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HASHIRAMOTO AkiraGraduate School of Health Sciences / Faculty of Health SciencesProfessor
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■ Paper- The IL-5 inhibitor mepolizumab is beneficial in eosinophilic granulomatosis with polyangiitis (EGPA), and the inhibition of antineutrophil cytoplasmic antibody (ANCA) production has been suggested as a possible mechanism. We herein report a 78-year-old Japanese man with EGPA who received solo mepolizumab 300 mg twice for elevated ANCA levels, which led to subsequent GC discontinuation after achieving remission. The patient was able to be freed from the adverse events associated with long-term GC treatment, and the sole addition of mepolizumab also proved that mildly elevated ANCA could be converted to a negative result, thus leading to GC discontinuation.Oct. 2024, Internal medicine (Tokyo, Japan), English, Domestic magazineScientific journal
- (一社)日本認知症学会, Oct. 2024, Dementia Japan, 38(4) (4), 678 - 678, Japaneseアルツハイマー病マーカーと連動する脳脊髄液・血漿中炎症性マイクロRNAの同定
- (一社)日本認知症学会, Oct. 2024, Dementia Japan, 38(4) (4), 704 - 704, Japanese認知機能低下を予測する因子としての血漿中マイクロRNA測定の意義
- OBJECTIVES: For appropriate glucocorticoid (GC) reduction, we investigated the optimal strategy including baseline factors that could reduce GC more than 50% with 96 weeks of belimumab. METHODS: This is a retrospective cohort study of Kakogawa Central City hospital from 2019 to 2023. We identified SLE patients who were receiving 200 mg of belimumab weekly by subcutaneous injection for 96 weeks. The background at baseline, trends in clinical indicators, and factors involved in GC reduction were statistically analyzed. Finally, univariate and multivariate logistic analyses were carried out to identify baseline factors associated ≥50% GC reduction at 96 weeks. RESULTS: Forty-seven patients were enrolled, with a median daily prednisolone of 5 mg. Almost 90% of them received concomitant immunosuppressants and/or hydroxychloroquine. Serological indices, daily GC dose, and SLEDAI-2K scores showed significant improvement in 96 weeks. At baseline, a significant negative correlation has been shown between the daily dose of GC and the duration from onset or last flare, as well as C4 levels. At 96 weeks, GC reduction rate and SLEDAI-2K scores were negatively correlated with duration from onset or last flare to initiation of belimumab. Mycophenolate mofetil use was significantly frequent in patients with lupus nephritis (LN), which also correlated with the frequency of past flares. In addition, LN presence was associated with higher SLEDAI-2K scores at 96 weeks, and baseline SLEDAI-2K ≥10 was associated with significantly higher GC dose at 96 weeks. Univariate analysis of the factor contributing to achieving ≥50% GC reduction at 96 weeks has pointed shorter disease duration and higher daily GC dose at baseline as significant variables. Finally, we performed a multivariate analysis by combining above two items with age, which extracted the higher daily GC dose at baseline as a significant variable (OR (95% CI) 1.25 (1.00 to 1.56), p = .047). CONCLUSIONS: Our study showed that a delay in belimumab initiation led to higher SLEDAI-2K score and difficulty in achieving a 50% GC reduction at 96 weeks. Since GC-related adverse events increase with long-term administration of GC though with small daily doses, we proposed here that belimumab should be started in combination with higher daily prednisolone.May 2024, Lupus, 33(6) (6), 598 - 607, English, International magazineScientific journal
- (一社)日本リウマチ学会, Mar. 2024, 日本リウマチ学会総会・学術集会プログラム・抄録集, 68回, 544 - 544, Japaneseリウマチ学の基礎研究1 時計遺伝子Bmal1はNF-κB転写活性を促進してRA-FLSにおける炎症性メディエーターの産生を制御する
- (一社)日本リウマチ学会, Mar. 2024, 日本リウマチ学会総会・学術集会プログラム・抄録集, 68回, 712 - 712, Japanese時計制御遺伝子Tefは細胞周期調節因子を介して細胞増殖活性を制御する
- OBJECT: To clarify the involvement of clock genes in the production of inflammatory mediators from RA-FLS, we examined the role of Bmal1, one of the master clock genes. METHODS: RA-FLSs were stimulated with IL-1β (0, 20 ng/mL), IL-6 (0, 20 ng/mL), IL-17 (0, 20 ng/mL), TNF-α (0, 20 ng/mL) or IFN-γ (0, 20 ng/mL) to examine the expression of Bmal1, MMP-3, CCL2, IL-6, IL-7 and IL-15 by qPCR and immunofluorescence staining. After silencing Bmal1, RA-FLSs were stimulated with IL-1β (0, 20 ng/mL), TNF-α (0, 20 ng/mL) or IFN-γ (0, 20 ng/mL) to examine the expressions of inflammatory mediators; MMP-3, CCL2, IL-6 and IL-15 by qPCR, ELISA and immunofluorescence staining. RESULTS: Bmal1 expressions were increased by IL-1β, TNF-α and IFN-γ stimulations. Under stimulations with TNF-α, IL-1β, and IFN-γ, mRNA and protein expressions of MMP-3, CCL2 and IL-6 were suppressed by siBmal1. CONCLUSION: Results indicate that Bmal1 contributes the production of MMP-3, CCL2, and IL-6 from RA-FLS, implying Bmal1 is involved in the pathogenesis of RA by regulating the inflammation.Nov. 2023, Biochemical and biophysical research communications, 691, 149315 - 149315, English, International magazineScientific journal
- (一社)日本認知症学会, Oct. 2023, Dementia Japan, 37(4) (4), 667 - 667, Japanese当院におけるMCIの背景病理についての検討
- (一社)日本認知症学会, Oct. 2023, Dementia Japan, 37(4) (4), 672 - 672, JapaneseMCIの背景病理による患者本人および家族の困りごとの違い
- (一社)日本認知症学会, Oct. 2023, Dementia Japan, 37(4) (4), 686 - 686, Japaneseアルツハイマー病を鑑別する上での血漿中炎症性マイクロRNA測定の意義
- (一社)日本認知症学会, Oct. 2023, Dementia Japan, 37(4) (4), 696 - 696, JapaneseMCIの背景病理による髄液バイオマーカー,脳形態画像,脳血流画像の検討
- (一社)日本認知症学会, Oct. 2023, Dementia Japan, 37(4) (4), 706 - 706, JapaneseAPOEε4アリルが脳脊髄液/血漿中の炎症性マイクロRNA発現量に及ぼす影響
