The human liver clears both asymmetric and symmetric dimethylarginine

Michiel P.C. Siroen, Joost R. M. van der Sijp, Tom Teerlink, Cors van Schaik, Robert J. Nijveldt, Paul A. M. van Leeuwen – 22 February 2005 – Asymmetric (ADMA) and symmetric dimethylarginine (SDMA) inhibit production of nitric oxide. The concentration of both dimethylarginines is regulated by urinary excretion, although ADMA, but not SDMA, is also subject to degradation by dimethylarginine dimethylaminohydrolase, which is highly expressed in the liver but also present in the kidney. The exact roles of the human liver and kidney in the metabolism of dimethylarginines are currently unknown.

Contribution of Toll‐like receptor/myeloid differentiation factor 88 signaling to murine liver regeneration

Ekihiro Seki, Hiroko Tsutsui, Yuji Iimuro, Tetsuji Naka, Gakuhei Son, Shizuo Akira, Tadamitsu Kishimoto, Kenji Nakanishi, Jiro Fujimoto – 22 February 2005 – Toll‐like receptors (TLRs) act as innate immune signal sensors and play central roles in host defense. Myeloid differentiation factor (MyD) 88 is a common adaptor molecule required for signaling mediated by TLRs. When the receptors are activated, cells bearing TLRs produce various proinflammatory cytokines in a MyD88‐dependent manner.

Kupffer cells and macrophages are not required for hepatic hepcidin activation during iron overload

Giuliana Montosi, Elena Corradini, Cinzia Garuti, Samuele Barelli, Stefania Recalcati, Gaetano Cairo, Linda Valli, Elisa Pignatti, Chiara Vecchi, Francesca Ferrara, Antonello Pietrangelo – 22 February 2005 – Hepcidin, the iron hormone, is produced by the liver in response to iron and inflammation. Its synthesis during inflammation is triggered by cytokines, but the details of iron activation are obscure.

Metalloproteinase inhibitor TIMP‐1 affects hepatocyte cell cycle via HGF activation in murine liver regeneration

Fazilat F. Mohammed, Caroline J. Pennington, Zamaneh Kassiri, Jeffrey S. Rubin, Paul D. Soloway, Ulrich Ruther, Dylan R. Edwards, Rama Khokha – 22 February 2005 – Liver regeneration depends on timely restoration of cellular mass while orchestrating structural matrix remodeling. Matrix metalloproteinases (MMPs) and their endogenous inhibitors (TIMPs) are known to regulate the extracellular matrix (ECM) turnover and, more recently, the processing of growth factors and cytokines.

Splitting of the middle hepatic vein in full‐right full‐left splitting of the liver

Dieter C. Broering, Pamela Bok, Lars Mueller, Christian Wilms, Xavier Rogiers – 17 February 2005 – Full‐right/full‐left splitting of the liver offers a chance to overcome the severe shortage of donor organs. During this procedure, the splitting surgeons are always faced with the question of how to share the middle hepatic vein (MHV), since this vein drains parts of both halves of the liver. Consequently, we developed a procedure that splits the MHV, thus creating an MHV on both grafts. In this short article, we report on this splitting technique and our first initial experience.

Microchimerism after liver transplantation: Absence of rejection without abrogation of anti‐donor cytotoxic T‐lymphocyte–mediated alloreactivity

Florence Bettens, Jean‐Marie Tiercy, Nathalie Campanile, Emiliano Giostra, Pietro Majno, Laura Rubbia, Eddy Roosnek, Gilles Mentha, Jean Villard – 17 February 2005 – Microchimerism (MC) is defined by the persistence of <1% circulating donor cells resulting from cell migration from the graft; MC may play a role in the induction of unresponsiveness to allogeneic tissues, or may be merely the consequence of the graft's acceptance following immunosuppression.

MARS treatment for a patient presenting with acquired hepatic glutamine synthetase deficiency after orthotopic liver transplantation

Alexander Chiu, Sidney Tam, Wing Yan Au, See Ching Chan, Chi Leung Liu, Sheung Tat Fan – 17 February 2005 – We report a 48‐year‐old man presenting with refractory hyperammonemia after orthotopic liver transplantation. On investigation he was found to have acquired hepatic glutamine synthetase deficiency, a rare condition that occurs after organ transplantations. The patient was started on continuous venovenous hemofiltration treatment, but the hyperammonemia did not respond.

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