Gastric mucosa as an additional extrahepatic localization of hepatitis C virus: Viral detection in gastric low‐grade lymphoma associated with autoimmune disease and in chronic gastritis

Salvatore De Vita, Valli De Re, Domenico Sansonno, Dario Sorrentino, Renato La Corte, Barbara Pivetta, Daniela Gasparotto, Vito Racanelli, Alessandra Marzotto, Antonella Labombarda, Annunziata Gloghini, Gianfranco Ferraccioli, Angelo Monteverde, Antonino Carbone, Franco Dammacco, Mauro Boiocchi – 30 December 2003 – The hepatitis C virus (HCV) has been linked to B‐cell lymphoproliferation and autoimmunity, and has been localized in several tissues.

Randomized controlled trial of interferon treatment for advanced hepatocellular carcinoma

Josep M. Llovet, Margarita Sala, Lluís Castells, Yanette Suarez, Ramon Vilana, Lluís Bianchi, Carmen Ayuso, Víctor Vargas, Joan Rodés, Jordi Bruix – 30 December 2003 – The aim of this randomized controlled trial was to assess the efficacy of interferon alfa–2b (IFN) for the treatment of advanced hepatocellular carcinoma (HCC).

Role for tumor necrosis factor α receptor 1 and interleukin‐1 receptor in the suppression of mouse hepatocyte apoptosis by the peroxisome proliferator nafenopin

Douglas A. West, Neil H. James, Sabina C. Cosulich, Peter R. Holden, Richard Brindle, Mark Rolfe, Ruth A. Roberts – 30 December 2003 – Peroxisome proliferators (PPs) cause rodent liver enlargement and tumors. In vitro, PPs induce rat and mouse hepatocyte DNA synthesis and suppress apoptosis, a response mimicked by exogenous tumor necrosis factor α (TNFα). Here, we determine the role of TNF receptor 1 (TNFR1), TNF receptor 2 (TNFR2), and nuclear factor κ beta (NFκB) in the response of mouse hepatocytes to the PP, nafenopin.

Pediatric and adult forms of type I autoimmune hepatitis in argentina: Evidence for differential genetic predisposition

Marcelo Pando, Julian Larriba, Gabriela C. Fernandez, Hugo Fainboim, Mirta Ciocca, Margarita Ramonet, Isabel Badia, Jorge Daruich, Jorge Findor, Hugo Tanno, Cristina Cañero‐Velasco, Leonardo Fainboim – 30 December 2003 – The aim of this study was to compare major histocompatibility complex (MHC) class II susceptibility to type 1 autoimmune hepatitis (AH) between children and adults of the same ethnic group. HLA‐DRB1, HLA‐DRB3, HLA‐DQA1, and HLA‐DQB1 gene subtypes were examined by high resolution oligonucleotide typing in 122 pediatric (PAH) and 84 adult (AAH) patients and in 208 controls.

Phospholipid metabolism of hypothermically stored rat hepatocytes

Jae‐Sung Kim, James H. Southard – 30 December 2003 – Isolated rat hepatocytes were suspended and stored in either Liebovitz‐15 medium (37°C or 4°C) or University of Wisconsin (UW) solution (4°C) containing [3H] arachidonic acid (AA). At varying times, membrane phospholipids were separated by thin layer chromatography. AA labeled phospholipids similarly at both 4°C and 37°C.

Suppression of lipopolysaccharide‐induced nitric oxide synthase expression by platelet‐activating factor receptor antagonists in the rat liver and cultured rat kupffer cells

Shamimunisa B. Mustafa, Brent D. Flickinger, Merle S. Olson – 30 December 2003 – Excessive nitric oxide (NO) generated by hepatic cells in response to lipopolysaccharide (LPS) and inflammatory substances (e.g., platelet‐activating factor [PAF]) is a key contributor to the pathophysiological outcomes observed in the liver during sepsis. In rats subjected to liver‐focused endotoxemia, inducible nitric oxide synthase (iNOS) levels in the intact liver were elevated by 6 hours; cell‐specific expression of iNOS messenger RNA (mRNA) was Kupffer cells (KCs), endothelial cells, and hepatocytes.

Endotoxin suppresses mouse hepatic low‐density lipoprotein–receptor expression via a pathway independent of the toll‐like receptor 4

Wei Liao, Mats Rudling, Bo Angelin – 30 December 2003 – Endotoxin provokes an inflammatory state in the infected host. C3H/HeJ mice are tolerant to endotoxin because of an Lps gene mutation. Recent studies have identified that this gene encodes the Toll‐like receptor 4. Endotoxin also induces hyperlipidemia and suppresses hepatic low‐density lipoprotein (LDL)–receptor expression. In the current study, we investigated whether a defective Lps gene would impair the hepatic LDL‐receptor response to endotoxin in C3H/HeJ mice.

Transjugular intrahepatic portosystemic shunt in the treatment of refractory bleeding from ruptured gastric varices

Karl Barange, Jean‐Marie Péron, Kamran Imani, Philippe Otal, Jean‐Louis Payen, Herve Rousseau, Jean‐Pierre Pascal, Francis Joffre, Jean‐Pierre Vinel – 30 December 2003 – The optimal management of ruptured gastric varices in patients with cirrhosis has not been codified yet. The present study reports the use of transjugular intrahepatic portosystemic shunt (TIPS) in patients with refractory gastric variceal bleeding. Thirty‐two consecutive patients were included.

Serum levels of soluble interferon alfa/beta receptor as an inhibitory factor of interferon in the patients with chronic hepatitis C

Eishiro Mizukoshi, Shuichi Kaneko, Kyosuke Kaji, Shuichi Terasaki, Eiki Matsushita, Masahiro Muraguchi, Yasukazu Ohmoto, Kenichi Kobayashi – 30 December 2003 – Human serum contains a soluble form of interferon alfa/beta (sIFN α/β) receptors, the functional and clinical significance of which has not been investigated in patients with chronic hepatitis C. In the present study, serum levels of sIFN α/β receptor were assessed in 81 patients with chronic hepatitis C and correlated with the effectiveness of IFN therapy in these patients.

Changing blood into liver: Adding further intrigue to the hepatic stem cell story

Alastair J. Strain – 30 December 2003 – Bone marrow stem cells develop into hematopoietic and mesenchymal lineages but have not been known to participate in production of hepatocytes, biliary cells, or oval cells during liver regeneration. Cross‐sex or cross‐stain bone marrow and whole liver transplantation were used to trace the origin of the repopulating liver cells. Transplanted rats were treated with 2‐acetylaminofluorene, to block hepatocyte proliferation, and then hepatic injury, to induce oval cell proliferation.

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