- Endogenous DNA is released into the bloodstream as cell-free DNA (cfDNA) following cell death and is associated with various pathological conditions. However, their association with therapeutic drugs against rheumatoid arthritis (RA) remains unknown. Therefore, we investigated the significance of cfDNA in RA treated with tocilizumab and tumour necrosis factor inhibitor (TNF-I). Biological DMARDs (bDMARDs), including tocilizumab and TNF-I, were administered to 77 and 59 RA patients, respectively. Plasma cfDNA levels were measured at weeks 0, 4, and 12 by quantitative polymerase chain reaction. Disease activity was evaluated at the same time point using DAS28ESR. cfDNA levels from RA synovial cells treated with tocilizumab or etanercept for 24 h were measured. Human toll-like receptor 9 (hTLR9)-expressing HEK293 cells, which release secreted embryonic alkaline phosphatase (SEAP) upon NF-κB activation, were stimulated by cfDNA from RA patients, and subsequently, SEAP levels were determined. NF-κB translocation was evaluated by immunofluorescence staining with or without tocilizumab. The DAS28ESR significantly improved in both bDMARD groups at week 12. However, plasma cfDNA levels significantly decreased in the tocilizumab group at week 12 compared to that in week 0. cfDNA levels correlated with DAS28ESR in biological treatment-naïve patients administered tocilizumab. cfDNA levels in synovial cells were significantly suppressed by tocilizumab treatment and unaltered with etanercept. HEK293 cells released SEAP upon cfDNA stimulation, and the observed NF-κB nuclear translocation was suppressed by tocilizumab. Tocilizumab suppressed inflammation via the TLR9 pathway by decreasing cfDNA levels. Regulation of cfDNA may be a therapeutic target for RA.Jul. 2023, Clinical and experimental immunology, 213(2) (2), 209 - 220, English, International magazineScientific journal
- Abstract Objectives To investigate the efficacy of mepolizumab in patients with eosinophilic granulomatosis with polyangiitis (EGPA) and factors contributing to glucocorticoid (GC) discontinuation. Methods We retrospectively studied EGPA patients treated with mepolizumab who were on GC at the time of induction of mepolizumab, at Japanese single center as of January 2023. Patients were classified into those who were able to discontinue GC at the time of the investigation (GC-free group) and those who continued (GC-continue group). Patient characteristics at the time of EGPA diagnosis (age, gender, absolute eosinophil counts, serum CRP level, serum IgE level, Rheumatoid factor (RF) / anti-neutrophil cytoplasmic antibody (ANCA) positivity, presence of asthma, affected organ, Five factor score (FFS), Birmingham Vasculitis Activity Score (BVAS) and characteristics at the time of mepolizumab induction (daily prednisolone dose, concomitant immunosuppressive maintenance therapy at the mepolizumab induction, prior history of GC pulse therapy, concomitant immunosuppressive therapy for remission induction,), history of relapse before mepolizumab induction and the duration of mepolizumab treatment were compared. We also followed the clinical indicators (absolute eosinophil counts, CRP and IgE levels, BVAS, Vascular Damage Index (VDI)) and daily prednisolone dosage at the EGPA diagnosis, at the mepolizumab induction and at the survey. Results Twenty-seven patients were included in the study. At the time of the study, patients had received mepolizumab for median 31 months (IQR, 26 to 40), the daily prednisolone dose was median 1 mg (IQR, 0 to 1.8) and GC-free was achieved in 13 patients (48%). Among clinical indicators that have improved by conventional therapy before the induction of mepolizumab, eosinophil counts, GC doses and BVAS have successively shown significant reductions throughout the observation period both GC-free and GC-continue. Of the GC-free patients, 7 were ANCA positive and 12 had FFS1 or more. Univariate analysis showed that the absolute eosinophil counts at diagnosis was significantly higher in the GC-free group (median 8165/µl (IQR, 5138 to 13,409) vs. 4360/µl (IQR, 151 to 8380), P = 0.037) and significantly fewer patients presented with gastrointestinal lesions (2 (15%) vs. 8 (57%), P = 0.025), while multivariate analysis showed no significant differences. Mepolizumab treatment significantly improved VDI in the GC-continue group (P = 0.004). Conclusions After three years of treatment with mepolizumab, approximately 50% of patients with EGPA achieved GC-free status. GC could be discontinued even in severe cases and ANCA-positive cases. Although multivariate analysis did not extract any significant factors contributing to achieving GC-free, we found that improvement in eosinophil counts and BVAS led to GC reduction, resulted in protection of organ damages in both the GC-free and continuation groups. The significance of achieving GC-free remission in EGPA patients was demonstrated.Last, Springer Science and Business Media LLC, Jun. 2023, Arthritis Research & Therapy, 25(1) (1), English[Refereed]Scientific journal
- Rationale: Chronic eosinophilic pneumonia (CEP) presents eosinophil infiltrations in the lung due to allergic reactions. Most CEP patients continue to take glucocorticoids, and their prolonged use induces various side effects. In this case report, based on the efficacy of baricitinib in patients with rheumatoid arthritis (RA) and CEP, we aimed to show that the administration of Janus kinase (JAK) inhibitors, when RA is complicated by an allergic disease, can stabilize the disease state and help avoid the adverse effects of long-term systemic glucocorticoid administration. Patients concerns: A 56-year-old woman developed RA at the age of 19 years. Treatment of the arthritis was initiated, but the joint destruction had progressed. At the age of 42, she developed eosinophilic pneumonia, which was relieved by glucocorticoid therapy. Since then, maintenance therapy has been continued with the diagnosis of CEP. She was treated with concomitant tacrolimus for persistent arthritis, and the prednisolone (PSL) dose was reduced to 3 mg/day after 10 years. However, around this time, an increase in peripheral blood eosinophil counts and respiratory symptoms was observed. Diagnosis: The peripheral blood eosinophil count was 4000/µL and computed tomography revealed multiple ground-glass opacities in the