H Ogawa

Tokyo Institute of Technology, Edo, Tōkyō, Japan

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Publications (550)1491.53 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Background Few studies have evaluated the effects of rabeprazole on low-dose aspirin (LDA)-induced gastroduodenal injuries.AimTo conduct a randomised, double-blind, triple-dummy, active-controlled, multicentre trial, named the PLANETARIUM study, to assess the efficacy, dose–response relationship and safety of rabeprazole for peptic ulcer recurrence in Japanese patients on long-term LDA therapy.Methods Eligible patients had a history of endoscopically confirmed peptic ulcers and were receiving long-term LDA (81 or 100 mg/day) therapy for cardiovascular or cerebrovascular protection. Subjects were randomly segregated into three groups receiving rabeprazole 10 mg once daily (standard dose in Japan), rabeprazole 5 mg once daily, or teprenone (geranylgeranylacetone; mucosal protective agent commercially available in Japan) 50 mg three times per day as an active control. The primary endpoint was recurrence of peptic ulcers over 24 weeks.ResultsAmong 472 randomised subjects, 452 subjects (n = 151, 150, 151, respectively) constituted the full analysis set. The cumulative recurrence rates of peptic ulcers over 24 weeks in the 10- and 5-mg rabeprazole groups were 1.4% and 2.8%, respectively, both of which were significantly lower than that in the teprenone group (21.7%). The cumulative occurrence rate of bleeding ulcers over 24 weeks in the teprenone group was 4.6%, while bleeding ulcers were not observed in the 10- or 5-mg rabeprazole groups. Rabeprazole was well tolerated at both doses.Conclusion Rabeprazole prevents the recurrence of peptic ulcers with no evidence of a major dose–response effect in subjects on low-dose aspirin therapy.
    Alimentary Pharmacology & Therapeutics 08/2014; · 4.55 Impact Factor
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    ABSTRACT: Autoantibodies to proliferating cell nuclear antigen (PCNA) are specifically, if rarely, present in systemic lupus erythematosus (SLE) patient sera. Even SLE patients lacking PCNA reactivity often show reaction to PCNA-binding protein. Here, immunoreactivity to chromatin assembly factor-1 (CAF-1), an essential molecule for DNA replication and a PCNA-binding protein, was compared for the sera of SLE patients, normal healthy controls (NHCs) and other disease controls, and in autoimmune sera reactive to standard autoantigens, by enzyme-linked immunosorbent assay (ELISA), indirect immunofluorescence, and immunoblotting. CAF1 and IRF1 expression in SLE and NHC peripheral mononuclear cells were compared by quantitative real-time polymerase chain reaction. Serum interferon-γ-inducing protein-10 and anti-double-stranded (ds)DNA antibody levels were measured by ELISA. Increased CAF-1 autoimmune reactivity was recognized in SLE or serum anti-dsDNA antibody-positive patients. Significantly greater central nervous system (CNS) involvement (aseptic meningitis) and serum anti-dsDNA antibody titers were present more often in anti-CAF-1 antibody-positive than antibody-negative SLE patients. IFN-γ positively regulated CAF-1 expression in vitro and was associated with anti-CAF-1 antibody production in SLE. Thus, a novel anti-CAF-1 autoantibody is frequently found in patients with SLE and is a useful biomarker for diagnosis, especially in cases with CNS involvement. Aberrant IFN-γ regulation appears to play an important role in anti-CAF-1 antibody production in SLE.
    Lupus 05/2014; · 2.48 Impact Factor
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    ABSTRACT: BackgroundS100A7/psoriasin is a member of the S100 protein family and is encoded in the epidermal differentiation complex, which contains genes for markers for epidermal differentiation. S100A7/psoriasin is overexpressed in hyperproliferative skin diseases, where it is believed to not only exhibit antimicrobial functions but also to induce immunomodulatory activities, including chemotaxis and cytokine/chemokine production.Objective To evaluate the effect of S100A7/psoriasin on keratinocyte differentiation and regulation of the tight junction barrier function.Methods Expression of differentiation markers and tight junction proteins in human keratinocytes was determined by real-time PCR and Western blot. The changes in tight junction barrier function were assessed by transepithelial electrical resistance and paracellular permeability assays. Glycogen synthase kinase-3 (GSK-3) and MAP kinase activation was analysed by Western blot, whereas β-catenin and E-cadherin activation was evaluated by Western blot and immunofluorescence.ResultsS100A7/psoriasin enhanced expression of several differentiation markers and selectively increased expression of tight junction proteins, such as claudins and occludin, that are known to strengthen the tight junction barrier. Furthermore, S100A7/psoriasin increased β-catenin and E-cadherin accumulation at cell-cell contact, and enhanced transepithelial electrical resistance while reducing the paracellular permeability of keratinocyte layers. The data suggested that S100A7/psoriasin-mediated regulation of tight junction barrier was via both the GSK-3 and MAP kinase pathways, as evidenced by the inhibitory effects of inhibitors for GSK-3 and MAPKs.Conclusions Our finding that S100A7/psoriasin regulates differentiation and strengthens tight junction barrier function provides novel evidence that S100A7/psoriasin is involved in skin innate immunity, in addition to its antimicrobial and immunoregulatory activities.This article is protected by copyright. All rights reserved.
