Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)  

Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)  

Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)  

Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)   Publisher：CAMBRIDGE UNIV PRESS  

In rats, maternal exposure to restraint stress during pregnancy can induce abnormalities in the cardiovascular and central nervous systems of the offspring. These effects are mediated by long-lasting hyperactivation of the hypothalamic-pituitary-adrenal axis. However, little is known about the potential effects of stress during pregnancy on metabolic systems. We examined the effect of restraint stress in pregnant mice on the liver function of their offspring. The offspring of stressed mothers showed significantly higher lipid accumulation in the liver after weaning than did the controls; this accumulation was associated with increased expression of lipid metabolism-related proteins such as alanine aminotransferase 2 diglyceride acyltransferase 1, peroxisome proliferator-activated receptor gamma and glucocorticoid receptor. Additionally, we observed increased levels of 11 beta-hydroxysteroid dehydrogenase type 1, an intercellular mediator that converts glucocorticoid from the inactive to the active form, in the foetal and postnatal periods. These results indicate that restraint stress in pregnancy in mice induces metabolic abnormalities via 11 beta-hydroxysteroid dehydrogenase type 1-related pathways in the foetal liver. It is therefore possible that exposure to stress in pregnant women may be a risk factor for metabolic syndromes (e.g. fatty liver) in children.

DOI： 10.1017/S2040174415000100

Web of Science

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)   Publisher：AMER SOC MICROBIOLOGY  

Equine hepacivirus (EHcV) has been identified as a closely related homologue of hepatitis C virus (HCV) in the United States, the United Kingdom, and Germany, but not in Asian countries. In this study, we genetically and serologically screened 31 serum samples obtained from Japanese-born domestic horses for EHcV infection and subsequently identified 11 PCR-positive and 7 seropositive serum samples. We determined the full sequence of the EHcV genome, including the 3' untranslated region (UTR), which had previously not been completely revealed. The polyprotein of a Japanese EHcV strain showed approximately 95% homology to those of the reported strains. HCV-like cis-acting RNA elements, including the stem-loop structures of the 3' UTR and kissing-loop interaction were deduced from regions around both UTRs of the EHcV genome. A comparison of the EHcV and HCV core proteins revealed that Ile(190) and Phe(191) of the EHcV core protein could be important for cleavage of the core protein by signal peptide peptidase (SPP) and were replaced with Ala and Leu, respectively, which inhibited intramembrane cleavage of the EHcV core protein. The loss-of-function mutant of SPP abrogated intramembrane cleavage of the EHcV core protein and bound EHcV core protein, suggesting that the EHcV core protein may be cleaved by SPP to become a mature form. The wild-type EHcV core protein, but not the SPP-resistant mutant, was localized on lipid droplets and partially on the lipid raft-like membrane in a manner similar to that of the HCV core protein. These results suggest that EHcV may conserve the genetic and biological properties of HCV.
IMPORTANCE
EHcV, which shows the highest amino acid or nucleotide homology to HCV among hepaciviruses, was previously reported to infect horses from Western, but not Asian, countries. We herein report EHcV infection in Japanese-born horses. In this study, HCV-like RNA secondary structures around both UTRs were predicted by determining the whole-genome sequence of EHcV. Our results also suggest that the EHcV core protein is cleaved by SPP to become a mature form and then is localized on lipid droplets and partially on lipid raft-like membranes in a manner similar to that of the HCV core protein. Hence, EHcV was identified as a closely related homologue of HCV based on its genetic structure as well as its biological properties. A clearer understanding of the epidemiology, genetic structure, and infection mechanism of EHcV will assist in elucidating the evolution of hepaciviruses as well as the development of surrogate models for the study of HCV.

DOI： 10.1128/JVI.02280-14

Web of Science

Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)  

Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：ELSEVIER SCIENCE BV  

We previously reported that enhanced ceramide production induces calpain-mediated proteolysis of protein kinase C (PKC) in leukocytes from Chediak-Higashi syndrome (CHS). In the present study, we demonstrated that phospholipase D (PLD) inhibitors ameliorated abnormal increases in concanavalin A (Con A) cap formation in polymorphonuclear leukocytes (PMNs) from beige mouse, an animal model of CHS. PLD activity in PMNs from beige mice enhanced at 30 to 60 s after Con A stimulation. In Con A-stimulated beige PMNs, both neutral sphingomyelinase (N-SMase) and acidic sphingomyelinase (A-SMase) activities enhanced, and ceramide levels are also increased. We found that ceramide levels were reversed by the treatment of beige PMNs with propranolol which inhibits phosphatidic acid phosphohydrolase. In addition, we showed that diacylgycerol (DAG) analogs enhance both N-SMase and A-SMase activities in PMNs from normal mice. We subsequently examined the association of CHS1 with PLD, and showed that expression of a truncated mutant of CHS1 in 293T cells induced abnormally rapid activation of PLO after phorbol ester stimulation. Moreover, we showed that specific inhibitors of 14-3-3 proteins, which interact with CHS1/LYST and bind PKC, did not affect abnormal increases in Con A cap formation in beige PMNs. These results suggest that the enhanced DAG production via the PLD pathway is associated with abnormal increases in Con A cap formation in beige PMNs, and that CHS1 may be involved in the regulation of PLD activity. (C) 2014 Elsevier B.V. All rights reserved.