peripheral lung fields. As interstitial pneumonia due to infection or other causes was ruled out, CEP relapse was diagnosed. Interventions: Pneumonia rapidly recovered when the PSL dose was increased to 15 mg/day, and asymptomatic eosinophilic infiltrates reappeared in the lung field along with a relapse of arthritis when the PSL dose was reduced to 5 mg/day. Concomitant use of methotrexate and baricitinib has been introduced to suppress allergic reactions to pneumonia. Outcomes: After starting combination therapy with baricitinib and methotrexate, both arthritis and eosinophilia improved, and glucocorticoid-free remission was achieved. Lessons: Recently, inhibition of IL-5 signaling via JAK2 has been reported to be effective in bronchial asthma and atopic dermatitis. Although complications of RA and CEP are not common, the actions of baricitinib are useful not only in arthritis but also in allergic diseases. The efficacy of some JAK inhibitors should be actively tested in patients with RA and these complications.Last, Ovid Technologies (Wolters Kluwer Health), Mar. 2023, Medicine, 102(13) (13), e33396 - e33396, English[Refereed]Scientific journal
- (一社)日本リウマチ学会, Mar. 2023, 日本リウマチ学会総会・学術集会プログラム・抄録集, 67回, 616 - 616, Japaneseリウマチ性疾患の基礎研究-2 時計制御遺伝子Tefは細胞増殖活性とTNFα産生を制御する
- (一社)日本リウマチ学会, Mar. 2023, 日本リウマチ学会総会・学術集会プログラム・抄録集, 67回, 766 - 766, JapaneseRA滑膜細胞におけるTNFα誘導性Tef遺伝子発現低下のメカニズム 3'UTR結合miRNAを対象とした研究
- (一社)日本リウマチ学会, Mar. 2023, 日本リウマチ学会総会・学術集会プログラム・抄録集, 67回, 812 - 812, Japanese時計遺伝子Bmal1はRA-FLSの炎症性メディエーター発現を制御する
- (一社)日本リウマチ学会, Mar. 2022, 日本リウマチ学会総会・学術集会プログラム・抄録集, 66回, 340 - 340, Japaneseリウマチ性疾患のヒト免疫研究 時計制御遺伝子TefはRA滑膜細胞の増殖に関与する
- (一社)日本リウマチ学会, Mar. 2022, 日本リウマチ学会総会・学術集会プログラム・抄録集, 66回, 340 - 340, Japaneseリウマチ性疾患のヒト免疫研究 C646はROREを介してTNFα誘導性CCL2発現による細胞遊走および細胞骨格形成を抑制する
- (一社)日本リウマチ学会, Mar. 2022, 日本リウマチ学会総会・学術集会プログラム・抄録集, 66回, 419 - 419, JapaneseBioの関節破壊抑制や大関節への効果・その他 関節リウマチ患者における細胞外遊離DNAの検討 トシリズマブとTNF阻害薬の比較
- (一社)日本リウマチ学会, Mar. 2022, 日本リウマチ学会総会・学術集会プログラム・抄録集, 66回, 570 - 570, Japanese時計遺伝子Bmal1はRA滑膜細胞の炎症性メディエーター産生を制御する
- Last, 2022, 医学のあゆみ, 281, 180体内時計による関節リウマチの制御
- Aug. 2021, 22(16) (16), 8941Cell-Free DNA in Rheumatoid Arthritis.[Refereed]
- (一社)日本リウマチ学会, Mar. 2021, 日本リウマチ学会総会・学術集会プログラム・抄録集, 65回, 546 - 546, Japanese時計制御遺伝子Tefは細胞周期調節因子を介してRA滑膜細胞の増殖を制御する
- (一社)日本リウマチ学会, Mar. 2021, 日本リウマチ学会総会・学術集会プログラム・抄録集, 65回, 547 - 547, JapaneseIL-6は時計遺伝子PAR-bZIPを介して関節リウマチ滑膜細胞に細胞死抵抗性をもたらす
- (一社)日本リウマチ学会, Mar. 2021, 日本リウマチ学会総会・学術集会プログラム・抄録集, 65回, 548 - 548, Japanese時計遺伝子Bmal1を介したRA滑膜細胞の炎症性メディエーター産生
- (一社)日本リウマチ学会, Aug. 2020, 日本リウマチ学会総会・学術集会プログラム・抄録集, 64回, 551 - 551, JapaneseTNFα誘導性CCL2は転写因子RORα/REV-ERBα、ヒストンアセチル化酵素CBP/p300を介してRA滑膜細胞の遊走に関与する
- (一社)日本リウマチ学会, Aug. 2020, 日本リウマチ学会総会・学術集会プログラム・抄録集, 64回, 649 - 649, JapaneseJAK阻害剤Baricitinibを用いた薬物時間療法はマウス関節炎を効果的に抑制する
- (一社)日本リウマチ学会, Aug. 2020, 日本リウマチ学会総会・学術集会プログラム・抄録集, 64回, 705 - 705, JapaneseIL-6はミトコンドリア内因性経路を介して関節リウマチ滑膜細胞に細胞死抵抗性をもたらす
- (一社)日本リウマチ学会, Aug. 2020, 日本リウマチ学会総会・学術集会プログラム・抄録集, 64回, 706 - 706, JapaneseIL-6、TNF-α刺激によるRA滑膜細胞の増殖は時計制御遺伝子Tefによって制御される
- Corresponding, May 2020, Int Immunopharmacol, EnglishChronotherapy targeting cytokine secretion attenuates collagen-induced arthritis in mice[Refereed]Scientific journal
- Jan. 2020, Front Immunol, 12(801897) (801897), EnglishIncreased Circulating Cell-Free DNA in Eosinophilic Granulomatosis With Polyangiitis: Implications for Eosinophil Extracellular Traps and Immunothrombosis[Refereed]Scientific journal
- Corresponding, Sep. 2019, Scandinavian Journal of Rheumatology, 48(5) (5), 353 - 361, EnglishInterleukin-6 and tumour necrosis factor-α cooperatively promote cell cycle regulators and proliferate rheumatoid arthritis fibroblast-like synovial cells.[Refereed]Scientific journal
- The cause of systemic lupus erythematosus (SLE) is unknown. IFN-α has been suggested as a causative agent of SLE; however, it was not proven, and to what extent and how IFN-α contributes to the disease is unknown. We studied the contribution of IFN-α to SLE by generating inducible IFN-α transgenic mice and directly show that conditional upregulation of IFN-α alone induces a typical manifestation of SLE in the mice not prone to autoimmunity, such as serum immune complex, autoantibody against dsDNA (anti-dsDNA Ab), and the organ manifestations classical to SLE, such as immune complex-deposited glomerulonephritis, classical splenic onion-skin lesion, alopecia, epidermal liquefaction, and positive lupus band test of the skin. In the spleen of mice, activated effector CD4 T cells, IFN-γ-producing CD8 T cells, B220+CD86+ cells, and CD11c+CD86+ cells were increased, and the T cells produced increased amounts of IL-4, IL-6, IL-17, and IFN-γ and decreased IL-2. In particular, activated CD3+CD4-CD8- double-negative T cells positive for TCRαβ, B220, CD1d-teteramer, PD-1, and Helios (that produced increased amounts of IFN-γ, IL-4, IL-17, and TNF-α) were significantly expanded. They infiltrated into kidney and induced de novo glomerulonephritis and alopecia when transferred into naive recipients. Thus, sole upregulation of IFN-α is sufficient to induce SLE, and the double-negative T cells expanded by IFN-α are directly responsible for the organ manifestations, such as lupus skin disease or nephritis.Aug. 2019, J Immunol, 203(4) (4), 835 - 843, English, International magazine[Refereed]Scientific journal
- Corresponding, May 2019, Modern Rheumatology, (2) (2), 1 - 8, EnglishExpressions of circadian clock genes represent disease activities of RA patients treated with biological DMARDs.[Refereed]Scientific journal
- (一社)日本リウマチ学会, Mar. 2019, 日本リウマチ学会総会・学術集会プログラム・抄録集, 63回, 446 - 446, Japaneseリウマチ性疾患の基礎研究-1 関節リウマチモデルマウスにおけるJAK阻害剤を用いた時間治療の検討
- (一社)日本リウマチ学会, Mar. 2019, 日本リウマチ学会総会・学術集会プログラム・抄録集, 63回, 489 - 489, Japanese関節リウマチの治療評価と予測-2 生物学的製剤治療が関節リウマチ患者白血球における時計遺伝子発現を変動させる
- (一社)日本リウマチ学会, Mar. 2019, 日本リウマチ学会総会・学術集会プログラム・抄録集, 63回, 603 - 603, Japanese滑膜細胞におけるTNFα誘導性CCL2発現増加に対するヒストンアセチル化酵素と転写因子RORα/REV-ERBαの役割