    British Journal of Dermatology 05/2014; · 3.76 Impact Factor
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    ABSTRACT: Epidermal hyperinnervation is considered one cause of sensitization to itch, and is thought to regulated by keratinocyte-derived axonal guidance molecules, including nerve growth factor (NGF) and semaphorin (Sema)3A. Neurotropin (NTP) shows antipruritic effects in allergic disease and is also used for pain relief. Using cultured rat dorsal root ganglion neurones, we previously found that NTP inhibited NGF-induced neurite outgrowth. However, no such inhibitory effect has been shown in vivo. We therefore assessed the effects of intraperitoneal administration of NTP on nerve density and expression of NGF and Sema3A mRNAs in the epidermis of acetone-treated mice showing epidermal hyperinnervation. We found that NTP significantly reduced intraepidermal nerve growth in these acetone-treated mice. NTP significantly upregulated epidermal Sema3A mRNA, but had no effect on expression of epidermal NGF mRNA. These findings indicate that NTP may reduce intraepidermal nerve density by inducing expression of Sema3A in the epidermis.
    Clinical and Experimental Dermatology 06/2013; · 1.23 Impact Factor
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    ABSTRACT: Excited states in 17C were investigated through the measurement of beta?-delayed neutrons and gamma rays emitted in the ? decay of 17B. In the measurement, three negative-parity states and two inconclusive states, were identified in 17C above the neutron threshold energy, and seven gamma-lines were identified in a beta?-delayed multiple neutron emission of the 17B ? decay. From these transitions, the beta?-decay scheme of 17B was determined. In the present work, the ?beta-NMR technique is combined with the ?-delayed particle measurements using a fragmentation-induced spin-polarized 17B beam. This new scheme allows us to determine the spin parity of beta?-decay feeding excited states based on the difference in the discrete ?beta-decay asymmetry parameters, provided the states are connected through the Gamow-Teller transition. In this work, 1/2-, 3/2-, and (5/2-) are assigned to the observed states at Ex = 2.71(2), 3.93(2), and 4.05(2) MeV in 17C, respectively.
    Physical Review C 01/2013; 87(3). · 3.88 Impact Factor
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    ABSTRACT: This study aimed to investigate the safety and feasibility of physical therapy in cytopenic patients undergoing allogeneic haematopoietic stem cell transplantation (allo-HSCT), and to investigate the effect of physical therapy on physiological functions and quality of life (QOL) in allo-HSCT patients. The study cohort included 321 patients who underwent allo-HSCT. To investigate the safety and feasibility of physical therapy during cytopenia, patients were assigned to the physical therapy group (n = 227) or the control group (n = 94). To determine the effects of physical therapy, patients were divided according to the frequency with which they underwent physical therapy (n = 51 per group). Handgrip strength, knee extensor strength and a 6-min walk test were used as measures of physiological function. Short-Form 36 was used to assess QOL. The physical therapy group had higher rate of achieving engraftment and lower death rate than the control group (P < 0.05). After HSCT, the high-frequency physical therapy group showed significantly less decline than the low-frequency physical therapy group with respect to physical functioning of QOL (P < 0.01). Physical therapy is quite beneficial and can be performed safely and feasibly in cytopenic patients during allo-HSCT.
