Junpei Hayashi

Nihon University, Edo, Tokyo, Japan

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Publications (12)30.42 Total impact

  • Yasuo Arakawa · Junpei Hayashi · Mitsuhiko Moriyama

    No preview · Article · May 2011 · Nippon rinsho. Japanese journal of clinical medicine
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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.
    Full-text · Article · Nov 2009 · Journal of Clinical Biochemistry and Nutrition
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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.
    Full-text · Article · Apr 2008 · World Journal of Gastroenterology
  • Junpei Hayashi · Mitsuhiko Moriyama
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    ABSTRACT: Hepatitis C virus (HCV) is a major cause of chronic hepatitis, liver cirrhosis and liver cancer. Previously, the consensus strategy against HCV infection was interferon mono-therapy. Now, pegylated interferon (PEG-IFN) with ribavirin combination therapy for 24-48 weeks is used against chronic hepatitis C and can achieve a sustained viral response (SVR) in about 50% of patients with genotype 1b and high viral loads. The number of elderly Japanese patients with chronic hepatitis C has increased compared to that in western countries. The efficacy of IFN therapy for elderly patients with genotype 1 and high viral titers is lower than in young patients, because the side effects of combination therapy with PEG-IFN and ribavirin are pronounced with a reduction in blood count. To avoid discontinuation of therapy and overcome the low SVR in elderly patients, ribavirin dosing, based on the total clearance of ribavirin (CL/F), may be considered to be increasingly valuable. Approximately 25% of HCV carriers have normal ranges of serum alanine amino transferase (ALT). The rate of SVR in patients with persistently normal serum ALT (PNALT) is almost as same as that in HCV carriers, in terms of IFN therapy. This evidence suggests that patients with PNALT should be considered for IFN therapy. Novel treatment options currently in development are focused on inhibition of HCV-specific enzymes, NS3 protease and NS5B polymerase, and several drugs have entered clinical trials. Now, patients with HCV and liver cirrhosis can be given IFN therapy, except in the case of genotype 1b and high viral loads. This therapy should contribute to an improvement in the prognosis. It would appears that interferon will remain an element of anti-HCV therapy for the immediate future, although new regimens will be necessary for advanced combination therapy. It is hoped that new forms of interferon that are more effective, less toxic, and more convenient can be developed.
    No preview · Article · Jan 2008
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    ABSTRACT: Ciliated foregut cysts (CHFC) originate from remnants of the embryonic foregut, and most of them locate in the subcapsular region of the medial segment of the liver. There are some CHFC which are hard to distinguish from hypovascular solid tumor, cystic neoplasm or hepatocellular carcinoma with severe necrosis. Although three cases of squamous cell carcinomas arising in CHFC have been reported in other countries, there are no such cases have been reported in Japan. We encountered a patient who was diagnosed as CHFC by needle biopsy. CHFC generally are benign lesions, therefore regular observation is thought to be enough. However in this case, the lesion was enucleated with an assistance of laparoscopy because it became larger and the possibility of malignant change could not be excluded.
    No preview · Article · Jan 2006 · Kanzo
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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.
    No preview · Article · Oct 2004 · Biochemical and Biophysical Research Communications
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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.
    No preview · Article · Nov 2002 · International Journal of Oncology
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    ABSTRACT: OBJECTIVE: Previously we hypothesized that the occurrence of hepatocellular carcinoma (HCC) is enhanced by genomic instability induced by the integrated hepatitis B virus (HBV) DNA. Using an in vitro recombination assay, we showed that a subgenomic fragment of HBV DNA designated 15AB (nt1855-1914) is indispensable for in vitro recombination, and also showed the existence of 15AB binding protein. On the assumption that the 15AB binding protein may be a candidate cellular recombinogenic protein which accelerates genomic instability and hepatocarcinogenesis, we tried to isolate it by southwestern screening. RESULTS AND CONCLUSION: We obtained several positive clones including mouse upstream binding factor (UBF) and DNA binding protein A (dbpA). UBF belongs to an HMG domain protein family and dbpA belongs to a Y box binding protein family. 15AB binding seemed to be mediated by the conserved DNA binding domains in these families, because other members in the families such as HMG1 and YB-1 also bound to 15AB. We report them here because several documents have already suggested the possible association of these families and DNA recombination.
