Meagan J. Walsh, Daina M. Vanags, Andrew D. Clouston, Michelle M. Richardson, David M. Purdie, Julie R. Jonsson, Elizabeth E. Powell – 26 April 2004 – Steatosis is increasingly recognized as a cofactor influencing the progression of fibrosis in chronic hepatitis C; however, the mechanisms by which it contributes to liver injury remain uncertain.
Neil Kaplowitz – 26 April 2004
Igor M. Sauer, Max Goetz, Ingo Steffen, Gesa Walter, Daniel C. Kehr, Ruth Schwartlander, Yoon J. Hwang, Andreas Pascher, Joerg C. Gerlach, Peter Neuhaus – 26 April 2004 – The detoxification capacities of single‐pass albumin dialysis (SPAD), the molecular adsorbents recirculation system, (MARS) and continuous veno‐venous hemodiafiltration (CVVHDF) were compared in vitro. In each experiment 4,100 mL of toxin‐loaded human plasma was processed for 6.5 hours. MARS treatment (n = 6) was undertaken in combination with CVVHDF.
Sándor Paku, Peter Nagy, László Kopper, Snorri S. Thorgeirsson – 26 April 2004 – The 2‐acetylaminofluorene (AAF)/partial hepatectomy (PH) model is one of the most extensively studied experimental systems for oval cell proliferation and differentiation. We have previously described the oval cells as forming ductular structures surrounded by basement membrane, representing extensions of the canals of Hering. Herein we analyze the differentiation of oval cells into hepatocytes after varying degrees of liver damage induced by AAF.
Nora V. Bergasa – 26 April 2004
26 April 2004
Ignazio Grattagliano, Stefan Russmann, Vincenzo O. Palmieri, Peter Jüni, Florian Bihl, Piero Portincasa, Giuseppe Palasciano, Bernhard H. Lauterburg – 26 April 2004 – Hemolysis is a frequent adverse effect of ribavirin (RBV). It has been suggested that oxidative stress plays a role, but mechanisms and predictive risk factors for severe forms remain unknown.
Gerald U. Denk, Carol J. Soroka, Albert Mennone, Hermann Koepsell, Ulrich Beuers, James L. Boyer – 26 April 2004 – The liver plays a major role in biotransformation and elimination of various therapeutic agents and xenobiotics, many of which are organic cations and substrates of the organic cation transporter 1 (Oct1, Slc22a1). Oct1 is expressed at the basolateral membranes of hepatocytes and proximal renal tubules. Although Oct1 is the major uptake mechanism in hepatocytes for many pharmaceutical compounds, little is known about the effects of liver injury on this process.
Nektarios Dikopoulos, Ursula Wegenka, Andrea Kröger, Hansjörg Hauser, Reinhold Schirmbeck, Jörg Reimann – 26 April 2004 – Large number of T cells traffic through the liver. In order to examine the effects of such traffic on the phenotype of hepatocytes, we vaccinated mice using DNA vaccines encoding antigens with MHC class I‐binding epitopes. Small numbers of activated CD8+ T blasts (105–106/liver) changed the surface phenotype and cytokine expression profile of hepatocytes (HCs).
Makoto Ochi, Hideki Ohdan, Hiroshi Mitsuta, Takashi Onoe, Daisuke Tokita, Hidetaka Hara, Kohei Ishiyama, Wendy Zhou, Yuka Tanaka, Toshimasa Asahara – 26 April 2004 – Although it is known that activation of natural killer (NK) cells causes liver injury, the mechanisms underlying NK cell‐induced killing of self‐hepatocytes are not clear. We demonstrated that liver NK cells have cytotoxicity against normal syngeneic hepatocytes in mice. Polyinosinic‐polycytidylic acid (poly I:C) treatment enhanced hepatocyte toxicity of liver NK cells but not that of spleen NK cells.