    European Journal of Cancer Care 12/2012; · 1.31 Impact Factor
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    ABSTRACT: Acute GVHD (aGVHD) is a major obstacle to allogeneic hematopoietic SCT (alloHSCT). Although it is thought that aGVHD is initiated in secondary lymphoid organs at a very early stage of alloHSCT, whether CD4(+)FOXP3(+) regulatory T-cells (Tregs) have an impact on aGVHD development during this period remains unclear. Here, we measured Tregs in peripheral blood as early as possible after HLA-mismatched alloHSCT, and assessed the incidence of aGVHD. Flow cytometric analyses revealed that at the second week after HSCT, patients with aGVHD had significantly (P=0.018) lower Treg:CD4(+)T-cell ratios than those without aGVHD. As these differences were seen before the development of aGVHD, these ratios can predict the incidence of aGVHD. The cumulative incidence of aGVHD in patients with ratios of <9% was significantly higher than that in patients with ratios of 9% (P=0.0082, log-rank test). Additionally, the specific ratio of Tregs:CD4(+)T-cells was the most significant value among all other possible lymphocyte-associated ratios and absolute cell counts. These findings suggest that the ratio of Tregs:CD4(+)T-cells at the second week post HLA-mismatched alloHSCT might be a potent predictor of aGVHD in these patients. The practical efficacy of this finding should be verified in further interventional studies.Bone Marrow Transplantation advance online publication, 19 November 2012; doi:10.1038/bmt.2012.232.
    Bone marrow transplantation 11/2012; · 3.00 Impact Factor
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    ABSTRACT:   ATP2A2 encoding the sarcoplasmic/endoplasmic reticulum Ca(2+) -ATPase2 (SERCA2) is a Darier disease (DD)-related gene. Ultraviolet (UV) B irradiation downregulates ATP2A2/SERCA2 expression in keratinocytes, whereas cyclooxygenase-2 (COX-2) expression is dramatically upregulated by UVB.  To analyse the involvement of COX-2 in ATP2A2/SERCA2 expression.   Keratinocytes were transfected with COX-2 siRNA or treated with COX-2 inhibitor, celecoxib, to evaluate the effect of COX-2 on ATP2A2/SERCA2 expression. Quantitative real-time polymerase chain reaction, Western blotting analysis and reporter assay were used to determine the amount of mRNA, protein level and transcription activity, respectively.   COX-2 knockdown by siRNA resulted in upregulation of ATP2A2 transcription. Treatment by celecoxib rescued UVB-mediated suppression of the ATP2A2 transcription and SERCA2 protein expression. Simple addition of prostaglandin (PG) E(2) , which is a product of COX-2 enzyme, reduced the amounts of ATP2A2 mRNA and SERCA2 protein in keratinocytes.   UVB downregulates ATP2A2/SERCA2 expression via induction of COX-2 expression and subsequent increase of PGE(2) production in keratinocytes. Considering that DD is caused by the decreased function of SERCA2 due to the reduced expression of the ATP2A2 gene, this finding shows the possibility that COX-2 inhibition may be useful to prevent and/or treat DD.
    British Journal of Dermatology 03/2012; 166(5):1017-22. · 3.76 Impact Factor
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    ABSTRACT: Pre-existing donor-specific HLA antibodies in patients undergoing HLA-mismatched SCT have increasingly been recognized as a risk factor for primary graft failure. However, the clinical implications of the presence of HLA antibodies in donors remain unknown. We prospectively examined 123 related donors for the presence of HLA antibodies by using a Luminex-based single antigen assay. Of these, 1/57 (1.8%) male, 6/27 (22%) parous female and 0/39 (0%) nonparous female donors were HLA antibody-positive. Then, we determined the presence of HLA antibodies in seven patients who received SCT from antibody-positive donors. Of these, four became HLA antibody-positive after SCT. The specificities of the antibodies that emerged in the patients closely resembled those of the antibodies found in the donors, indicating their production by donor-derived plasma cells. Moreover, the kinetics of the HLA antibody levels were similar in all four patients: levels started increasing within 1 week after SCT and peaked at days 10-21, followed by a gradual decrease. These results suggest that donor-derived HLA antibody production frequently occurs in patients undergoing SCT from antibody-positive donors. Further studies are warranted for clarifying the clinical significance of donor-derived HLA antibodies, including the role of these antibodies in post transplant platelet transfusion refractoriness.
