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Nippon rinsho. Japanese journal of clinical medicine 05/2011; 69 Suppl 4:128-33.
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Shunichi Matsuoka,
Hiroshi Matsumura,
Hitomi Nakamura,
Shu Oshiro,
Yasuo Arakawa, Junpei Hayashi,
Naoki Sekine,
Kazushige Nirei,
Hiroaki Yamagami,
Masahiro Ogawa,
Noriko Nakajima,
Shuichi Amaki,
Naohide Tanaka,
Mitsuhiko Moriyama
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ABSTRACT: We treated patients with C-viral chronic hepatitis (CH) and liver cirrhosis (LC) with polaprezinc and determined prospectively the effect on long-term outcome. 62 patients were enrolled. Of these, 32 were administered 1.0 g polaprezinc and the remainder were not administered polaprezinc. We measured the serum zinc concentrations using conventional atomic absorption spectrometry and conducted a prospective study to determine the long-term outcome of the polaprezinc therapy. Changes of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels in the polaprezinc administration group were significantly lower than those of the untreated group. The decrease in platelet count was clearly less than that of the untreated group. The factors that inhibited increases in serum zinc concentrations following administration of polaprezinc included low serum zinc concentration states. Furthermore, the reductions of AST and ALT levels in the low zinc group were significantly greater than those of the high zinc group. When the patients who were administered polaprezinc were divided into two groups whose zinc concentrations increased (zinc responders) or remained stable or decreased (zinc non-responders), the zinc responders had a clearly lower cumulative incidence of HCC than the zinc non-responders. We conclude zinc supplementation improved the long-term outcome in C-viral CH and LC patients.
Journal of Clinical Biochemistry and Nutrition 11/2009; 45(3):292-303. · 1.98 Impact Factor
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Junpei Hayashi,
Shyunichi Matsuoka,
Makiko Inami,
Shu Ohshiro,
Akiyasu Ishigami,
Hirotoshi Fujikawa,
Masahide Miyagawa,
Kenji Mimatsu,
Youichi Kuboi,
Hisao Kanou,
Takatsugu Oida,
Mitsuhiko Moriyama
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ABSTRACT: A 65-year-old woman was found to have dilatation of the intrahepatic bile duct in the right anterior segment during a general health. Laboratory data were within normal ranges and no solid mass was detected in her abdominal computer tomography (CT) or nuclear magnetic resonance imaging (MRI). However, endoscopic retrograde cholangiopancreatography (ERCP) demonstrated an obstruction of the right bile duct. Intraoperative cholangiography showed stenosis of the intrahepatic bile duct in the anterior inferior segment (B5) and narrowness of the intrahepatic bile duct in the anterior superior segment (B8), so that we strongly suspected intrahepatic cholangiocarcinoma (ICC). Histologically, surgically resected liver specimens, without tumor mass by macroscopic observation, showed intraductal papillary proliferation with fibrovascular cores and intraductal spreading of carcinoma in situ throughout a considerable area, especially in bile ductules around the peripheral small portal area. Furthermore, the immunohistochemical profile of the tumor (MUC5AC+/CK7+) was compatible with an intraductal papillary neoplasm of the bile duct (IPN-B). Consequently, this case was diagnosed as IPN-B with spreading CIS, stage I (pT1, pN0, P0, H1, M0). We report a case of IPN-B with interesting histopathological findings and emphasize that cholangiography is especially helpful for the diagnosis of bile duct dilatation due to infiltration of carcinoma cells.
World Journal of Gastroenterology 04/2008; 14(10):1625-9. · 2.47 Impact Factor
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ABSTRACT: We have used DNA microarray analysis of human hepatoma and epithelial carcinoma cells expressing hepatitis C virus (HCV) subgenomic replicons to test whether HCV replication alters gene expression and influences the alpha interferon (IFN-alpha) response. We directly compared the HCV replicon system with a similar system based on a subgenomic replicon of the West Nile virus (WNV) subtype Kunjin virus. We found that in contrast to WNV replicons, persistent replication of HCV replicons did not significantly alter the transcriptome of infected cells nor did it inhibit the nature of the IFN-stimulated genes (ISGs). Our results also provided evidence for the existence of a small number of ISGs that could play a role in the inhibition of HCV replication by IFN-alpha. Finally, we identified ISGs that are activated by the cytokine in a cell-type specific fashion.
