Pamela B. Sylvestre, Alvaro R. Gonzalez‐Koch, Michael B. Ishitani – 30 December 2003

Nadim Joni Shah, Heiko Neeb, Maxim Zaitsev, Sven Steinhoff, Gerald Kircheis, Katrin Amunts, Dieter Häussinger, Karl Zilles – 30 December 2003 – Changes are shown in the spin‐lattice (T1) relaxation time caused by the putative deposition of manganese in various brain regions of hepatic encephalopathy (HE) patients using a novel and fast magnetic resonance imaging (MRI) method for quantitative relaxation time mapping. A new method, T1 mapping with partial inversion recovery (TAPIR), was used to obtain a series of T1‐weighted images to produce T1 maps.

Hiroyasu Ito, Kazuki Ando, Toshinori Nakayama, Masaru Taniguchi, Takayuki Ezaki, Kuniaki Saito, Masao Takemura, Kenji Sekikawa, Michio Imawari, Mitsuru Seishima, Hisataka Moriwaki – 30 December 2003 – Although we have previously demonstrated that IL‐12 stimulation increases the number of hepatic natural killer (NK) T (NKT) cells and enhances liver injury during the early phase of liver regeneration, the role of NKT cells has remained unknown.

David Milich, T. Jake Liang – 30 December 2003 – The function of the hepatitis B e antigen (HBeAg) is largely unknown because it is not required for viral assembly, replication, or infection. In this report we chronicle clinical and experimental studies in an attempt to understand the role of HBeAg in natural infection. These studies largely have focused on clinical‐pathologic features of HBeAg‐negative variants in acute and chronic HBV infection, mutational analysis in animal models of hepadnavirus infection, and the use of transgenic murine models.

Irina G. Kessova, Ye‐Shih Ho, Swan Thung, Arthur I. Cederbaum – 30 December 2003 – Because alcoholic liver disease has been linked to oxidative stress, we investigated the effect of a compromised antioxidant defense system, Cu, Zn‐superoxide dismutase (Sod1) deficiency, on alcohol‐induced liver injury. C57BL/129SV wild‐type (Sod1+/+) and Sod1 knockout (Sod1−/−) mice were fed dextrose or ethanol (10% of total calories) liquid diets for 3 weeks.

Olga Coll, Anna Colell, Carmen García‐Ruiz, Neil Kaplowitz, J. C. Fernández‐Checa – 30 December 2003 – The mitochondrial pool of reduced glutathione (mGSH) is known to play a protective role against liver injury and cytokine‐mediated cell death. However, the identification of the mitochondrial carriers involved in its transport in hepatocellular mitochondria remains unestablished.

Hao Zhang, Iwata Ozaki, Toshihiko Mizuta, Tohru Yoshimura, Sachiko Matsuhashi, Akitaka Hisatomi, Jutaro Tadano, Takahiro Sakai, Kyosuke Yamamoto – 30 December 2003 – Although cooperative interactions between growth factors and integrins, cell surface receptors for extracellular matrices (ECM), have been reported, little is known about the interaction between hepatocyte growth factor (HGF) and integrin in hepatoma cells. We investigated the effects and mechanisms of integrin on the proliferation of hepatoma cells regulated by HGF.

Maria Rius, Anne T. Nies, Johanna Hummel‐Eisenbeiss, Gabriele Jedlitschky, Dietrich Keppler – 30 December 2003 – The liver is the major source of reduced glutathione (GSH) in blood plasma. The transport protein mediating the efflux of GSH across the basolateral membrane of human hepatocytes has not been identified so far. In this study we have localized the multidrug resistance protein 4 (MRP4; ABCC4) to the basolateral membrane of human, rat, and mouse hepatocytes and human hepatoma HepG2 cells.

Andreas Geier, Christoph G. Dietrich, Sebastian Voigt, Suk‐Kyum Kim, Thomas Gerloff, Gerd A. Kullak‐Ublick, Johann Lorenzen, Siegfried Matern, Carsten Gartung – 30 December 2003 – Hepatobiliary transporters are down‐regulated in toxic and cholestatic liver injury. Cytokines such as tumor necrosis factor α (TNF‐α) and interleukin 1β (IL‐1β) are attributed to mediate this regulation, but their particular contribution in vivo is still unknown. Thus, we studied the molecular mechanisms by which Ntcp, Oatp1, Oatp2, and Mrp2 are regulated by proinflammatory cytokines during liver injury.

Ichiro Ogushi, Yuji Iimuro, Ekihiro Seki, Gakuhei Son, Tadamichi Hirano, Toshikazu Hada, Hiroko Tsutsui, Kenji Nakanishi, Ryuichi Morishita, Yasufumi Kaneda, Jiro Fujimoto – 30 December 2003 – Endotoxin syndrome is a systemic inflammatory response mediated by inflammatory cytokines. Nuclear factor κB (NF‐κB) is the dominant regulator of the production of these cytokines by inflammatory cells.