    Bone marrow transplantation 02/2012; 47(10):1338-42. · 3.00 Impact Factor
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    ABSTRACT: The role of HLA antibodies in SCT has drawn increasing attention because of the significantly increased number of patients who receive HLA-mismatched SCT, including cord blood transplantation, haploidentical SCT and unrelated SCT. Technical advancements in the methods of HLA Ab testing have realized rapid, accurate and objective identification, as well as quantification of specific HLA antibodies. Recent clinical studies have suggested that the presence of donor-specific HLA antibodies (DSA) in patients is associated with graft failure in HLA-mismatched SCT when the above-listed stem cell sources are used and results in different impacts. Of note, most of the 'HLA-matched' unrelated SCT actually involve HLA mismatches in HLA-DP and the presence of antibodies against this locus has been reported to be associated with graft failure. Thus, HLA Ab should be examined as a work-up for all patients who undergo SCT from 'alternative donors.' The simplest route for preventing HLA Ab-mediated graft failure in Ab-positive patients is to avoid donors who possess the target Ag of HLA antibodies. If SCT from such donors must be performed, treatment for DSA before SCT may improve the chances of successful donor engraftment.Bone Marrow Transplantation advance online publication, 9 January 2012; doi:10.1038/bmt.2011.249.
    Bone marrow transplantation 01/2012; · 3.00 Impact Factor
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    Clinical and experimental rheumatology 12/2011; 30(1):145-6. · 2.97 Impact Factor
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    ABSTRACT: Changes in gene expression in CD3+ T cells associated with disease progression in systemic lupus erythematosus (SLE) patients were determined. The genes related to SLE disease-related activities were identified and their gene regulatory networks were investigated. Analyses of gene expression were performed by both DNA microarray and real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR). The expression of certain genes including interferon (IFN) regulatory factor (IRF)-related genes, such as IFN-regulated, -related, and -signature genes was increased in the active phase of SLE. Pathway network analyses suggested that these IRF-related genes are regulated through the Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway. JAK/STAT pathway-mediated regulation of IRF-related genes may have an important role in the disease activity of SLE. Inhibitors of JAK/STAT cascade may be useful as therapeutic agents.
    Lupus 10/2011; 20(12):1231-9. · 2.48 Impact Factor
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    ABSTRACT: Extramedullary (EM) relapse of leukemia after allo-SCT in patients with AML/myelodysplastic syndrome has been increasingly reported. The reduced effectiveness of the GVL effect in EM sites, as compared with BM, has been suggested to underlie this problem. We retrospectively analyzed the pattern of relapse after haploidentical SCT (haplo-SCT), performed as the first or second SCT. Among 38 patients who received haplo-SCT as their first SCT, the cumulative incidences of BM and EM relapse at 3 years were 40.5 and 10.9%, respectively. Among 19 patients who received haplo-SCT as their second SCT, the cumulative incidences of BM and EM relapse were 30.9 and 31.9%, respectively. Moreover, most of the patients who underwent repeat haplo-SCT for the treatment of EM relapse had further EM relapse at other sites. Post-relapse survival did not differ significantly with different patterns of relapse. The frequent occurrence of EM relapse after haplo-SCT, particularly when performed as a second SCT, suggests that the potent GVL effect elicited by an HLA disparity also occurs preferentially in BM. Our findings emphasize the need for a treatment strategy for EM relapse that recognizes the reduced susceptibility of EM relapse to the GVL effect.
    Bone marrow transplantation 08/2011; 47(5):669-76. · 3.00 Impact Factor
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    ABSTRACT: A role of donor-specific HLA antibodies (DSA) in graft failure after SCT has been suggested, but the relevance of DSA in unmanipulated haploidentical SCT (haplo-SCT) remains unknown. We prospectively examined HLA antibodies using the Luminex-based single Ag assay for 79 adult patients undergoing unmanipulated haplo-SCT. Among them, 16 (20.2%) were HLA Ab-positive, including five patients with antibodies not corresponding to donor HLA Ags and 11 DSA-positive patients. Of the 11 DSA-positive patients, five received treatments to decrease DSA levels, including two, who received plasma exchange and rituximab, two who received platelet transfusions from healthy-related donors having DSA-corresponding HLA Ags and one who received bortezomib. Platelet transfusion was the most simple and effective treatment option for class I DSA. The cumulative incidence of neutrophil recovery was significantly lower in pretransplant (post-treatment) DSA-positive patients than in DSA-negative patients (61.9 vs 94.4%, P=0.026). Notably, three of five patients with high levels of DSA had graft failure. Donors should be selected on the basis of an evaluation of HLA antibodies. If haplo-SCT from donors with HLA Ags that correspond to high levels of DSA must be performed, then recipients should be treated for DSA to improve the chances of successful donor engraftment.