- (一社)日本リウマチ学会, Mar. 2019, 日本リウマチ学会総会・学術集会プログラム・抄録集, 63回, 604 - 604, JapaneseIL-6は時計遺伝子Hlfを介して関節リウマチ滑膜細胞に細胞死抵抗性をもたらす
- Corresponding, BioMed Central Ltd., Mar. 2018, Arthritis Research and Therapy, 20(1) (1), 55, English[Refereed]Scientific journal
- (一社)日本リウマチ学会, Mar. 2018, 日本リウマチ学会総会・学術集会プログラム・抄録集, 62回, 539 - 539, Japaneseリウマチ性疾患の基礎研究2 IL-6とTNFαは細胞周期調節因子を介して協調的に滑膜細胞増殖に関与する
- (一社)日本リウマチ学会, Mar. 2018, 日本リウマチ学会総会・学術集会プログラム・抄録集, 62回, 706 - 706, JapaneseTNF-αはc-Mycを介してリウマチ滑膜細胞のp27Kip発現を変化させる
- (一社)日本リウマチ学会, Mar. 2018, 日本リウマチ学会総会・学術集会プログラム・抄録集, 62回, 779 - 779, Japanese時計遺伝子Bmal1は細胞周期調節因子を介して関節リウマチ滑膜細胞の増殖能を制御する
- (一社)日本リウマチ学会, Mar. 2018, 日本リウマチ学会総会・学術集会プログラム・抄録集, 62回, 782 - 782, JapaneseIL-6は時計遺伝子を介して滑膜細胞に細胞死抵抗性をもたらす
- Corresponding, Elsevier B.V., Jan. 2018, Biochemical and Biophysical Research Communications, 495(2) (2), 1675 - 1680, English[Refereed]Scientific journal
- Corresponding, 2018, J Transl Sci., 4(4) (4), 1, EnglishChronobiology of rheumatoid arthritis; now and future.[Refereed]Scientific journal
- Lead, American Society for Biochemistry and Molecular Biology Inc., 2018, Journal of Biological Chemistry, 293(6) (6), 1933 - 1943, English[Refereed]Scientific journal
- Corresponding, Jun. 2017, INTERNATIONAL JOURNAL OF RHEUMATIC DISEASES, 20(6) (6), 722 - 730, English[Refereed]Scientific journal
- (一社)日本リウマチ学会, Mar. 2017, 日本リウマチ学会総会・学術集会プログラム・抄録集, 61回, 589 - 589, Japaneseリウマチ性疾患の基礎研究/サイトカイン・ケモカイン 転写因子群PAR bZIPを介したメトトレキサートの新しい薬理作用
- (一社)日本リウマチ学会, Mar. 2017, 日本リウマチ学会総会・学術集会プログラム・抄録集, 61回, 711 - 711, Japanese時計遺伝子が滑膜細胞の細胞周期を調節する
- (一社)日本リウマチ学会, Mar. 2017, 日本リウマチ学会総会・学術集会プログラム・抄録集, 61回, 712 - 712, JapaneseIL-6とTNF-αが関節リウマチ滑膜細胞の細胞周期調節因子の発現を制御する
- (一社)日本リウマチ学会, Mar. 2017, 日本リウマチ学会総会・学術集会プログラム・抄録集, 61回, 713 - 713, JapaneseTNFαはヒストンアセチル化酵素を介してRA滑膜細胞内の時計遺伝子Bmal1発現を調節する
- (一社)日本リウマチ学会, Mar. 2017, 日本リウマチ学会総会・学術集会プログラム・抄録集, 61回, 804 - 804, JapaneseDNA integrity indexを用いたTCZの新しい薬理効果の検証
- (一社)日本リウマチ学会, Mar. 2017, 日本リウマチ学会総会・学術集会プログラム・抄録集, 61回, 589 - 589, Japaneseリウマチ性疾患の基礎研究/サイトカイン・ケモカイン リウマチ滑膜の低ミトコンドリア生合成は滑膜増殖を亢進させ関節破壊の誘導に寄与する[Refereed]
- Oct. 2016, ARTHRITIS & RHEUMATOLOGY, 68, EnglishDouble-Negative T (DNT) Cell over-Expressing PD-1 and Helios Is Responsible for Lupus Tissue Injury in Systemic Lupus Erythematosus (SLE): Direct Proof That Increased Interferon Alpha (IFN alpha) Expression Is Sufficient to Induce SLE in Ifn alpha-Transgenic Mice[Refereed]
- (一社)日本リウマチ学会, Mar. 2016, 日本リウマチ学会総会・学術集会プログラム・抄録集, 60回, 334 - 334, Japanese関節リウマチの治療 バイオマーカー RA滑膜細胞由来の遊離DNA産生はTCZにより制御される
- (一社)日本リウマチ学会, Mar. 2016, 日本リウマチ学会総会・学術集会プログラム・抄録集, 60回, 449 - 449, Japanese関節リウマチの治療評価と予測 関節リウマチ患者における血清遊離DNAの臨床的意義
- (一社)日本リウマチ学会, Mar. 2016, 日本リウマチ学会総会・学術集会プログラム・抄録集, 60回, 492 - 492, JapaneseCa2+イオンによる時計遺伝子発現リズムの制御
- (一社)日本リウマチ学会, Mar. 2016, 日本リウマチ学会総会・学術集会プログラム・抄録集, 60回, 492 - 492, JapaneseメトトレキサートがRA-FLSの時計遺伝子に与える影響
- (一社)日本リウマチ学会, Mar. 2016, 日本リウマチ学会総会・学術集会プログラム・抄録集, 60回, 489 - 489, Japaneseミトコンドリア生合成の亢進はコラーゲン誘導性関節炎(CIA)マウスの関節破壊を抑制する[Refereed]
- (一社)日本リウマチ学会, Mar. 2015, 日本リウマチ学会総会・学術集会プログラム・抄録集, 59回, 337 - 337, Japaneseリウマチ性疾患の基礎研究 IL-6は転写調節因子RORαに作用してRA滑膜細胞の時計遺伝子発現を調節する
- (一社)日本リウマチ学会, Mar. 2015, 日本リウマチ学会総会・学術集会プログラム・抄録集, 59回, 471 - 471, JapaneseCalcium signal伝達系を介したTNF-αによる時計遺伝子発現制御
- (一社)日本リウマチ学会, Mar. 2015, 日本リウマチ学会総会・学術集会プログラム・抄録集, 59回, 484 - 484, Japaneseトシリズマブ治療によるRA患者血清ccf-DNA量の変化と疾患活動性の相関
- (一社)日本リウマチ学会, Mar. 2015, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集 59回, 59回, 479 - 479, JapaneseRA滑膜細胞のミトコンドリア活性化は細胞増殖とMMP-3/RANKLの分泌を抑制する[Refereed]Research society
- 【目的】DNAは細胞傷害やアポトーシスにより末梢血中に放出される.近年,末梢血の遊離DNAがさまざまな疾患のバイオマーカーとして認識されてきているが,関節リウマチ(RA)患者においては,その意義は不明である.今回,RA患者に関して血清遊離DNAと疾患活動性の関連について調べたので報告する.【方法】当院で生物学的製剤を開始したRA患者21例について,投与前から24週まで4週おきに血液検査を行い,リアルタイムPCRを用いて血清遊離DNAを測定し,疾患活動性も同時に評価した.比較対象として,健常人10例でも血清遊離DNAを測定した.加えて,RA患者5例の膝関節液を採取し遊離DNAを測定した.【結果】生物学的製剤投与前のRA患者と健常人で,血清遊離DNAに差はなかった.継時的にみると,投与開始後12週までに遊離DNAが上昇する群(n = 10)と変化しない群(n = 11)に分かれた.2群を比較すると,遊離DNA上昇群では罹病期間が短く(P = 0.012),治療前疾患活動性(SDAI)が高かった(P = 0.041).またΔSDAI(P = 0.021),ΔCDAI(P = 0.027)も高く,疾患活動性が有意に改善していた.DNAは白血球にも含まれるが,この変化に差はなかった.関節液遊離DNAは著増していた.【結論】遊離DNAが血球系とは相関せず,関節液中で著増していたことを考慮すると,血清遊離DNAが滑膜細胞由来であることが示唆される.高疾患活動性のRA患者で遊離DNAが生物学的製剤の治療反応性を予測するマーカーとなるかもしれない.The Japan Society for Clinical Immunology, 2015, 日本臨床免疫学会会誌, 38(4) (4), 361a - 361a, Japanese
- Corresponding, 2015, International Journal of clinical rheumatology., 10(5) (5), 315 - 318, EnglishCircadian rhythm and joint stiffness/destruction in rheumatoid arthritis.[Refereed]Scientific journal
- (一社)日本リウマチ学会, Mar. 2014, 日本リウマチ学会総会・学術集会プログラム・抄録集, 58回, 661 - 661, JapaneseIL-6シグナルは関節リウマチ患者滑膜細胞の時計遺伝子発現を変化させる
- Corresponding, 2014, JOURNAL OF IMMUNOLOGY RESEARCH, 2014, 282495, English[Refereed]Scientific journal
- Corresponding, Nov. 2013, Modern Rheumatology, 23(6) (6), 1192 - 1197, English[Refereed]Scientific journal
- Jul. 2013, Journal of Immunology, 191(1) (1), 91 - 96, English[Refereed]Scientific journal
- (一社)日本リウマチ学会, Mar. 2013, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 57回・22回, 555 - 555, JapaneseTNFαは関節リウマチ滑膜細胞の時計遺伝子Per2発現量をD-box配列を介して抑制する
- Corresponding, 2013, Advances in Neuroimmune Biology, 4(1) (1), 7 - 11, English[Refereed]Scientific journal
- Corresponding, 2013, Scandinavian Journal of Rheumatology, 42(4) (4), 276 - 280, English[Refereed]Scientific journal
- Jan. 2013, TISSUE ANTIGENS, 81(1) (1), 44 - 45, English[Refereed]Scientific journal
- Jan. 2013, TISSUE ANTIGENS, 81(1) (1), 44 - 45, English[Refereed]Scientific journal
- Nov. 2012, ANNALS OF THE RHEUMATIC DISEASES, 71(11) (11), 1820 - 1826, English[Refereed]Scientific journal
- Oct. 2012, ARTHRITIS AND RHEUMATISM, 64(10) (10), S186 - S186, EnglishTNF alpha Modulates the Expression of Circadian Clock Gene, Per2, Via D-Box Motif in the Promoter Region in Rheumatoid Synovial Cells.[Refereed]
- Aug. 2012, ARTHRITIS CARE & RESEARCH, 64(8) (8), 1125 - 1134, English[Refereed]Scientific journal
- May 2012, JOURNAL OF IMMUNOLOGY, 188, EnglishAnti-U1C autoantibody interferes with the U1C-mediated splicing of both Ang1 and Tie2 genes in human pulmonary artery smooth muscle cells[Refereed]
