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.

Progelatinase A is produced and activated by rat hepatic stellate cells and promotes their proliferation

R. Christopher Benyon, Christopher J. Hovell, Marianna Da Gaça, Emma H. Jones, John P. Iredale, Michael J. P. Arthur – 30 December 2003 – Activated hepatic stellate cells (HSCs) are a potential source of gelatinase A, which accumulates in fibrotic livers. Progelatinase A activation requires its binding to a complex of membrane‐type matrix metalloproteinase (MT‐MMP) and tissue inhibitor of metalloproteinases (TIMP)‐2. These studies examine gelatinase A, MT1‐MMP, and TIMP‐2 synthesis by HSCs during activationin vitroand the potential role of gelatinase A in promoting HSC proliferation.

In situ nucleic acid detection of human telomerase in intrahepatic cholangiocarcinoma and its preneoplastic lesion

Satoru Ozaki, Kenichi Harada, Takahiro Sanzen, Kishichiro Watanabe, Wilson Tsui, Yasuni Nakanuma – 30 December 2003 – Human telomerase, an enzyme associated with cellular immortality and tumorigenesis, is expressed by most malignant tumor cells. Human telomerase consists of human telomerase RNA (hTR) and telomerase protein components. One of the latter has been cloned and was termed telomerase‐associated protein 1 (TP1).

Liver fibrosis progression in human immunodeficiency virus and hepatitis C virus coinfected patients

Yves Benhamou, Marie Bochet, Vincent Di Martino, Frederic Charlotte, Felipe Azria, Anne Coutellier, Michel Vidaud, François Bricaire, Pierre Opolon, Christine Katlama, Thierry Poynard, for the MULTIVIRC Group – 30 December 2003 – The natural history of hepatitis C virus (HCV) infection in human immunodeficiency virus (HIV)‐infected patients has never been studied according to the concept of liver fibrosis progression. The aim of this work was to assess the fibrosis progression rate in HIV‐HCV coinfected patients and in patients infected by HCV only.

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