    Bone marrow transplantation 06/2011; 47(4):508-15. · 3.00 Impact Factor
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    ABSTRACT: Graft failure is a major concern after cord blood transplantation (CBT) or HLA-haploidentical transplantation (haplo-SCT). As patients who undergo CBT or haplo-SCT almost always lack both matched-related and -unrelated donors, salvage transplantation would also be limited to either CBT or haplo-SCT. In this study, we assessed eight patients who received haplo-SCT as salvage therapy for graft failure. Five and three patients had received haplo-SCT and CBT, respectively, which resulted in graft failure. The median interval from the failed transplantation to salvage transplantation in six patients with primary graft failure was 33.5 days. The reduced-intensity conditioning regimen consisted of fludarabine, thiotepa, rabbit antithymocyte globulin and low-dose TBI. All eight patients achieved neutrophil engraftment, and seven patients achieved platelet recovery. The median times to neutrophil recovery and platelet recovery were 10 and 20 days, respectively. Three patients died from treatment-related causes: two from GVHD and one from rupture of carotid artery aneurysm. Five patients are alive, at a median follow-up of 946 days. The probability of overall survival at 5 years was 75%. These findings may serve as a rationale for giving precedence to haplo-SCT over CBT in salvage SCT after graft failure.
    Bone marrow transplantation 04/2011; 47(3):369-73. · 3.00 Impact Factor
  • Biology of Blood and Marrow Transplantation 02/2011; 17(2). · 3.35 Impact Factor
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    ABSTRACT: Two promoter polymorphisms of the high-affinity IgE receptor alpha-subunit (FcepsilonRIalpha) gene (FCER1A), -66T>C (rs2251746) and -315C>T (rs2427827), were analysed in Japanese atopic dermatitis subjects. Patients with the -315CT/TT genotype tended to have higher total serum IgE levels, while the proportion of -315CT/TT genotype or the -315T allele was significantly higher in those with highly elevated total serum IgE concentrations.
    International Journal of Immunogenetics 02/2010; 37(2):139-41. · 1.34 Impact Factor
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    ABSTRACT: We investigated the efficacy and safety of cyclosporine A (CsA; targeted serum trough level: 80-150 ng/ml) in a daily clinical practice for treating patients with systemic lupus erythematosus (SLE), who had been, or were expected to be, refractory to glucocorticoids (GCs) and other immunosuppressants. Fifty-nine patients with SLE receiving CsA were observed for at least 6 months (21.5 months on average). A significant reduction of proteinuria was noted 2 weeks after initiation of treatment in patients with nephritis, resulting in a clinical response in five of eight patients in the GC dose-up group and 11 of 18 patients in the stable GC dose group, respectively. Notably, the mean score for disease activity on the SLE Disease Activity Index decreased significantly from 8.6 +/- 5.3 to 4.4 +/- 2.5 after CsA treatment in patients in the stable GC dose group (n = 40). Moreover, the mean flare rate decreased by approximately 60% with CsA. Side effects of CsA appeared in 32.2% of patients and all of them subsided through dose reduction or discontinuation (n=8) of CsA. Consequently, the cumulative 2-year survival rate of CsA was 75%. The results suggest that CsA should be considered for patients with SLE refractory to GCs.
    Lupus 12/2009; 19(2):162-9. · 2.48 Impact Factor
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    ABSTRACT: Epidermal hyperinnervation occurs in dermatoses with intractable pruritus, such as atopic dermatitis, suggesting that the hyperinnervation is partly responsible for abnormal itch perception. To investigate the mechanisms of penetration of sensory nerve fibres into the basement membrane of the skin. A rat dorsal root ganglion neurone culture system consisting of Matrigel and a Boyden chamber containing a nerve growth factor (NGF) concentration gradient was used. In some experiments, matrix metalloproteinase (MMP) blockers and semaphorin 3A (Sema3A) were added to the culture system. Matrigel-coated membranes were stained with anti-Tau antibody, and the number of nerve fibres that crossed the membrane was counted. Expression of MMPs in the cultured neurones was examined at mRNA and protein levels by quantitative reverse transcription-polymerase chain reaction and immunocytochemistry, respectively. The activity was also examined by zymography. Nerve fibres penetrated into Matrigel in the presence of an NGF concentration gradient, which was dose-dependently inhibited by GM6001, a broad-spectrum MMP inhibitor. Transcripts for MMP2, but not MMP9, were increased in the cultured neurones, and the penetration was dose-dependently inhibited by MMP-2 blockers. MMP-2 and its activity were partially localized on the NGF-responsive growth cones. NGF also upregulated pro-MMP-2 activation molecules in the cultured neurones. Sema3A stimulation showed the opposite effects on these NGF-dependent events. Interestingly, MMP2 expression was modulated by extracellular matrix (ECM) substrates for this enzyme. Membrane-associated MMP-2 contributes to penetration of nerve fibres into Matrigel through modulation by axonal guidance molecules and/or ECM. These findings provide insight for understanding the development of intractable pruritus involving epidermal nerve density.