DOI： 10.1016/j.intimp.2014.05.003

Web of Science

Language：Japanese   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)   Publisher：WILEY-BLACKWELL  

Microglia survey the brain environment by sensing several types of diffusible molecules, among which extracellular nucleotides released/leaked from damaged cells have central roles. Microglia sense ATP or other nucleotides by multiple P2 receptors, after which they change into several different phenotypes. However, so far, it is largely unknown whether microglia themselves release ATP and, if so, by what mechanism. Here we show that exocytosis is the mechanism by which microglia release ATP. When we stimulated microglia with ionomycin, they released ATP and the release was dependent on Ca2+, vesicular H+-ATPase, or SNAREs but independent of connexin/pannexin hemichannels. VNUT was found to be expressed in microglia and exhibited no colocalization with lysosome. We also visualized the exocytosis of ATP by a quinacrine-based fluorescent time-lapse imaging. Moreover, we found that lipopolysaccharide increased the ionomycin-induced release of ATP, which was dependent on the increase in VNUT. Taken together, our data suggested that exocytosis is the mechanism of ATP release from microglia. When activated, they would release ATP by increasing VNUT-dependent exocytotic mechanisms. GLIA 2013;61:1320-1330

DOI： 10.1002/glia.22517

Web of Science

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

We previously reported that administration of a potent calpain inhibitor, E-64-d, which protects protein kinase C (PKC) from proteolysis, in a mouse model of Chediak-Higashi syndrome (CHS) (beige mice), decreases its susceptibility to Staphylococcus aureus infection. In the present study, we examined the in vitro effect of E-64-d on both deficient natural killer (NK) and delayed bactericidal activities of leukocytes from six CHS patients. Our results showed that pretreatment of peripheral blood mononuclear cells (PBMCs) obtained from CHS patients with E-64-d (1 μg/ml) significantly enhanced NK activity against K562 cells. The delayed bactericidal activity of polymorphonuclear cells (PMNs) against S. aureus also showed marked improvement. This was recovered to almost normal levels when PMNs were pretreated with E-64-d (1 μg/ml). On the other hand, the same concentration of E-64-d did not affect either the NK or bactericidal activity of normal controls. In addition, we confirmed that following E-64-d treatment, the abnormal down-regulation of PKC activity after concanavalin A (Con A) stimulation was eliminated in PBMCs obtained from CHS patients. To examine whether PKC is involved in the NK cell-mediated cytolysis and bactericidal activity of PMNs, two potent PKC inhibitors, chelerythrin and GÖ6976, were used. We found that chelerythrin inhibits NK activity of normal PBMCs in a dose-dependent manner, and GÖ6976 inhibits NK activity at doses that inhibit Ca2+-dependent PKC isozymes. These inhibitors also suppressed the bactericidal activity of PMNs against S. aureus. Taken together, our findings suggested that E-64-d improved the compromised NK and bactericidal activity of leukocytes from CHS patients by reversing the down-regulation of PKC activity. © 2009 Elsevier B.V. All rights reserved.

DOI： 10.1016/j.intimp.2009.01.003

Scopus

PubMed

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)   Publisher：AMER ASSOC IMMUNOLOGISTS  

IL-7 plays a critical role in B cell fate decision by regulating early B cell factor (EBF) expression. However, it was not clear when IL-7 stimulation is necessary in hemato-/lymphopoiesis in adult mice. Here we show that pre-proB cells derived from IL-7(-/-) mice have lost B cell potential, despite up-regulation of EBF expression following IL-7 stimulation. Pre-proB cells from wild-type mice can give rise to proB cells in the absence of IL-7. In this case, EBF up-regulation during the transition from the pre-proB to proB stages occurs normally. In contrast, EBF expression by IL-7(-/-) pre-proB cells after IL-7 stimulation is similar to 20 times lower than wild-type pre-proB cells. In addition, only multipotent progenitors with higher levels of ectopic EBF can give rise to proB cells in the absence of IL-7. Therefore, the primary function of IL-7 before the pre-proB stage in B cell development is to maintain the EBF expression level above a certain threshold, which is necessary for pre-proB cells to further transit to the proB stage.