    No preview · Article · Feb 2001 · Intervirology
  • J Hayashi · H Aoki · K Kajino · M Moriyama · Y Arakawa · O Hino
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    ABSTRACT: Persistent hepatitis C virus (HCV) infection is associated with the development of human hepatocellular carcinoma (HCC), although the mechanism of HCV-related hepatocarcinogenesis remains unclear. Recently, however, the close relationships between the development of HCC and the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated protein kinase (ERK) cascade have been described. In the present study, we investigated the effects of HCV core protein on this MAPK/ERK cascade. HCV core protein significantly activated the MAPK/ERK cascade, including Elk1. We also examined whether HCV core protein acted synergistically along with hepatocyte mitogen-mediated MAPK/ERK activation. Interestingly, Elk-1 activities were further enhanced by the tumor promoter, 12-O-tetradecanoyl phorbol 13-acetate (TPA), but not by hepatocyte mitogens (epidermal growth factor [EGF] and transforming growth factor alpha [TGF-alpha]) in NIH3T3 cells and HepG2 cells expressing HCV core protein. Moreover, the MAPK/ERK activation by HCV core protein was blocked in the presence of the specific MEK1 inhibitor, PD98059. These results indicate that ERK activation by HCV core protein may be independent of hepatocyte mitogen-mediated signaling but synergistic with TPA, and HCV core protein may function at MEK1 or farther upstream of that component.
    No preview · Article · Dec 2000 · Hepatology
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    ABSTRACT: Persistent hepatitis C virus (HCV) infection is a major cause of chronic liver dysfunction in humans and is epidemiologically closely associated with the development of human hepatocellular carcinoma. Among HCV components, core protein has been reported to be implicated in cell growth regulation both in vitro and in vivo, although mechanisms explaining those effects are still unclear. In the present study, we identified that members of the 14-3-3 protein family associate with HCV core protein. 14-3-3 protein bound to HCV core protein in a phosphoserine-dependent manner. Introduction of HCV core protein caused a substantial increase in Raf-1 kinase activity in HepG2 cells and in a yeast genetic assay. Furthermore, the HCV core–14-3-3 interaction was essential for Raf-1 kinase activation by HCV core protein. These results suggest that HCV core protein may represent a novel type of Raf-1 kinase-activating protein through its interaction with 14-3-3 protein and may contribute to hepatocyte growth regulation.
    Preview · Article · Mar 2000 · Journal of Virology
  • J Hayashi · H Aoki · Y Arakawa · O Hino
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    ABSTRACT: Although human hepatocellular carcinoma (HCC) is one of the most common types of tumors in the world, the molecular mechanisms underlying hepatitis-C-related human hepatocarcinogenesis are still not clear. HCC is accompanied by virus infections in most cases, and it is suggested that hepatitis B virus and hepatitis C virus (HCV) significantly influence the oncogenic process. The persistence of inflammation following HCV infection is reportedly related to carcinogenesis, and the mechanism of chronic inflammation has been approached by taking viral, immunologic, cytokine and apoptotic responses into consideration. With the progress made in molecular biology, the functional abnormality of oncogenes/tumor suppressor genes has been identified and, apart from the p53 gene, involvement of the IGF-II gene has also been described recently. Furthermore, it has been suggested that uncontrolled proliferation of cancer cells might be based on abnormal regulation of intracellular signal transduction pathways. Here we review the cutting edge of molecular hepatitis C virology in terms of virus-cell interactions, which may contribute to the development of human HCCs. We also discuss the recent progress made in the molecular and cell biology of human hepatocarcinogenesis.
    No preview · Article · Feb 1999 · Intervirology
  • Junpei Hayashi · Hiroshi Aoki · Yasuyuki Arakawa · Okio Hino

    No preview · Article · Jan 1999 · Intervirology

Publication Stats

343 Citations
30.42 Total Impact Points


  • 2000-2009
    • Nihon University
      • School of Medicine
      Edo, Tokyo, Japan
  • 2002
    • Kinki University
      • Department of Gastroenterology and Hepatology
      Ōsaka, Ōsaka, Japan