    British Journal of Dermatology 11/2009; 161(5):1028-37. · 3.76 Impact Factor
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    ABSTRACT: Low-affinity IgE receptor gene (FCER2) rs3760687 polymorphism was found to be associated with differential binding affinity of transcription factors Sp1 and Sp3 leading to altered transcriptional activity. Haplotypic interaction of functional FCER2 polymorphisms (rs28364072, rs2228137 and rs3760687) might potentially provide a background for genotype-phenotype associations previously observed for some rather non-functional FCER2 variants.
    Tissue Antigens 10/2009; 74(6):534-8. · 2.35 Impact Factor

Publication Stats

9k Citations
1,491.53 Total Impact Points


  • 1995–2013
    • Tokyo Institute of Technology
      • Department of Physics
      Edo, Tōkyō, Japan
  • 2008–2011
    • Hyogo College of Medicine
      • Department of Internal Medicine
      Nishinomiya, Hyōgo, Japan
  • 2009
    • Saitama Medical University
      • Saitama Medical Center
      Saitama, Saitama-ken, Japan
  • 1979–2009
    • Juntendo University
      • • Department of Medicine
      • • Atopy (Allergy) Research Center
      • • Department of Dermatology
      Tokyo, Tokyo-to, Japan
  • 1979–2008
    • National Institute of Radiological Sciences
      • Research Center for Charged Particle Therapy
      Tiba, Chiba, Japan
  • 2007
    • Tokyo Medical University
      • Division of Dermatology
      Edo, Tōkyō, Japan
  • 1920–2007
    • Saga University
      • • Department of Electrical & Electronic Engineering
      • • Synchrotron Light Application Center
      Сага Япония, Saga, Japan
  • 2003–2006
    • Osaka City University
      • Department of Neurosurgery
      Ōsaka, Ōsaka, Japan
    • National Institute of Advanced Industrial Science and Technology
      Tsukuba, Ibaraki, Japan
    • Hiroshima Institute of Technology
      Hirosima, Hiroshima, Japan
  • 1998–2003
    • RIKEN
      • Nishina Center for Accelerator-Based Science (RNC)
      Вако, Saitama, Japan
    • Tokyo Metropolitan Institute of Gerontology
      Edo, Tōkyō, Japan
  • 2002
    • Shanghai Jiao Tong University
      • Department of Physics
      Shanghai, Shanghai Shi, China
  • 2001
    • Kinki University
      • Faculty of Agriculture
      Ōsaka-shi, Osaka-fu, Japan
  • 1998–2001
    • Kyoto Prefectural University of Medicine
      • Department of Cell Biology
      Kioto, Kyōto, Japan
  • 2000
    • Aichi Medical University
      • Division of Internal Medicine
      Okazaki, Aichi, Japan
    • Chiba University
      Tiba, Chiba, Japan
    • Meiji Pharmaceutical University
      Edo, Tōkyō, Japan
  • 1997
    • Tokyo Metropolitan Tama Medical Center
      Edo, Tōkyō, Japan
    • Kagoshima University
      Kagosima, Kagoshima, Japan
  • 1992–1995
    • Osaka University
      • Department of Biological Sciences
      Ōsaka-shi, Osaka-fu, Japan
  • 1994
    • Takamatsu Red Cross Hospital
      Takamatu, Kagawa, Japan
    • Tokyo Gakugei University
      Koganei, Tōkyō, Japan
  • 1993
    • Kyoto University
      • Department of Dermatology
      Kyoto, Kyoto-fu, Japan
    • Kobe University
      • Department of Chemistry
      Kōbe, Hyōgo, Japan
  • 1987
    • Catholic University of Korea
      • Department of Dermatology
      Sŏul, Seoul, South Korea