Web of Science

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)   Publisher：B M J PUBLISHING GROUP  

DOI： 10.1136/ard.2007.076117

Web of Science

Authorship：Last author   Language：English   Publishing type：Research paper (scientific journal)  

Authorship：Last author   Language：English   Publishing type：Research paper (scientific journal)  

Authorship：Last author   Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Authorship：Last author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：OXFORD UNIV PRESS  

We examined the effects of hemicellulase-treated Agaricus blazei (AB fraction H, ABH) on growth of several tumor cell lines. ABH inhibited the proliferation of some cell lines without cytotoxic effects. It markedly prolonged the S phase of the cell cycle. ABH also induced mitochondria-mediated apoptosis in different cell lines. However, it had no impact on the growth of other cell lines. ABH induced strong activation of p38 mitogen-activated protein kinase (MAPK) in the cells in which it evoked apoptosis. On the other hand, ABH showed only a weak p38 activation effect in those cell lines in which it delayed cell cycle progression with little induction of apoptosis. However, p38 MAPK-specific inhibitor inhibited both ABH-induced effects, and ABH also caused apoptosis in the latter cells under conditions of high p38 MAPK activity induced by combined treatment with TNF-alpha. These results indicate that the responsiveness of p38 MAPK to ABH, which differs between cell lines, determines subsequent cellular responses on cell growth.

DOI： 10.1093/ecam/nel059

Web of Science

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

DOI： 10.1136/ard.2006.054874

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)   Publisher：MARY ANN LIEBERT INC  

Human immunodeficiency virus type-1 (HIV-1) is a leading cause of mortality and morbidity in the world, with almost 46 million people infected globally. HIV-1 subtype C accounts for 55% of these infections. In Zambia, the majority of HIV-1 infections are subtype C. However, to its north most countries have non-subtype C as the most predominant HIV-1 subtype while to its south most of them are predominantly subtype C. The aim of this study was to determine the subtype distribution and to analyze the long terminal repeat (LTR) region of HIV-1 isolates from the northern part of Zambia. We amplified as well as directly sequenced the LTR, gag, and env regions of 78 HIV-1 peripheral blood samples from adult Zambians. Our results show 95% (74/78) of our isolates were HIV-1 subtype C. Furthermore, of the subtype C samples analyzed across the LTR, 61% (25/41) carried 3 NF-kappa B signature binding site sequences.

Web of Science

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English  

Language：Japanese  

Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)  

Language：Japanese   Publishing type：Research paper (scientific journal)  

Language：Japanese   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

CD69, mitogenic reaction, stress, granulocyte, natural killer cell

Language：Japanese  

Authorship：Lead author   Language：English   Publishing type：Research paper (scientific journal)   Publisher：OXFORD UNIV PRESS  

Agaricus blazei Murill is an edible fungus used in traditional medicine, which has various well-documented medicinal properties. In the present study, we investigated the effects of hemicellulase-derived mycelia extract (Agaricus blazei fraction H: ABH) on the immune system. First, we examined the cytokine-inducing activity of ABH on human peripheral mononuclear cells (PBMC). The results indicated that ABH induced expression of IL-12, a cytokine known to be a critical regulator of cellular immune responses. Flow cytometric analysis demonstrated the induction of IL-12 production by the CD14-positive cell population, consisting of monocytes/macrophages (Mo/M phi). Furthermore, the elimination of Mo/M phi attenuated IL-12 production in PBMC. ABH-induced IL-12 production was inhibited by anti-CD14 and anti-TLR4 antibodies but not by anti-TLR2 antibody. The activity of ABH was not inhibited by polymyxin B, while the activity of lipopolysaccharide used as a reference was inhibited. Oral administration of ABH enhanced natural killer (NK) activity in the spleen. These findings suggest that ABH activated Mo/M phi in a manner dependent on CD14/TLR4 and NK activity.

DOI： 10.1093/ecam/neh043

Web of Science

Language：Japanese  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)  

Molecular epidemiology of HIV-1 in Zambia was investigated by direct sequencing of PCR products from samples collected from antenatal attendees in Lusaka, Zambia. One hundred and forty samples were initially screened for HIV, using antibody assays. Thirty-three (23.6%) samples were HIV-1 positive. Sequences of the HIV-1 env gp120 region were obtained from 28 of 33 (85%) HIV-1-positive samples. Twenty-six of the 28 sequences were HIV-1 env subtype C-like as previously reported. However, one HIV-1 env subtype D-like virus and one HIV-1 env subtype G-like virus were identified. This is the first time that these two HIV-1 env subtype viruses have been identified in Zambia, suggesting that more subtypes could be in existence.