- (一財)甲南病院, Apr. 2012, 甲南病院医学雑誌, 29, 44 - 47, Japanese皮膚筋炎に伴う急性間質性肺炎の3剖検例
- 2012, Kobe Journal of Medical Sciences, 58(2) (2), 41 - 50, EnglishA study on the selection of DMARDs for the combination therapy with adalimumab---E41-E50[Refereed]Scientific journal
- Oct. 2011, ARTHRITIS AND RHEUMATISM, 63(10) (10), S141 - S142, EnglishTNF alpha Modulates the Expression of Circadian Clock Genes in Rheumatoid Synovial Cells.[Refereed]
- Oct. 2011, ARTHRITIS AND RHEUMATISM, 63(10) (10), S444 - S444, EnglishInhibitory Effect of c-Fos/AP-1 Inhibitor T-5224 on the Levels of Cytokines and Chemokines in the Arthritic Lesion of Mice with Collagen-Induced Arthritis[Refereed]
- Oct. 2011, ARTHRITIS AND RHEUMATISM, 63(10) (10), S707 - S707, EnglishIL-6 and TNF-alpha Enhance the Expression of U1C and Affect the Splicing of Functional Defective Angiopoietin-1 (Ang1) Gene Mediated by Anti-U1C Antibody in the Patients with MCTD[Refereed]
- Oct. 2011, ARTHRITIS AND RHEUMATISM, 63(10) (10), 3058 - 3066, English[Refereed]Scientific journal
- Jul. 2011, JOURNAL OF RHEUMATOLOGY, 38(7) (7), 1258 - 1264, English[Refereed]Scientific journal
- (一社)日本リウマチ学会, Jun. 2011, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 55回・20回, 302 - 302, Japaneseアダリムマブ アダリムマブの治療成績と、併用抗リウマチ薬の検討
- Lead, May 2011, RHEUMATOLOGY, 50(5) (5), 852 - 861, English[Refereed]Scientific journal
- Apr. 2011, JOURNAL OF IMMUNOLOGY, 186, EnglishAnti-U1 autoantibody interferes with the U1RNP-mediated splicing of Angiopoietin-1 gene and induces functionally defective Ang-1/ins variant in the patients with MCTD[Refereed]
- Apr. 2011, JOURNAL OF IMMUNOLOGY, 186Lupus psychosis in IFN alpha transgenic mice[Refereed]
- Apr. 2011, JOURNAL OF IMMUNOLOGY, 186, EnglishInterferon alpha causes SLE by expanding CD4(-) CD8(-) double negative T cell[Refereed]
- Apr. 2011, ARCHIVUM IMMUNOLOGIAE ET THERAPIAE EXPERIMENTALIS, 59(2) (2), 89 - 95, English[Refereed]Scientific journal
- 血管新生因子Angiopoietin-1(Ang-1)は,ERK/MAPキナーゼ系とPI3キナーゼ/Akt系を介してリウマチ性疾患の病態形成に関与する.関節リウマチ滑膜細胞においては,Ang-1の刺激によってAktおよびNFκBの活性化がもたらされ,滑膜細胞のアポトーシス抵抗性獲得に寄与している.また,Ang-1はRhoファミリー低分子量GTP結合蛋白質群も活性化し,滑膜細胞の遊走能を亢進させて骨軟骨破壊を促進させる.一方,新規に同定された269Gry挿入型ANG-1蛋白は,肺血管内皮細胞のERK/MAPキナーゼ系の活性化とendtohelin-1産生亢進を介して混合性結合組織病や強皮症患者に合併する肺高血圧症の病因となることが示唆された.The Japanese Society for Clinical Rheumatology and Related Research, 2011, Clinical Rheumatology and Related Research, 23(1) (1), 11 - 15, Japanese
- (公社)日本生化学会, Dec. 2010, 日本生化学会大会・日本分子生物学会年会合同大会講演要旨集, 83回・33回, 3P - 1065, English混合性結合組織病(MCTD)患者における抗U1C自己抗体は血管新生因子Angiopoietin-1(Ang-1)スプライシングを攪乱する(Anti-U1RNP C autoantibody specifically interferes with the splicing of Angiopoietin-1 (Ang1) gene and induces functionally defective Ang-1/ins in the patients with mixed connective tissue disease)
- Last, Mar. 2010, EXPERT REVIEW OF CLINICAL IMMUNOLOGY, 6(2) (2), 181 - 183, English[Refereed]Scientific journal
- Lead, Feb. 2010, JOURNAL OF IMMUNOLOGY, 184(3) (3), 1560 - 1565, English[Refereed]Scientific journal
- The Japanese Society for Clinical Rheumatology and Related Research, 2010, Clinical Rheumatology and Related Research, 22(1) (1), 139 - 141, Japanese
- Lead, Dec. 2009, MODERN RHEUMATOLOGY, 19(6) (6), 637 - 642, English[Refereed]Scientific journal
- Adult-onset Still's disease (AOSD) is an inflammatory disease of unknown etiology. AOSD is typically characterized by a spiking fever, arthritis, rashes, leukocytosis, and involvement of various organs. We report a case of a 59-year-old Japanese male presenting rapid and progressive polyarthritis. He complained of bilateral knee joint pain and swelling of 3 months duration which was accompanied by a fever over 39°C for one month. On admission, he showed arthritis on bilateral MP, PIP, wrist, knee, and foot joints. X-ray study revealed distinct erosion of bilateral wrist joints and PIP joints even a few months after the disease onset. Laboratory tests showed CRP 8.95 mg/dl, FDP 14.0 μg/ml, and ferritin1 143 nm/ml. Rheumatoid factor, anti-CCP antibody or anti-nuclear antibody was negative. The patients' disease was diagnosed as AOSD because his clinical manifestation fulfilled the diagnostic criteria proposed by Cush et al. He was treated successfully with prednisolone and Methotrexate. Recently, anti-cytokine therapy was reported to be introduced for AOSD; i.e. anti-interleukin (IL)-6 receptor antibody or anti-IL-1 antibody, and serum IL-6 level was increased in this patient. We discussed the early progression of arthritic joint destruction in the wrists in a patient with AOSD. We propose that early intervention of arthritis may be useful for such conditions.The Japanese Society for Clinical Rheumatology and Related Research, Sep. 2009, 臨床リウマチ, 巻, 213, pp. 261-265(3) (3), 261 - 265, JapaneseScientific journal
- Sep. 2009, 炎症と免疫, 巻, 213, pp. 279-283(5) (5), Japanese自己免疫疾患における選択的スプライシング[Refereed]Scientific journal
- Aug. 2009, MODERN RHEUMATOLOGY, 19(4) (4), 416 - 419, English[Refereed]Scientific journal
- Behçet's disease (BD) is a systemic disease presenting oral and genital ulceration, other skin lesions, uveitis and manifestations affecting the blood vessels. Among those, entero-Behçet's disease is characterized by bowel inflammation with round and oval ulcers associated with gastro-entero-intestinal symptoms. BD is frequent in the Middle and Far East but is rare in the Europe and Western world, suggesting the contribution of a racial or genetic factor. Indeed, Human leukocyte antigen (HLA)-B 51 is a well-known genetic factor associated with BD. We report a case of a 25-year-old man with a 3-year history of entero-Behçet's disease having surgical treatment three times after the disease onset. This patient was introduced to our hospital presenting with melena and lower abdominal pain, while he has been treated with prednisone, colchicine, mesalazine and infliximab for 3 years. Laboratory test results on admission were as follows; WBC 14000/ml, Hb 9.8 g/ml, CRP 0.55 mg/dl, AST 30 U/ml, ALT 75 U/ml, total protein 5.2 g/dl and albumin 2.6 g/dl. After entering our hospital, despite an additional treatment of neutrophil apheresis (G-CAP) for 5 times, he underwent surgery twice owing to massive hematochezia and sature-failure due to long-term steroid usage. The efficacy and indication of steroid, biologics, neutrophil apheresis and surgical therapy for entero-Behçet's disease were discussed.The Japanese Society for Clinical Rheumatology and Related Research, Aug. 2009, 臨床リウマチ, 巻, 175, pp. 495-500(3) (3), 279 - 283, JapaneseScientific journal
