrypsin deficiency (AATD) due to homozygosity of the protease inhibitor (Pi) Z variant predisposes to childhood liver disease and pulmonary emphysema. About 10% of all neonates with AATD develop liver disease, and about 3% overall progress to severe disease. AATD is a principal genetic indication for liver transplantation in children.

Hepatocyte transplantation and drug‐induced perturbations in liver cell compartments

Yao‐Ming Wu, Brigid Joseph, Ekaterine Berishvili, Vinay Kumaran, Sanjeev Gupta – 26 December 2007 – The potential for organ damage after using drugs or chemicals is a critical issue in medicine. To delineate mechanisms of drug‐induced hepatic injury, we used transplanted cells as reporters in dipeptidyl peptidase IV–deficient mice. These mice were given phenytoin and rifampicin for 3 days, after which monocrotaline was given followed 1 day later by intrasplenic transplantation of healthy C57BL/6 mouse hepatocytes.

A pilot project examining the predicted preferences of patients and physicians in the primary prophylaxis of variceal hemorrhage

Anna V. Longacre, Avlin Imaeda, Guadalupe Garcia‐Tsao, Liana Fraenkel – 26 December 2007 – Endoscopic variceal ligation (EVL) and nonselective beta‐blockers (hereafter just called beta‐blockers) are both effective for primary prophylaxis for variceal hemorrhage; however, the route of administration and side effects of these treatments are distinct. The objective of this study was to examine predicted preferences of patients and physicians for the primary prevention of variceal hemorrhage.

ATP8B1 requires an accessory protein for endoplasmic reticulum exit and plasma membrane lipid flippase activity

Coen C. Paulusma, Dineke E. Folmer, Kam S. Ho‐Mok, D. Rudi de Waart, Petra M. Hilarius, Arthur J. Verhoeven, Ronald P. J. Oude Elferink – 26 December 2007 – Mutations in ATP8B1 cause progressive familial intrahepatic cholestasis type 1 and benign recurrent intrahepatic cholestasis type 1. Previously, we have shown in mice that Atp8b1 deficiency leads to enhanced biliary excretion of phosphatidylserine, and we hypothesized that ATP8B1 is a flippase for phosphatidylserine. However, direct evidence for this function is still lacking.

Ethanol induces oxidative stress in primary rat hepatocytes through the early involvement of lipid raft clustering

Philippe Nourissat, Marion Travert, Martine Chevanne, Xavier Tekpli, Amélie Rebillard, Gwenaelle Le Moigne‐Müller, Mary Rissel, Josiane Cillard, Marie‐Thérèse Dimanche‐Boitrel, Dominique Lagadic‐Gossmann, Odile Sergent – 26 December 2007 – The role of the hepatocyte plasma membrane structure in the development of oxidative stress during alcoholic liver diseases is not yet fully understood. Previously, we have established the pivotal role of membrane fluidity in ethanol‐induced oxidative stress, but no study has so far tested the involvement of lipid rafts.

Impact of inflammatory bowel disease and ursodeoxycholic acid therapy on small‐duct primary sclerosing cholangitis

Phunchai Charatcharoenwitthaya, Paul Angulo, Felicity B. Enders, Keith D. Lindor – 26 December 2007 – A longitudinal, cohort study was performed to characterize the clinical features of patients with small‐duct primary sclerosing cholangitis (PSC) occurring with and without inflammatory bowel disease (IBD) and to determine the influence of IBD and the effect of ursodeoxycholic acid (UDCA) therapy on the course of the liver disease. Forty‐two patients with small‐duct PSC (14 women and 28 men; mean age, 36.7 ± 13.3 years) were followed for up to 24.9 years.

Cholangiocarcinoma in primary sclerosing cholangitis is associated with NKG2D polymorphisms

Espen Melum, Tom H. Karlsen, Erik Schrumpf, Annika Bergquist, Erik Thorsby, Kirsten M. Boberg, Benedicte A. Lie – 26 December 2007 – Primary sclerosing cholangitis (PSC) is often complicated by the development of cholangiocarcinoma (CCA). Genetic variation of natural killer cell receptor G2D (NKG2D) has been associated with cancer susceptibility. An important ligand for NKG2D, major histocompatibility complex class I chain‐related molecule A (MICA), serves as a marker of cellular stress. The 5.1 allele of the gene encoding MICA has been associated with PSC.

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