DOI： 10.1089/088922201750237031

Scopus

PubMed

Language：English   Publishing type：Research paper (scientific journal)  

Interleukin-12 (IL-12) is a monocyte/macrophage-derived cytokine that plays a prominent role in the development of T helper type 1 (Th1) cell-mediated immune responses. Glycyrrhizin (GL), an aqueous extract of liquorice root, used as Chinese medicine, is known to have various immunomodulating activities. In this study, GL showed a dose-dependent priming effect on lipopolysaccharide (LPS)-induced IL-12 p40 and IL-12 p70 (heterodimer of p40 and p35) protein production by peritoneal macrophages (PM). The maximal effect was observed when GL was intraperitoneally administered 12 hr before the PM were harvested and stimulated in vitro with LPS. The increases in IL-12 p70 and p40 protein production were primarily due to up-regulated transcription of IL-12 p35 and p40 messenger RNAs (mRNAs), as demonstrated by RNase protection assay. The augmentation of IL-12 p40 mRNA expression induced by GL pretreatment was associated with increased NF-κB activation. Moreover, GL exhibited the same priming effect on IL-12 production in interferon-γ knockout (IFN-γ -/-) mice. The production of granulocyte-macrophage colony-stimulating factor (GM-CSF) was not induced at any time point after GL pretreatment. These findings demonstrated the ability of GL to enhance LPS-induced IL-12 production by peritoneal macrophages, and indicated that the priming effect of GL on IL-12 production was independent of both IFN-γ and GM-CSF.

DOI： 10.1046/j.1365-2567.2001.01224.x

Scopus

PubMed

Language：English   Publishing type：Research paper (scientific journal)  

Language：English   Publishing type：Research paper (scientific journal)   Publisher：ELSEVIER SCIENCE BV  

We here cloned a cDNA encoding STAM2, a new member of the STAM family, which contains an SH3 domain and ITAM, STAM2 like STAM1 is associated with Jak2 and Jak3, and involved in the signaling for DNA synthesis and c-myc induction mediated by IL-2 and GM-CSF. Go-expression of the SH3 deletion mutants of STAM1 and STAM2 induces an additive effect on suppressing DNA synthesis upon stimulation with IL-2 and GM-CSF, suggesting that STAM1 and STAM2 exhibit compensatory effects on the signaling pathways downstream of Jak2 and Jak3 upon stimulation with GM-SCF and IL-2, respectively, (C) 2000 Federation of European Biochemical Societies. Published by Elsevier Science B.V. All rights reserved.

Web of Science

Event date： 2022.11

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：長崎  

Event date： 2022.11

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：長崎  

Event date： 2022.11

Language：Japanese   Presentation type：Poster presentation  

Venue：長崎  

Event date： 2021.11

Language：Japanese   Presentation type：Oral presentation(general)  

Event date： 2021.11

Language：Japanese   Presentation type：Oral presentation(general)  

Event date： 2021.11

Language：Japanese   Presentation type：Oral presentation(general)  

Event date： 2021.11

Language：Japanese   Presentation type：Oral presentation(general)  

Event date： 2019.10

Language：English   Presentation type：Oral presentation(general)  

Event date： 2019.10

Language：English   Presentation type：Poster presentation  

Event date： 2019.10

Language：English   Presentation type：Oral presentation(general)  

Language：English   Presentation type：Poster presentation  

Venue：船橋テルサ  

Language：English   Presentation type：Oral presentation(general)  

Language：English   Presentation type：Oral presentation(general)  

Event date： 2019.10

Language：English   Presentation type：Oral presentation(general)  

Language：English   Presentation type：Oral presentation(general)  

Event date： 2018.10

Language：English  

Event date： 2018.10

Language：English   Presentation type：Oral presentation(general)  

Language：English  

Venue：京都  

Language：English   Presentation type：Oral presentation(general)  

Venue：京都  

Event date： 2018.10

Language：English   Presentation type：Poster presentation  

Language：English   Presentation type：Poster presentation  

Venue：京都  

Event date： 2017.10

Language：English   Presentation type：Oral presentation(general)  

Language：English   Presentation type：Oral presentation(general)  

Event date： 2017.10

Language：English   Presentation type：Poster presentation  

Event date： 2017.10

Language：English   Presentation type：Oral presentation(general)  

