Management of HCV‐infected health care workers
Nicola Magnavita, Ivo Iavicoli, Roberta Anna Placentino, Angelo Sacco, Vincenzo Puro – 30 December 2003
Nicola Magnavita, Ivo Iavicoli, Roberta Anna Placentino, Angelo Sacco, Vincenzo Puro – 30 December 2003
Mark J. Czaja, Hailing Liu, Yongjun Wang – 30 December 2003 – Oxidative stress has been implicated as a mechanism for a variety of forms of liver injury. Although reactive oxygen species (ROS) may damage cellular macromolecules directly, oxidant‐induced cell death may result from redox effects on signal transduction pathways. To understand the mechanisms of hepatocyte death from oxidative stress, the functions of the mitogen‐activated protein kinases (MAPKs) were determined during oxidant‐induced hepatocyte injury from menadione.
Zuo‐Liang Xiao, Piero Biancani, Martin C. Carey, Jose Behar – 30 December 2003 – The pathogenesis of acute cholecystitis (AC) is controversial. Bile acids may be involved in the pathogenesis of AC because the hydrophobic chenodeoxycholic acid (CDCA) reproduced in vitro the muscle dysfunction observed in AC and was prevented by the hydrophilic ursodeoxycholic acid (UDCA). The present study examined the in vivo effects of UDCA or CDCA on gallbladder muscle dysfunction caused by AC.
Naoya Kato, Yue Wang, Yujin Hoshida, Masao Omata – 30 December 2003
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.
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.
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.
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.
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.
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.