Monocyte chemotactic protein‐1 as a chemoattractant for human hepatic stellate cells

Fabio Marra, Roberto G. Romanelli, Carlo Giannini, Paola Failli, Sabrina Pastacaldi, Maria Cristina Arrighi, Massimo Pinzani, Giacomo Laffi, Paolo Montalto, Paolo Gentilini – 30 December 2003 – Following liver injury, hepatic stellate cells (HSC) undergo proliferation and migrate into damaged areas in response to chemotactic factors. HSC have been shown to regulate leukocyte trafficking by secreting monocyte chemotactic protein‐1 (MCP‐1), a chemokine that recruits monocytes and lymphocytes. In this study, we explored whether MCP‐1 exerts biological actions on HSC.

Entry and integration of transplanted hepatocytes in rat liver plates occur by disruption of hepatic sinusoidal endothelium

Sanjeev Gupta, Pankaj Rajvanshi, Rana Sokhi, Sanjeev Slehria, Ana Yam, Andrew Kerr, Phyllis M. Novikoff – 30 December 2003 – To establish the process by which transplanted cells integrate into the liver parenchyma, we used dipeptidyl peptidase IV‐deficient F344 rats as hosts. On intrasplenic injection, transplanted hepatocytes immediately entered liver sinusoids, along with attenuation of portal vein radicles on angiography. However, a large fraction of transplanted cells (>70%) was rapidly cleared from portal spaces by phagocyte/macrophage responses.

Detection of genomic‐ and minus‐strand of hepatitis C virus RNA in the liver of chronic hepatitis C patients by strand‐specific semiquantitative reversetranscriptase polymerase chain reaction

Francesco Negro, Krzysztof Krawczynski, Rafael Quadri, Laura Rubbia‐Brandt, Mario Mondelli, Jean‐Pierre Zarski, Antoine Hadengue – 30 December 2003 – Studies aimed at correlating the intrahepatic hepatitis C virus (HCV)‐RNA level and anatomo‐clinical features have been difficult because of sensitivity and specificity shortcomings of available techniques. We titered the genomic‐ and minus‐strand HCV RNAs by a strand‐specific, semiquantitative, genotype‐independent reverse‐transcriptase polymerase chain reaction (RT‐PCR) in the liver tissue of 61 patients with chronic hepatitis C.

Expression of inducible nitric oxide synthase in endotoxemic rat hepatocytes is dependent on the cellular glutathione status

Thera A. Vos, Harry van Goor, Leonore Tuyt, Alie de Jager‐Krikken, Ron Leuvenink, Folkert Kuipers, Peter L. Jansen, Han Moshage – 30 December 2003 – The inducible nitric oxide synthase (iNOS) promoter contains nuclear factor κB (NF‐κB) binding sites. NF‐κB activation is determined, in part, by the intracellular redox status. The aim of this study was to determine the importance of the cellular glutathione status in relation to NF‐κB activation and iNOS expression in hepatocytes in vivo and in vitro. For in vivo experiments, rats were injected with endotoxin and sacrificed 6 hours later.

Increased carbon monoxide production in patients with cirrhosis with and without spontaneous bacterial peritonitis

Dara De Las Heras, Javier Fernández, Pere Ginès, Andres Cárdenas, Rolando Ortega, Miguel Navasa, Joan Albert Barberá, Blas Calahorra, Mónica Guevara, Ramón Bataller, Wladimiro Jiménez, Vicente Arroyo, Juan Rodés – 30 December 2003 – Carbon monoxide, a product of the heme‐oxygenase (HO) pathway, is an important endogenous vasoactive substance. Production of CO has not been assessed in human cirrhosis. The aim of this study was to assess production of CO in patients with cirrhosis with and without spontaneous bacterial peritonitis (SBP).

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