Deficient assembly and function of gap junctions in Trf1, a trafficking mutant of the human liver–derived cell line HuH‐7

Richard J. Stockert, David C. Spray, Yang Gao, Sylvia O. Suadicani, Catherine R. Ripley, Phyllis M. Novikoff, Allan W. Wolkoff, Elliot L. Hertzberg – 30 December 2003 – The Trf1 cell line, selected from the human hepatoma cell line HuH‐7, manifests altered trafficking of various plasma membrane proteins. In particular, there is a striking loss of State 2 asialoglycoprotein receptors. This cell line is shown here to also manifest defects in function and assembly of gap junctions comprising connexin43 (Cx43). No alteration of Cx43 expression or phosphorylation was apparent.

Nitric oxide production and inducible nitric oxide synthase expression in peritoneal macrophages of cirrhotic patients

Wladimiro Jiménez, Josefa Ros, Manuel Morales‐Ruiz, Miguel Navasa, Manuel Solé, Jordi Colmenero, Pau Sort, Francisca Rivera, Vicente Arroyo, Juan Rodés – 30 December 2003 – The present study assessed whether peritoneal macrophages isolated from cirrhotic patients produce nitric oxide (NO) and express NO synthase type II (NOS II) mRNA and protein. Patients with cirrhosis and ascites without peritonitis or with unresolved or resolved spontaneous bacterial peritonitis (SBP) were studied. Following paracentesis, ascites NO + NO content (NOx) was measured.

Racial differences in responses to therapy with interferon in chronic hepatitis C

K. Rajender Reddy, Jay H. Hoofnagle, Myron J. Tong, William M. Lee, Paul Pockros, E. Jenny Heathcote, Donald Albert, Tenshang Joh – 30 December 2003 – The likelihood of a sustained response to a course of interferon in patients with chronic hepatitis C correlates with several clinical and viral factors, including age, viral genotype and initial levels of hepatitis C virus (HCV) RNA in serum. The role of race and ethnicity has not been assessed.

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.

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).

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.

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.

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.

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.

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.

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