M Menegazzi, A Carcereri‐De Prati, H Suzuki, H Shinozuka, M Pibiri, R Piga, A Columbano, G M Ledda‐Columbano – 30 December 2003 – Our previous studies have shown a different pattern of immediate early gene and growth factor gene expression between compensatory liver regeneration occurring after cell loss/death and direct hyperplasia induced by primary mitogens.

R Gratzl, R Lassacher, A Majcen, J Graf – 30 December 2003

M A Zern, T F Kresina – 30 December 2003 – On September 21‐22, 1995, an international meeting entitled “Targeting of Novel Therapeutics to the Liver and GI Tract” was held at the Natcher Conference Center on the campus of the National Institutes of Health. The conference was sponsored by the National Institute of Diabetes and Digestive and Kidney Diseases through the Division of Digestive Diseases and Nutrition and Digestive Diseases Interagency Coordinating Committee (DDICC).

K Sakitani, H Kitade, K Inoue, Y Kamiyama, M Nishizawa, T Okumura, S Ito – 30 December 2003 – Recent evidence suggests that nitric oxide (NO) mediates cellular injury under the pathological conditions such as endotoxemia in the liver of rats. Regulation of NO production is crucial for improving the hepatic dysfunction. We have previously reported that, in cultured rat hepatocytes, a single cytokine interleukin‐1β (IL‐1β) stimulated a release of nitrite, an oxidation product of NO, into culture medium dose‐ and time‐dependently.

T Kim, H Shijo, H Kokawa, H Tokumitsu, K Kubara, K Ota, N Akiyoshi, T Iida, M Yokoyama, M Okumura – 30 December 2003 – The incidence and the risk factors of hemorrhage from gastric fundal varices (FV) have not been fully evaluated. We therefore conducted a retrospective and prospective study to define the incidence and risk factors for such episodes. We investigated 132 patients with cirrhosis and gastric FV. Of these 132 patients, 15 patients had hemorrhagic FV at the time of enrollment.

M G Swain, M Maric – 30 December 2003 – Fatigue is a common complaint in patients with liver disease; however, the etiology of fatigue is poorly understood and no therapeutic options are available to treat it. Altered central neurotransmission, especially serotonergic, appears to play a role in the genesis of fatigue. In this study, we describe a rat model of fatigue assessment using a swim tank, and we used this model to document the degree of fatigue in rat models of cholestasis caused by bile duct resection (BDR) and of hepatitis caused by carbon tetrachloride (CCl4) administration.

R H Peters, J H van Doorninck, P J French, R Ratcliff, M J Evans, W H Colledge, J Bijman, B J Scholte – 30 December 2003 – We have studied the physiological role of the cystic fibrosis (CF) gene product (cystic fibrosis transmembrane conductance regulator [CFTR]) in gallbladder epithelium using a knockout mouse model for CF. We found that normal mouse gallbladder epithelium expresses functional CFTR as shown by reverse‐transcription polymerase chain reaction (RT‐PCR) analysis and Ussing chamber experiments.

Alan P. Venook – 30 December 2003

Anastasios Armonis, David Patch, Andrew Burroughs – 30 December 2003

A. Okajima, K. Miyazawa, Y. Naitoh, K. Inoue, N. Kitamura – 30 December 2003 – Hepatocyte growth factor activator (HGFA) is a serine protease that is responsible for localized activation of hepatocyte growth factor (HGF) in injured tissue. The activated HGF may be involved in regeneration of the injured tissue. HGFA is produced and secreted by the liver and circulates in the plasma as an inactive zymogen. In response to tissue injury, the HGFA zymogen is converted to the active form by limited proteolysis.