Lichuan Liu, Ming Zhang, Bao Luo, Gary A. Abrams, Michael B. Fallon – 30 December 2003 – The hepatopulmonary syndrome (HPS) results from pulmonary microvascular dilatation in cirrhosis and is associated with increased pulmonary endothelial nitric oxide synthase (eNOS) levels. In the common bile duct ligation (CBDL) model, endothelin‐1 (ET‐1) released from the liver contributes to the rise in pulmonary eNOS and intrapulmonary vasodilatation.

Hisashi Taniai, Makoto Suematsu, Tsuneharu Suzuki, Shinji Norimizu, Rio Hori, Yuzuru Ishimura, Yuji Nimura – 30 December 2003 – This study aimed to investigate the roles of endothelin (ET) receptors in biliary dysfunction and cell injury in postischemic livers. Rat livers perfused with oxygenated Krebs‐Henseleit solution were exposed to reoxygenation following 20‐minute hypoxia. The anoxic perfusion decreased bile output and reduced cyclic guanosine monophosphate (cGMP) contents, an index of nitric oxide (NO) generation.

Yoshimichi Haruna, Tsutomu Kanda, Masaharu Honda, Tetsuto Takao, Norio Hayashi – 30 December 2003 – The pathobiology of hepatitis C virus (HCV) in the biliary system has not been clarified yet, although bile duct damage is a histological finding characteristic of chronic hepatitis C. In this study, we examined whether HCV infects bile ducts and is released into the bile. Twelve patients positive for serum HCV antibody were examined in this study, and eight were seropositive for HCV RNA by polymerase chain reaction (PCR).

Carol J. Soroka, John M. Lee, Francesco Azzaroli, James L. Boyer – 30 December 2003 – The hepatic expression of the ATP‐dependent conjugate export pump multidrug resistance–associated protein 2 (Mrp2) is diminished in experimentally induced models of cholestasis. In this study we have examined the localization and expression of Mrp3, another member of the multidrug resistance–associated protein family, in normal liver and after obstructive cholestasis in the rat.

Marius C. Van Den Heuvel, Maarten J. H. Slooff, Lydia Visser, Michael Muller, Koert P. De Jong, Sibrand Poppema, Annette S. H. Gouw – 30 December 2003 – Following hepatic injury, proliferation of anastomosing ductules can be observed. The origin of this ductular reaction is not completely clear, although there is considerable evidence for proliferation of a putative hepatic progenitor cell, reported to be located in the canals of Hering (CoH) and showing morphologic similarities with rat oval cells.

John W. Barnwell – 30 December 2003

Nancy W. Y. Leung, Ching‐Lung Lai, Ting‐Tsung Chang, Richard Guan, Chuan‐Mo Lee, Keng‐Yeen Ng, Seng‐Gee Lim, Pui‐Chee Wu, Julie C. Dent, Sally Edmundson, Lynn D. Condreay, Rong‐Nan Chien, on behalf of the ASIA HEPATITIS LAMIVUDINE STUDY GROUP – 30 December 2003 – A study in Chinese patients with chronic hepatitis B showed that treatment with lamivudine for 1 year significantly improves liver histology and enhances hepatitis B e antigen (HBeAg) seroconversion compared with placebo.

Hari S. Conjeevaram, Anna S. Lok – 30 December 2003

Miguel R. Arguedas, Anita Johnson, Mohamad A. Eloubeidi, Michael B. Fallon – 30 December 2003 – Hepatitis A virus (HAV) vaccination is recommended in chronic liver disease because of an increased morbidity and mortality associated with HAV superinfection. However, data regarding the efficacy of HAV vaccination in patients with advanced chronic liver disease is limited. We assessed the efficacy of a standard HAV vaccination schedule in decompensated chronic liver disease in comparison with compensated disease and defined clinical predictors associated with seroconversion.

Tuan H. Vu, Kurenai Tanji, Stephen A. Holve, Eduardo Bonilla, Ronald J. Sokol, Russell D. Snyder, Stephany Fiore, Gail H. Deutsch, Salvatore DiMauro, Darryl De Vivo – 30 December 2003 – Navajo neurohepatopathy (NNH) is an autosomal recessive disease of full‐blooded Navajo children living in the Navajo Reservation of southwestern United States. Clinical features of NNH include peripheral and central nervous system involvement, acral mutilation, corneal scarring or ulceration, liver failure, and metabolic and immunologic derangement.