- (一社)日本リウマチ学会, Mar. 2009, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 53回・18回, 172 - 172, English基礎 変異MICAは野生型MICAに比較してNK細胞からのIFNγ産生を増強する(Basic Mutant MICA enhances IFNγ production from NK cells as compared with wild type MICA)
- Sep. 2008, ARTHRITIS AND RHEUMATISM, 58(9) (9), S515 - S515, EnglishArthritis modulates biological clock: Cry directly regulates the transactivation, of TNF-alpha gene[Refereed]
- Sep. 2008, ARTHRITIS AND RHEUMATISM, 58(9) (9), S657 - S657, EnglishHsp 90 modulates actin filament rearrangement in rheumatoid synovial cell via IIk-dependent pathway[Refereed]
- Sep. 2008, ARTHRITIS AND RHEUMATISM, 58(9) (9), S660 - S660, EnglishVla-5 is an alternative receptor for angiopoietin-1/tie2 signaling via map kinase in rheumatoid synovial cells[Refereed]
- Sep. 2008, ARTHRITIS AND RHEUMATISM, 58(9) (9), S705 - S706, EnglishFull maturation of CD8+T cell[Refereed]
- Sep. 2008, ARTHRITIS AND RHEUMATISM, 58(9) (9), S841 - S841, EnglishInduction of autoantibody and autoimmune tissue injury is differentially regulated BCD4+ and CD8+ T cells[Refereed]
- Aug. 2008, JOURNAL OF IMMUNOLOGY, 181(3) (3), 1737 - 1745, EnglishLow- versus high-baseline epinephrine output shapes opposite innate cytokine profiles: Presence of Lewis- and Fischer-like neurohormonal immune phenotypes in humans?[Refereed]Scientific journal
- Aug. 2008, JOURNAL OF IMMUNOLOGY, 181(3) (3), 1737 - 1745, EnglishLow- versus high-baseline epinephrine output shapes opposite innate cytokine profiles: Presence of Lewis- and Fischer-like neurohormonal immune phenotypes in humans?Scientific journal
- Jul. 2008, NATURE BIOTECHNOLOGY, 26(7) (7), 817 - 823, English[Refereed]Scientific journal
- Mar. 2008, JOURNAL OF RHEUMATOLOGY, 35(3) (3), 414 - 420, EnglishEasy and accurate diagnosis of rheumatoid arthritis using anti-cyclic citrullinated peptide 2 antibody, swollen joint count, and C-reactive protein/rheumatoid factor[Refereed]Scientific journal
- The Japanese Society for Clinical Rheumatology and Related Research, 2008, Clinical Rheumatology and Related Research, 20(3) (3), 171 - 175, Japanese
- Lead, Jul. 2007, ARTHRITIS AND RHEUMATISM, 56(7) (7), 2170 - 2179, English[Refereed]Scientific journal
- Apr. 2007, ARTHRITIS AND RHEUMATISM, 56(4) (4), 1067 - 1075, English[Refereed]Scientific journal
- (NPO)日本免疫学会, Nov. 2006, 日本免疫学会総会・学術集会記録, 36, 289 - 289, English関節リウマチ〜臨床解析と新治療 リウマチ線維芽細胞様滑膜細胞においてアンギオポエチン-1はVLA-5(α5β1インテグリン)を介してMAPキナーゼを活性化させる(Angiopoietin-1 activates MAP kinases via VLA-5 (α5β1 integrin) in rheumatoid fibroblast-like synoviocytes)
- Sep. 2006, ARTHRITIS AND RHEUMATISM, 54(9) (9), S232A novel small molecule AP-1 inhibitor T-5224 resolves mouse type II collagen-induced arthritis in a c-Fos/AP-1-Specific fashion.[Refereed]
- Sep. 2006, ARTHRITIS AND RHEUMATISM, 54(9) (9), S355Once-anergized T cell in autoimmune-prone MRL/Ipr mice cannot be reactivated from anergy and generate autoantibodies after repeated priming with exogenous antigen.[Refereed]
- Sep. 2006, ARTHRITIS AND RHEUMATISM, 54(9) (9), S358Therapeutic efficacy of a novel small molecule AP-1 inhibitor T-5224 on collagen-induced arthritis in mice: Characterization of antiarthritic effect directly inhibiting IL-1 ss and matrix degrading MMPs.[Refereed]
- Sep. 2006, ARTHRITIS AND RHEUMATISM, 54(9) (9), S751 - S752, EnglishDistribution of apoptosis-inducing death receptor 3 (DR3) and Fas is significantly different among T cell subsets: DR3+ naive CD8+ T cell population is contracted in patients with rheumatoid arthritis.[Refereed]
- Sep. 2006, ARTHRITIS AND RHEUMATISM, 54(9) (9), S812 - S812, EnglishAngiopoietin-1 acts onto alpha 5 beta 1 integrin (VLA-5) to activate MAP kinases in rheumatoid synovial cells.[Refereed]
- Jun. 2006, ANNALS OF THE RHEUMATIC DISEASES, 65(6) (6), 721 - 727, English[Refereed]Scientific journal
- Jun. 2006, ONCOGENE, 25(28) (28), 3948 - 3955, EnglishScientific journal
- Jun. 2006, ANNALS OF THE RHEUMATIC DISEASES, 65(6) (6), 721 - 727, EnglishScientific journal
- (一社)日本リウマチ学会, Mar. 2006, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 50回・15回, 137 - 137, Japanese全身性エリテマトーデスの病因・病態/全身性エリテマトーデスのシグナル伝達異常 SLEにおけるDR3プロモータ領域DNAのメチル化
- (一社)日本リウマチ学会, Mar. 2006, 日本リウマチ学会総会・学術集会抄録集, pp.137-137, 139 - 139, Japanese全身性エリテマトーデスの病因・病態/全身性エリテマトーデスのシグナル伝達異常 SLEにおけるDR3プロモータ領域DNAのメチル化International conference proceedings
- (一社)日本リウマチ学会, Mar. 2006, 日本リウマチ学会総会・学術集会抄録集, pp.176-176, 176 - 176, Japanese関節リウマチの臨床 リウマチ性疾患患者の不安と抑鬱状態の評価International conference proceedings
- (一社)日本リウマチ学会, Mar. 2006, 日本リウマチ学会総会・学術集会抄録集, pp.106-106, 106 - 106, Japanese関節リウマチの治療 メトトレキサートとレフルノミド 当科におけるレフルノミドの使用成績と,中止後の治療方法の検討International conference proceedings
- Mar. 2006, 日本リウマチ学会総会・学術集会抄録集, pp.241-241, Japanese関節リウマチの関節破壊機序 Angiopoietin-1(Ang-1)は関節リウマチの軟骨破壊を促進するInternational conference proceedings
- (一社)日本リウマチ学会, Mar. 2006, 日本リウマチ学会総会・学術集会抄録集, pp.194-194, 194 - 194, Japanese滑膜増殖と制御 関節リウマチ滑膜細胞におけるdecoy receptor 3の機能解析International conference proceedings
- (一社)日本リウマチ学会, Mar. 2006, 日本リウマチ学会総会・学術集会抄録集, pp.218-218, 218 - 218, Japaneseリウマチ性疾患の病因としての微生物感染/リウマチ性疾患の遺伝子解析 関節リウマチ患者における変異型death receptor 3(DR3)遺伝子の頻度 日本人および韓国人2,480例の遺伝調査International conference proceedings
- (一社)日本リウマチ学会, Mar. 2006, 日本リウマチ学会総会・学術集会抄録集, pp.293-293, 293 - 293, Japaneseステロイドによる特発性大腿骨頭壊死症に及ぼすスタチンの作用についての前向き研究International conference proceedings
