Interleukin‐1 receptor type I gene‐deficient bile duct–ligated mice are partially protected against endotoxin

Miguel E. Sewnath, Tom Van Der Poll, Fiebo J. W. Ten Kate, Cornelis J. F. Van Noorden, Dirk J. Gouma – 30 December 2003 – Cholestatic liver injury is associated with an increased susceptibility toward endotoxin‐induced toxicity. To determine the role of interleukin 1 (IL‐1) herein, extrahepatic cholestasis was induced by bile duct ligation (bdl) in IL‐1 receptor type I gene‐deficient (IL‐1R−/−) mice, which are unresponsive to IL‐1α and IL‐1β, and normal IL‐1R+/+ mice. Bdl elicited increases in hepatic IL‐1α and IL‐1β messenger RNA (mRNA) and protein.

High frequency of epithelial chimerism in liver transplants demonstrated by microdissection and STR‐analysis

Wolfram Kleeberger, Thomas Rothämel, Sabine Glöckner, Peer Flemming, Ulrich Lehmann, Hans Kreipe – 30 December 2003 – It has recently been shown that epithelial cells derived from stem cells originating outside the liver are integrated into liver allografts. Whether epithelial intragraft chimerism protects transplants from rejection or chronic transplant dysfunction, and whether it interferes with recurrence of primary liver disease, is not known. Twenty‐seven sequential biopsies derived from 9 liver‐transplant recipients were studied for chimerism of hepatocytes and cholangiocytes.

Proangiogenic role of tumor‐activated hepatic stellate cells in experimental melanoma metastasis

Elvira Olaso, Clarisa Salado, Eider Egilegor, Virginia Gutierrez, Aitor Santisteban, Pau Sancho‐Bru, Scott L. Friedman, Fernando Vidal‐Vanaclocha – 30 December 2003 – Myofibroblasts infiltrate malignant liver tumors, although their pathogenic implications are unclear. Immunohistochemical detection of α‐smooth muscle actin, glial fibrillary acidic protein (GFAP), and CD31 and CD34 expression was used to analyze the contribution of myofibroblasts to angiogenesis in hepatic metastasis produced by intrasplenically‐injected B16 melanoma (B16M).

Arterial and portal circulation and parenchymal changes in Budd‐Chiari syndrome: A study in 17 explanted livers

Dominique Cazals‐Hatem, Valérie Vilgrain, Pascal Genin, Marie‐Hélène Denninger, François Durand, Jacques Belghiti, Dominique Valla, Claude Degott – 30 December 2003 – Hepatic parenchymal changes associated with Budd‐Chiari syndrome (BCS) have been tentatively explained by combined arterial and portal perfusion disturbances in addition to the complete occlusion of hepatic veins. The aim of this study was to correlate pretransplant course and vascular imaging with pathologic findings in livers explanted for BCS.

Hepatic cytochrome P450 2E1 activity in nondiabetic patients with nonalcoholic steatohepatitis

Naga Chalasani, J. Christopher Gorski, Maleeha S. Asghar, Ali Asghar, Brian Foresman, Stephen D. Hall, David W. Crabb – 30 December 2003 – Cytochrome P450 2E1 (CYP2E1) plays an important role in the pathogenesis of nonalcoholic steatohepatitis (NASH) in animal models, but its role in the pathogenesis of human NASH is unclear. Therefore, we measured hepatic CYP2E1 activity and its correlates in a cohort of nondiabetic patients with NASH (NDN) and controls to explore its role in the pathogenesis of human NASH.

Mouse A6–positive hepatic oval cells also express several hematopoietic stem cell markers

Bryon E. Petersen, Brian Grossbard, Heather Hatch, Liya Pi, Jie Deng, Edward W. Scott – 30 December 2003 – Hepatic oval cells (HOC) are thought to be a type of facultative stem cell that arises as a result of certain forms of hepatic injury. A new and more efficient model has been established to activate the oval cell compartment in mice by incorporating 3,5‐diethoxycarbonyl‐1,4‐dihydro‐collidine (DDC) in a standard chow at a concentration of 0.1%. At the present time, very few markers exist for the mouse oval cells.

p18(INK4c) collaborates with other CDK‐inhibitory proteins in the regenerating liver

Tom Luedde, Maria E. Rodriguez, Frank Tacke, Yue Xiong, David A. Brenner, Christian Trautwein – 30 December 2003 – p18(INK4c) belongs to the family of cyclin‐dependent kinase inhibitory proteins that target the cyclin‐dependent kinases and inhibit their catalytic activity. The role of p18(INK4c) for cell cycle progression in vivo is characterized poorly. Therefore, we studied the expression and physiologic relevance of p18 in quiescent and proliferating hepatocytes during liver regeneration.

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