Yukiyasu Kuzumoto, Masayuki Sho, Naoya Ikeda, Kaoru Hamada, Takashi Mizuno, Satoru Akashi, Yoshikazu Tsurui, Hisanori Kashizuka, Takeo Nomi, Atsushi Kubo, Hiromichi Kanehiro, Yoshiyuki Nakajima – 17 August 2005 – Prostaglandin E2 (PGE2) mediates a variety of innate and adaptive immunity through four distinct receptors: EP1‐EP4. It has been suggested that each EP plays a unique and pivotal role in various disease conditions. We investigated the pathophysiological role of EP receptors in hepatic ischemia/reperfusion (I/R) injury.

Renato Costi, Vincenzo Violi, Luigi Roncoroni, Leopoldo Sarli – 17 August 2005

Zsolt Sarang, Péter Molnár, Tamás Németh, Szabolcs Gomba, Tamás Kardon, Gerry Melino, Susanna Cotecchia, László Fésüs, Zsuzsa Szondy – 17 August 2005 – Tissue transglutaminase (TG2) is a protein cross‐linking enzyme known to be expressed by hepatocytes and to be induced during the in vivo hepatic apoptosis program. TG2 is also a G protein that mediates intracellular signaling by the alpha‐1b‐adrenergic receptor (AR) in liver cells.

Stefano Fiorucci, Elisabetta Antonelli, Andrea Mencarelli, Stefano Orlandi, Barbara Renga, Giovanni Rizzo, Eleonora Distrutti, Vijay Shah, Antonio Morelli – 17 August 2005 – The regulation of sinusoidal resistance is dependent on the contraction of hepatic stellate cells (HSC) around sinusoidal endothelial cell (SEC) through paracrine cross‐talk of vasoconstrictor and vasodilator agents. Hydrogen sulfide (H2S), a recently discovered gas neurotransmitter, is a putative vasodilator whose role in hepatic vascular regulation and portal hypertension is unexplored.

Mical S. Campbell, Colleen M. Brensinger, Arun J. Sanyal, Chris Gennings, Florence Wong, Kris V. Kowdley, Timothy McCashland, K. Rajender Reddy – 17 August 2005 – Uncontrolled studies suggest that transjugular intrahepatic portal‐systemic shunting (TIPS) may improve quality of life in patients with refractory ascites. We hypothesized that any improvement of quality of life in patients with TIPS would be matched in controls due to the competing effects of improved ascites and worsened hepatic encephalopathy.

Karla J. Helbig, Daryl T.‐Y. Lau, Ljiljana Semendric, Hugh A. J. Harley, Michael R. Beard – 17 August 2005 – Interferon (IFN) α inhibits hepatitis C virus (HCV) replication both clinically and in vitro; however, the complete spectrum of interferon‐stimulated genes (ISGs) expressed in the HCV‐infected liver or the genes responsible for control of HCV replication have not been defined. To better define ISG expression in the chronically infected HCV liver, DNA microarray analysis was performed on 9 individuals with chronic hepatitis C (CHC).

Yusuke Yamamoto, Takumi Teratani, Hanako Yamamoto, Gary Quinn, Sigenori Murata, Rieko Ikeda, Kenji Kinoshita, Kenichi Matsubara, Takashi Kato, Takahiro Ochiya – 15 August 2005 – Hepatic differentiation at the molecular level is poorly understood, mainly because of the lack of a suitable model. Recently, using adherent monoculture conditions, we demonstrated the direct differentiation of hepatocytes from embryonic stem (ES) cells.

Michael Shim, Inessa Khaykis, James Park, Edmund J. Bini – 15 August 2005 – Hepatitis A virus (HAV) superinfection is associated with a high risk of liver failure and death in patients with underlying chronic liver disease. Although HAV vaccination is recommended for all patients with chronic hepatitis C virus (HCV) infection, little is known about adherence to these recommendations in clinical practice. The aims of this study were to determine the frequency of HAV testing and vaccination among patients with chronic HCV infection.

Xamila Salcedo, Jesús Medina, Paloma Sanz‐Cameno, Luisa García‐Buey, Samuel Martín‐Vilchez, María J. Borque, Manuel López‐Cabrera, Ricardo Moreno‐Otero – 15 August 2005 – Angiogenesis, the formation of new vessels, has been reported to play a significant pathogenic role in liver damage–associated hepatitis C virus infection. Most of our current knowledge derives from immunohistochemical studies of hepatic biopsy samples obtained from chronic hepatitis C (CHC) patients.

David A. Rudnick, David H. Perlmutter – 25 July 2005 – Liver disease in alpha‐1‐antitrypsin (α1AT) deficiency is caused by a gain‐of‐toxic function mechanism engendered by the accumulation of a mutant glycoprotein in the endoplasmic reticulum (ER). The extraordinary degree of variation in phenotypical expression of this liver disease is believed to be determined by genetic modifiers and/or environmental factors that influence the intracellular disposal of the mutant glycoprotein or the signal transduction pathways that are activated.