Event date： 2017.10

Language：Japanese   Presentation type：Poster presentation  

Language：Japanese   Presentation type：Poster presentation  

Language：English   Presentation type：Poster presentation  

Event date： 2016.12

Language：Japanese   Presentation type：Poster presentation  

Language：Japanese   Presentation type：Poster presentation  

Event date： 2016.10

Language：English   Presentation type：Oral presentation(general)  

Event date： 2016.10

Language：English   Presentation type：Oral presentation(general)  

Event date： 2016.10

Language：English   Presentation type：Oral presentation(general)  

Language：English   Presentation type：Oral presentation(general)  

Venue：札幌コンベンションセンター  

Language：English   Presentation type：Oral presentation(general)  

Venue：札幌コンベンションセンター  

Language：English   Presentation type：Oral presentation(general)  

Venue：札幌コンベンションセンター  

Event date： 2016.10

Language：English   Presentation type：Poster presentation  

Language：English   Presentation type：Poster presentation  

Event date： 2016.10

Language：English   Presentation type：Poster presentation  

Venue：Kyoto  

Language：English   Presentation type：Poster presentation  

Venue：Kyoto  

Event date： 2016.3

Language：Japanese   Presentation type：Oral presentation(general)  

Language：Japanese   Presentation type：Oral presentation(general)  

Event date： 2015.12

Language：Japanese   Presentation type：Other  

Language：Japanese   Presentation type：Other  

Venue：第 38回日本分子生物学会年会、第 88回日本生化学会大会  

Event date： 2015.11

Language：English   Presentation type：Oral presentation(general)  

Event date： 2015.11

Language：English   Presentation type：Oral presentation(general)  

Language：English   Presentation type：Oral presentation(general)  

Venue：第６3回日本ウイルス学会学術総会 福岡国際会議場  

Event date： 2015.7

Language：Japanese   Presentation type：Oral presentation(general)  

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：第38回日本神経科学大会  

Event date： 2014.10

Language：Japanese   Presentation type：Oral presentation(general)  

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：第６2回日本ウイルス学会学術総会  

Event date： 2013.11

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：神戸国際会議場  

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：神戸国際会議場  

Event date： 2012.12

Language：Japanese   Presentation type：Other  

Language：Japanese   Presentation type：Other  

Venue：第３５回日本分子生物学会年会  

Event date： 2012.11

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：第６０回日本ウイルス学会学術総会  

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：第６０回日本ウイルス学会学術総会  

Event date： 2012.10

Language：English   Presentation type：Other  

Language：English   Presentation type：Other  

Venue：19th International Symposium on Hepatitis C Virus and Related Viruses  

Event date： 2011.12

Language：English   Presentation type：Oral presentation(general)  

Language：English   Presentation type：Oral presentation(general)  

Venue：横浜  

Event date： 2011.9

Language：English   Presentation type：Oral presentation(general)  

Language：English   Presentation type：Oral presentation(general)  

Venue：Seattle  

Event date： 2006.11

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：東京  

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：東京  

Event date： 2004.12

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：静岡市  

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：静岡市  

Event date： 2004.12

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：静岡市  

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：静岡市  

Event date： 2004.11

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：富山市  

Event date： 2004.11

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：静岡市  

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：静岡市  

Event date： 2003.12

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：東京  

Event date： 2003.12

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：福岡市  

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：福岡市  

Event date： 2003.11

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：神戸市  

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：神戸市  

Event date： 2003.10

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：京都市  

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：京都市  

Event date： 2003.5

Language：Japanese   Presentation type：Oral presentation(invited, special)  

Venue：甲府市  

Language：Japanese   Presentation type：Oral presentation(invited, special)  

Venue：甲府市  

Event date： 2001.12

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：大阪  

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：大阪  

Event date： 2001.11

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：東京  

Event date： 2001.11

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：東京  

Event date： 2001.11

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：大阪  

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：東京  

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：東京  

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：大阪  

Event date： 2001.9

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：東京  

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：東京  

Event date： 2001.7

Language：English   Presentation type：Oral presentation(general)  

Venue：Buenos Aires  

Language：English   Presentation type：Oral presentation(general)  

Venue：Buenos Aires  

Event date： 2000.11

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：京都  

Event date： 2000.11

Language：English   Presentation type：Oral presentation(general)  

Event date： 2000.11

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：京都  

Event date： 2000.11

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：京都  

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：京都  

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：京都  

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：京都  

Language：English   Presentation type：Oral presentation(general)  

Venue：京都  

Event date： 2000.10

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：津  

Language：Japanese   Presentation type：Oral presentation(general)  

Venue：津