Virology 06/2005; 335(2):264-75. · 3.35 Impact Factor
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ABSTRACT: West Nile virus (WNV) is a human pathogen that can cause neurological disorders, including meningoencephalitis. Experiments with mice and mammalian cell cultures revealed that WNV exhibited resistance to the innate immune program induced by alpha interferon (IFN-alpha). We have investigated the nature of this inhibition and have found that WNV replication inhibited the activation of many known IFN-inducible genes, because it prevented the phosphorylation and activation of the Janus kinases JAK1 and Tyk2. As a consequence, activation of the transcription factors STAT1 and STAT2 did not occur in WNV-infected cells. Moreover, we demonstrated that the viral nonstructural proteins are responsible for this effect. Thus, our results provided an explanation for the observed resistance of WNV to IFN-alpha in cells of vertebrate origin.
Journal of Virology 03/2005; 79(3):1343-50. · 5.40 Impact Factor
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ABSTRACT: The chromosomal features that influence retroviral integration site selection are not well understood. Here, we report the mapping of 226 avian sarcoma virus (ASV) integration sites in the human genome. The results show that the sites are distributed over all chromosomes, and no global bias for integration site selection was detected. However, RNA polymerase II transcription units (protein-encoding genes) appear to be favored targets of ASV integration. The integration frequency within genes is similar to that previously described for murine leukemia virus but distinct from the higher frequency observed with human immunodeficiency virus type 1. We found no evidence for preferred ASV integration sites over the length of genes and immediate flanking regions. Microarray analysis of uninfected HeLa cells revealed that the expression levels of ASV target genes were similar to the median level for all genes represented in the array. Although expressed genes were targets for integration, we found no preference for integration into highly expressed genes. Our results provide a more detailed description of the chromosomal features that may influence ASV integration and support the idea that distinct, virus-specific mechanisms mediate integration site selection. Such differences may be relevant to viral pathogenesis and provide utility in retroviral vector design.
Journal of Virology 12/2004; 78(21):11656-63. · 5.40 Impact Factor
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ABSTRACT: Human hepatocellular carcinoma is one of the most common cancers in the world. We previously showed that dbpA, a member of the Y box family of proteins, could accelerate the process of inflammation-induced hepatocarcinogenesis, and that dbpA is more abundantly expressed in hepatocellular carcinoma than in non-tumorous tissue. In this study, to clarify the mechanism by which expression of dbpA is enhanced in the proliferative state, we examined the transcriptional activity of the dbpA promoter region. We focused on the sequence 5'-TTTGGGGC-3' (-8 to -1 in the promoter region) resembling the E2F binding site (one base mismatch, TFSEARCH score 86.2). By overexpressing E2F1 in Huh-7 cells, transcriptional activity of dbpA was significantly increased, and this increase was abolished by mutating or deleting this sequence. Thus, expression of dbpA was positively regulated by E2F1, suggesting that one of the effects of E2F1 on cell proliferation might be mediated by dbpA at the carcinogenesis step.
Biochemical and Biophysical Research Communications 10/2004; 322(1):297-302. · 2.48 Impact Factor
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ABSTRACT: Human DNA-binding protein (dbpA) is a member of a Y-box binding protein family containing a cold shock domain. The increased expression of Y box binding proteins in somatic cells is associated with cell proliferation and transformation. Recently, we isolated a splicing variant of dbpA as a candidate for the cellular recombinogenic protein that leads to genomic instability and inflammation-mediated hepatocarcinogenesis. The expression of dbpA is enhanced in proliferating cells, but the manner in which it regulates transcription is largely unknown. In this study, we analyzed the transcriptional regulatory region of dbpA, and searched for the mutation in this region by a direct sequence method. In 3 of 55 human hepatocellular carcinoma (HCC) cases, we identified one nucleotide replacement (T right curved arrow G transversion) in nucleotide position -6 of the promoter region. Among 3 cases showing this transversion, one HCC case was due to a somatic mutation and the other two were due to single nucleotide polymorphism (SNP). By luciferase assay, we showed that the transcriptional activity of the promoter region with the transversion was significantly higher than that of the wild-type. Using the Southwestern blotting, we also confirmed the existence of a cellular proteins (about 25 and 50 kDa) that specifically bind to the sequence with this transversion. Our results suggested the biological significance of the transversion of dbpA's promoter region as one of the factors accelerating hepatocarcinogenesis.
International Journal of Oncology 11/2002; 21(4):847-50. · 2.40 Impact Factor
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Intervirology 08/1970; 42(2-3):205-210. · 2.34 Impact Factor
