Regulation of tissue inhibitor of metalloproteinases‐1 gene expression by cytokines and dexamethasone in rat hepatocyte primary cultures

Elke Roeb, Lutz Graeve, Rolf Hoffmann, Karl Decker, Dylan R. Edwards, Peter C. Heinrich – 1 December 1993 – The steady‐state levels of extracellular matrix proteins are regulated by the rates of their synthesis and degradation. Metalloproteinases and their specific inhibitors, tissue inhibitor of metalloproteinases‐1 and ‐2 are believed to play a crucial role in extracellular matrix protein degradation. Here we show that the tissue inhibitor of metalloproteinases‐1 is expressed in rat hepatocytes in primary culture and regulated by inflammatory cytokines.

Interferon‐α2b therapy reduces liver fibrosis in chronic non‐A, non‐B hepatitis: A quantitative histological evaluation

Noboru Manabe, Michèle Chevallier, Philippe Chossegros, Xavier Causse, Sylviane Guerret, Christian Trépo, Jean‐Alexis Grimaud – 1 December 1993 – The aim of this study was to evaluate the effect of interferon‐α on liver fibrosis with an established quantitative histochemical method for determining collagen as a marker. 59 patients (31 men, 28 women; 47 ± 14 yr) with chronic non‐A, non‐B hepatitis (92% with hepatitis C virus antibody) received subcutaneous injections of 3 or 1 MU recombinant interferon‐α2b or placebo thrice weekly for 24 wk.

Evidence for neurological dysfunction in end‐stage protoporphyric liver disease

Jeffrey M. Rank, Robert Carithers, Joseph Bloomer – 1 December 1993 – Protoporphyria is a genetic disorder characterized by a defect in the enzyme ferrochelatase, which catalyzes the chelation of iron to protoporphyrin. This causes excessive accumulation and excretion of protoporphyrin. The predominant clinical feature is photosensitivity. Progressive and fatal liver disease occurs in a small percentage of cases.

Erythropoietin production in hepatocellular carcinoma cells associated with polycythemia: Immunohistochemical evidence

Shotaro Sakisaka, Masahide Watanabe, Hideo Tateishi, Masaru Harada, Satoshi Shakado, Yoshihiro Mimura, Kazuhisa Gondo, Masao Yoshitake, Kazunori Noguchi, Teruko Hino, Ryuichi Nohno, Yasuo Majima, Kenji Hirai, Michio Sata, Hiroshi Yoshida, Kyuichi Tanikawa – 1 December 1993 – Patients with hepatocellular carcinoma sometimes have erythrocytosis and high plasma erythropoietin levels. However, previous studies have not revealed direct evidence that the carcinoma cells produce the erythropoietin.

Quantitation and typing of serum hepatitis C virus RNA in patients with chronic hepatitis C treated with interferon‐β

Yoshinao Kobayashi, Shozo Watanabe, Masayoshi Konishi, Masato Yokoi, Ryuichi Kakehashi, Masahiko Kaito, Masahiro Kondo, Yuji Hayashi, Takahito Jomori, Shiro Suzuki – 1 December 1993 – We quantified serum hepatitis C virus RNA titers and determined hepatitis C virus subtypes in chronic hepatitis C patients treated with interferon‐β to investigate relationships among serum ALT response, serum hepatitis C virus titer and hepatitis C virus subtype.

Persistence of hepatitis B virus DNA in the liver after loss of HBsAg in chronic hepatitis B

Tse‐Ling Fong, Adrian M. Di Bisceglie, Michael A. Gerber, Jeanne G. Waggoner, Jay H. Hoofnagle – 1 December 1993 – To determine whether patients with chronic hepatitis B who lose hepatitis B virus DNA and HBsAg from the serum completely resolve the hepatitis and virus infection, we evaluated serum and liver tissue from 11 patients who had lost HBsAg. These patients were evaluated for clinical, histological and serological features and for hepatitis B virus DNA by use of hybridization and polymerase chain reaction techniques.

Monitoring of antiviral therapy with quantitative evaluation of hbeag: A comparison with HBV DNA testing

Robert Perrillo, Larry Mimms, Kenneth Schechtman, David Robbins, Carolyn Campbell – 1 December 1993 – The serological endpoint of response in the treatment of chronic hepatitis B is the loss of hepatitis B virus DNA and HBeAg. Because the quantitative measurement of hepatitis B virus DNA in serum has been shown to be useful for monitoring and predicting response to interferon‐α therapy, we decided to evaluate whether changes in HBeAg concentration could also be used in this manner.

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