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Your search keyword '"Tur-Kaspa R"' showing total 40 results
Start Over Author "Tur-Kaspa R" Journal journal of hepatology
40 results on '"Tur-Kaspa R"'

12. 2010 Q2WEEK CONTROLLED-RELEASE-INTERFERON-ALPHA2B + RIBAVRIN REDUCES FLU-LIKE SYMPTOMS >50% AND PROVIDES EQUIVALENT EFFICACY IN COMPARISON TO WEEKLY PEGYLATED-INTERFERON-ALPHA2B + RIBAVIRIN IN TREATMENT-NAIVE-GENOTYPE-1-CHRONIC-HEPATITIS-C: RESULTS FROM EMPOWER, A RANDOMIZED-OPEN-LABEL-12-WEEK-COMPARISON IN 133 PATIENTS

Author

Long, W.A., primary, Takov, D., additional, Tchernev, K., additional, Kotzev, I., additional, Rigney, A., additional, Krastev, Z., additional, Stoynov, S., additional, Balabanska, R., additional, Lawitz, E., additional, Younossi, Z., additional, Ghalib, R., additional, Zuckerman, E., additional, Safadi, R., additional, Tur-Kaspa, R., additional, Assy, N., additional, and Lurie, Y., additional

Published
2010
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19. [743] IMMUNE RESPONSES AND FIBROSIS IN ALCOHOLIC HEPATITIS

Author

Neuman, M.G., primary, Katz, G.G., additional, Malkiewitz, I., additional, Benhamou, J.-P., additional, Marcelin, P., additional, Valla, D.C., additional, Bourliere, M., additional, Schmilovitz-Weiss, H., additional, Ben-Ari, Z., additional, Tur-Kaspa, R., additional, and Trepo, C., additional

Published
2007
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38. Inhibition of hepatitis C virus NS3-mediated cell transformation by recombinant intracellular antibodies.

Author

Zemel R, Berdichevsky Y, Bachmatov L, Benhar I, and Tur-Kaspa R

Subjects
Amino Acid Sequence, Animals, Cell Transformation, Viral, Cells, Cultured, Cloning, Molecular, Hepacivirus drug effects, Hepacivirus genetics, Molecular Sequence Data, Plasmids, Polymerase Chain Reaction, Reverse Transcriptase Polymerase Chain Reaction, Viral Nonstructural Proteins chemistry, Hepacivirus physiology, Viral Nonstructural Proteins genetics
Abstract

Background/aims: Hepatitis C virus (HCV) infection is a major worldwide health problem, causing chronic hepatitis, liver cirrhosis and primary liver cancer. In addition to its role in the viral polyprotein-processing, the viral NS3 serine protease has been implicated in interactions with various cell constituents resulting in phenotypic changes including malignant transformation. NS3 is currently regarded a prime target for anti-viral drugs thus specific inhibitors of its activities should be of importance. With the aim of inhibiting NS3-mediated cell transformation, we used antibody-phage display to isolate NS3-specific single-chain antibodies (scFv)., Methods: We have isolated and characterized eight anti-NS3 scFvs. We investigated the phenotypic changes that NS3-expressing cells undergo upon intracellular expression of these antibodies in different subcellular compartments (intracellular immunization), assayed by their proliferation rate and their ability to grow anchorage independently. The intracellular location of NS3 and the scFvs were analyzed by immunofluorescent staining using confocal microscopy., Results: Nuclear targeted anti-NS3 intrabodies shuttle NS3 from the cytosol to the nucleus with concomitant inhibition of cell proliferation and loss of the transformed phenotype., Conclusions: Intracellular immunization-based gene therapy strategies may emerge as a promising antiviral approach to interfere with the life cycle and tumorigenicity of HCV.

Published
2004
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39. Lipoamide dehydrogenase deficiency: a newly discovered cause of acute hepatitis in adults.

Author

Barak N, Huminer D, Segal T, Ben Ari Z, Halevy J, and Tur-Kaspa R

Subjects
Acute Disease, Adult, Female, Humans, Treatment Outcome, Dihydrolipoamide Dehydrogenase deficiency, Hepatitis enzymology
Abstract

Lipoamide dehydrogenase deficiency is a rare disease, manifested in early childhood by lactic acidemia, progressive neurological damage and death in most cases. We report a case of lipoamide dehydrogenase deficiency in a 34-year-old Ashkenazi-Jewish woman. The deficiency manifested as acute hepatitis without cognitive impairment or acidosis. The patient's brother also had lipoamide dehydrogenase deficiency, diagnosed at the age of 20, and manifested as hepatocellular damage, lactic acidemia and myoglobinuria. We assume that the trigger for this hepatocellular damage was prolonged fasting, and that otherwise the patient might have gone undiagnosed. Other cases in Ashkenazi Jews of mild lipoamide dehydrogenase deficiency with hepatocellular injury but without central nervous system involvement are reviewed.

Published
1998
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40. Corticosteroids stimulate hepatitis B virus DNA, mRNA and protein production in a stable expression system.

Author

Tur-Kaspa R and Laub O

Subjects
Carcinoma, Hepatocellular genetics, Carcinoma, Hepatocellular microbiology, Carcinoma, Hepatocellular pathology, DNA Replication drug effects, DNA, Viral drug effects, Dexamethasone pharmacology, Gene Expression drug effects, Humans, Liver Neoplasms genetics, Liver Neoplasms microbiology, Liver Neoplasms pathology, RNA, Messenger drug effects, RNA, Viral drug effects, Transcription, Genetic drug effects, Viral Structural Proteins metabolism, Adrenal Cortex Hormones pharmacology, DNA, Viral genetics, Hepatitis B virus genetics, RNA, Messenger genetics, RNA, Viral genetics, Viral Structural Proteins genetics
Abstract

The effect of corticosteroids (Dexamethasone) on hepatitis B virus was investigated in human hepatoblastoma cells stable transfected with recombinant HBV DNA. Dexamethasone was found to cause elevation of HBsAg, HBeAg and viral DNA production. HBV poly(A)+ RNA was significantly increased in cells treated with Dexamethasone. Furthermore, pulse labelled nuclear HBV RNA was also stimulated by Dexamethasone. These findings, suggest that corticosteroids enhance expression of viral gene products by stimulating HBV transcription.

Published
1990
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