- Mar. 2006, ARTHRITIS AND RHEUMATISM, 54(3) (3), 779 - 787, English[Refereed]Scientific journal
- Serum levels and pharmacodynamics of methotrexate and its metabolite 7-hydroxymethotrexate in Japanese patients with rheumatoid arthritis treated with 2-mgcapsule of methotrexate three times per week.Methotrexate (MTX) is the first-choice drug for rheumatoid arthritis (RA); however, the pharmacodynamics of MTX in Japanese patients with RA treated legitimately according to the government recommended dosage, 6 mg per week, are unknown. Methotrexate and its metabolite, 7-hydroxy MTX (7-OH MTX), were measured in sera of 16 outpatients with active RA in the first week of MTX treatment and 4-12 weeks after the introduction at 0, 1, 2, 4, and 8 h after administration of the first and the third 2-mg capsule, followed by sampling at 48, 96, and 168 h. The mean maximal serum drug concentration (mean C(max)) of MTX attained at 1-2 h after ingestion of the first capsule was 0.215 and 0.252 microM, respectively, in the first and the follow-up week. The mean C(max) after ingestion of the third capsule was 0.223 microM and 0.357 microM. The mean C(max) of 7-OH MTX was 0.0334 and 0.0289 microM for the first capsule, and 0.0495 and 0.0672 microM for the third capsule. The results indicate that MTX does not accumulate or deposit in the body of Japanese patients with RA when treated with 6 mg per week, and pharmacodynamics of MTX are comparable to those in overseas patients treated with 7.5 mg per week.2006, Mod Rheumatol, 15(6) (6), 405 - 9, English, International magazine[Refereed]Scientific journal
- Dec. 2005, Nihon rinsho. Japanese journal of clinical medicine, 63 Suppl 12, 228 - 231, Japanese, Domestic magazine[Molecular genetics of rheumatic diseases].[Refereed]Scientific journal
- Dec. 2005, Modern Rheumatology, 15(6) (6), 405 - 409, English[Refereed]Scientific journal
- May 2005, INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, 15(5) (5), 827 - 832, EnglishEstrogen specifically stimulates expression and production of osteoprotegerin from rheumatoid synovial fibroblasts[Refereed]Scientific journal
- (一社)日本リウマチ学会, Apr. 2005, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 49回・14回, 127 - 127, Japanese関節リウマチ疾患遺伝子変異型DR3のトランスジェニックマウスを用いた機能解析
- (一社)日本リウマチ学会, Apr. 2005, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 49回・14回, 157 - 157, JapanesePoncet病 その異同及び最近の動向に関する症例による考察
- (一社)日本リウマチ学会, Apr. 2005, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 49回・14回, 181 - 181, Japanese混合性結合織病(MCTD)および強皮症(SSc)におけるANG-1遺伝子変異と臨床所見の関連
- (一社)日本リウマチ学会, Apr. 2005, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 49回・14回, 181 - 181, Japanese関節リウマチ(RA)患者末梢血リンパ球(PBL)におけるDeath Receptor 3(DR3)発現細胞の解析
- (一社)日本リウマチ学会, Apr. 2005, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 49回・14回, 212 - 212, JapaneseTリンパ球系腫瘍細胞におけるDR3発現がTL1A誘導アポトーシスに及ぼす影響
- (一社)日本リウマチ学会, Apr. 2005, 日本リウマチ学会総会・学術集会抄録集, pp.233-233, 233 - 233, Japanese関節リウマチ滑膜細胞発現Death Receptor 3(DR3)の機能解析International conference proceedings
- (一社)日本リウマチ学会, Apr. 2005, 日本リウマチ学会総会・学術集会抄録集, pp.210-210, 210 - 210, Japanese関節リウマチ滑膜細胞におけるDR3プロモータ領域DNAの高度メチル化International conference proceedings
- (一社)日本リウマチ学会, Apr. 2005, 日本リウマチ学会総会・学術集会抄録集, pp.234-234, 234 - 234, Japanese関節リウマチ滑膜細胞におけるDcR3発現の解析[Refereed]International conference proceedings
- (一社)日本リウマチ学会, Apr. 2005, 日本リウマチ学会総会・学術集会抄録集, pp.211-211, 211 - 211, Japanese関節リウマチの疾患遺伝子候補Angiopoietin-1変異体の機能解析International conference proceedings
- (一社)日本リウマチ学会, Apr. 2005, 日本リウマチ学会総会・学術集会抄録集, pp.233-233, 233 - 233, Japanese関節リウマチ(RA)の疾患候補遺伝子Angiopoietin-1(Ang-1)の機能解析International conference proceedings
- (一社)日本リウマチ学会, Apr. 2005, 日本リウマチ学会総会・学術集会抄録集, pp.211-211, 211 - 211, Japanese関節リウマチ(RA)の滑膜細胞におけるRA疾患遺伝子Dblプロトオンコジーンエクソン23,24欠失型の機能異常International conference proceedings
- (一社)日本リウマチ学会, Apr. 2005, 日本リウマチ学会総会・学術集会抄録集, pp.122-122, 122 - 122, Japaneseリウマチ治療の新機軸 DR3特異的リガンドTL1AのRA滑膜細胞増殖及びマウスCIAに対する抑制効果International conference proceedings
- Apr. 2005, INTERNATIONAL JOURNAL OF MOLECULAR MEDICINE, 15(4) (4), 649 - 653, EnglishHeat shock protein 90 is required for increased DNA binding activity of activator protein-1, a heterodimer of Fos/JunD, in rheumatoid synovial cells under inflammatory stimuli[Refereed]Scientific journal
- (一社)日本臨床リウマチ学会, Mar. 2005, 臨床リウマチ, 17巻, 1号, pp. 48-52(1) (1), 48 - 52, Japanese血漿交換が著効したSLEに合併したTTPの1例[Refereed]Scientific journal
- Jan. 2005, Nihon rinsho. Japanese journal of clinical medicine, 63 Suppl 1, 122 - 6, Japanese, Domestic magazine[Susceptibility genes in rheumatoid arthritis: mutation in DR3 gene].[Refereed]Scientific journal
- Dec. 2004, 第27回日本分子生物学会年会, 27巻, pp. 995, Japanese関節リウマチ滑膜細胞におけるDR3プロモーター領域DNAの高度メチル化International conference proceedings
- (NPO)日本免疫学会, Nov. 2004, 日本免疫学会総会・学術集会記録, 34, 160 - 160, English慢性関節リウマチ患者の好中球及び滑膜細胞のCdc42エフェクター蛋白質(Cdc42 effector proteins of neutrophils and synovial cells of rheumatoid arthritis)
- Sep. 2004, GENES AND IMMUNITY, 5(6) (6), 439 - 443, English[Refereed]Scientific journal
- Sep. 2004, Modern Rheumatology, 14(4) (4), 323 - 326, English[Refereed]Scientific journal
- (一社)日本リウマチ学会, Mar. 2004, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 48回, 253 - 253, Japaneseシェーグレン症候群に対する塩酸セビメリンの治療効果とγグロブリン高値
- (一社)日本リウマチ学会, Mar. 2004, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 48回, 288 - 288, Japanese滑膜細胞におけるRA疾患遺伝子Db1プロトオンコジーンエフェクター分子の同定
- (一社)日本リウマチ学会, Mar. 2004, 日本リウマチ学会総会・学術集会抄録集, pp. 116-116, 116 - 116, Japanese早期関節リウマチの診断と治療 関節リウマチ 疾患遺伝子DR3からみた早期診断と臨床経過の予知International conference proceedings
- (一社)日本リウマチ学会, Mar. 2004, 日本リウマチ学会総会・学術集会抄録集, pp. 288-288, 288 - 288, Japanese好中球のアクチン重合に影響を及ぼす関節リウマチ(RA)の疾患遺伝子DBL proto-oncogeneInternational conference proceedings
- (一社)日本リウマチ学会, Mar. 2004, 日本リウマチ学会総会・学術集会抄録集, pp. 173-173, 173 - 173, Japanese関節リウマチ滑膜細胞におけるHSP90を介したシグナル伝達系の解析International conference proceedings
- (一社)日本リウマチ学会, Mar. 2004, 日本リウマチ学会総会・学術集会抄録集, pp. 279-279, 279 - 279, Japanese関節リウマチ滑膜細胞におけるDeath Receptor3(DR3)の発現International conference proceedings
- (一社)日本リウマチ学会, Mar. 2004, 日本リウマチ学会総会・学術集会抄録集, pp. 173-173, 173 - 173, Japanese関節リウマチ(RA)の疾患候補遺伝子Angiopoietin-1(Ang-1)の機能解析International conference proceedings
- Mar. 2004, 日本リウマチ学会総会・学術集会抄録集, pp. 288-288, Japanese滑膜細胞におけるRA疾患遺伝子Dblプロトオンコジーンエフェクター分子の同定International conference proceedings
- (一社)日本リウマチ学会, Mar. 2004, 日本リウマチ学会総会・学術集会抄録集, pp. 289-289, 289 - 289, JapaneseRNA干渉法を用いた関節リウマチ滑膜細胞におけるCyclooxygenase-2の発現抑制International conference proceedings
- (一社)日本リウマチ学会, Mar. 2004, 日本リウマチ学会総会・学術集会抄録集, pp. 286-286, 286 - 286, JapaneseAnti nuclear envelope antibodies(ANEA)陽性例の臨床的検討International conference proceedings
- (公社)日本生化学会, 2004, 生化学, 76巻, 8, pp. 925-925(8) (8), 925 - 925, JapaneseIdentification of effector proteins of Cdc42 in synovia and neutrophils that was down-regulated by exon-skipped form of Dbl proto-oncogene with genetic association with rheumatoid arthritis (RA)International conference proceedings
- 2004, Int. J. Mol. Med., 15(4) (4), 649, EnglishHeat shock protein 90 (HSP90) is required for increased DNA Binding activity of activator protein-1 (AP-1), a heterodimer of Fos JunD, inrheumatoid synovial cells under inflammatory stimuli.[Refereed]Scientific journal
- Oxford University Press, Dec. 2003, Modern Rheumatology, 13(4) (4), 380 - 381, English慢性関節リウマチのゲノム解析 近年の進歩と今後の方向性 慢性関節リウマチ疾患遺伝子,death receptor 3(DR3),angiopoietin-1(Ang-1)及びDbl含有ヌクレオチド多型性の分子遺伝学及び生化学(Genome Analysis of Rheumatoid Arthritis: Recent Advances and Future Directions: Molecular genetics and biochemistry of the rheumatoid arthritis disease genes, death receptor 3 (DR3), angiopoietin-1 (Ang-1), and Dbl containing nucleotide polymorphisms)
- 日本医学会, Dec. 2003, 日本医学会総会26回会誌, 2号, pp. 194-194(2) (2), 194 - 194, Japanese医学・医療の進歩を世界へ向けて ゲノム医科学 ゲノム時代からポストゲノム時代へ 疾患遺伝子の膠原病発症における役割International conference proceedings
- (株)メジカルビュー社, Oct. 2003, 関節外科, 22(10月増刊) (10月増刊), 87 - 96, Japanese【最近の関節リウマチ診療】RAのaggressive therapyとは
- 日本臨床分子医学会, Jul. 2003, 日本臨床分子医学会40回学術総会プログラム・抄録集, pp. 48-48, 48 - 48, Japanese関節リウマチ(RA)疾患遺伝子候補アンジオポエチン-1International conference proceedings
- 日本臨床分子医学会, Jul. 2003, 日本臨床分子医学会40回学術総会プログラム・抄録集, pp. 47-47, 47 - 47, Japanese関節リウマチ(RA)疾患遺伝子DBLの遺伝生化学的解析International conference proceedings
- Apr. 2003, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 304(1) (1), 143 - 147, English[Refereed]Scientific journal
- (一社)日本リウマチ学会, Mar. 2003, リウマチ, 43(2) (2), 253 - 253, English古典的初期胚中心と似ていない関節リウマチ滑膜組織リンパ節集合体でのB細胞クローン性増殖(B cell clonal expansion in rheumatoid arthritis synovial tissue lymphoid aggregates that do not resemble classical germinal centers)
- (一社)日本リウマチ学会, Mar. 2003, リウマチ, 43(2) (2), 266 - 266, Japanese関節リウマチ(RA)の疾患遺伝子DR3変異陽性例の臨床像の特徴
- Mar. 2003, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 100(6) (6), 3445 - 3449, English[Refereed]Scientific journal
- Feb. 2003, JCR-JOURNAL OF CLINICAL RHEUMATOLOGY, 9(1) (1), 1 - 3, EnglishFasciitis: What is the significance of various forms?[Refereed]Scientific journal
- Feb. 2003, JCR-JOURNAL OF CLINICAL RHEUMATOLOGY, 9(1) (1), 1 - 3, EnglishFasciitis: What is the significance of various forms?[Refereed]Scientific journal
- Oct. 2002, JOURNAL OF BONE AND MINERAL RESEARCH, 17(10) (10), 1761 - 1767, EnglishLocalization of the mutation responsible for osteopetrosis in the op rat to a 1.5-cM genetic interval on rat chromosome 10: Identification of positional candidate genes by radiation hybrid mapping[Refereed]Scientific journal
- Aug. 2002, ARTHRITIS AND RHEUMATISM, 46(8) (8), 2225 - 2234, English[Refereed]Scientific journal
- Jun. 2002, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 294(5) (5), 1114 - 1120, EnglishMutation of macrophage colony stimulating factor (Csf1) causes osteopetrosis in the tl rat[Refereed]Scientific journal
- Jun. 2002, MAMMALIAN GENOME, 13(6) (6), 299 - 301, English[Refereed]Scientific journal
- 2002, Modern Rheumatology, 12(3) (3), 206 - 212, English[Refereed]Scientific journal
- Dec. 2001, JOURNAL OF RHEUMATOLOGY, 28(12) (12), 2591 - 2596, EnglishInhibitory effect of T-614 on tumor necrosis factor-alpha induced cytokine production and nuclear factor-kappa B activation in cultured human synovial cells[Refereed]Scientific journal
- Sep. 2001, JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 86(9) (9), 4344 - 4352, EnglishUrocortin expression in synovium of patients with rheumatoid arthritis and osteoarthritis: Relation to inflammatory activity[Refereed]Scientific journal
- Jul. 2001, IMMUNOGENETICS, 53(5) (5), 427 - 429, EnglishPolymorphisms of the tumor necrosis factor receptor type 1 locus among autoimmune susceptible and resistant inbred rat strains[Refereed]Scientific journal
- Jun. 2001, GENES AND IMMUNITY, 2(4) (4), 229 - 232, EnglishPolymorphisms of the tumor necrosis factor alpha locus among autoimmune disease susceptible and resistant inbred rat strains[Refereed]Scientific journal
- Jul. 2000, JOURNAL OF CLINICAL INVESTIGATION, 106(2) (2), 189 - 197, English15-deoxy-Delta(12,14)-PGJ(2) induces synoviocyte apoptosis and suppresses adjuvant-induced arthritis in rats[Refereed]Scientific journal
- Jun. 2000, ARTHRITIS AND RHEUMATISM, 43(6) (6), 1278 - 1289, EnglishIdentification of four new quantitative trait loci regulating arthritis severity and one new quantitative trait locus regulating autoantibody production in rats with collagen-induced arthritis[Refereed]Scientific journal
- May 2000, EUROPEAN JOURNAL OF PHARMACOLOGY, 395(3) (3), 255 - 263, EnglishPreferential inhibition of cyclooxygenase-2 by meloxicam in human rheumatoid synoviocytes[Refereed]Scientific journal
- Mar. 2000, BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 269(2) (2), 415 - 421, EnglishSelective inhibition of cyclooxygenase-2 with antisense oligodeoxynucleotide restricts induction of rat adjuvant-induced arthritis[Refereed]Scientific journal
- Nov. 1999, EUROPEAN JOURNAL OF PHARMACOLOGY, 385(1) (1), 71 - 79, EnglishAuranofin inhibits interleukin-1 beta-induced transcript of cyclooxygenase-2 on cultured human synoviocytes[Refereed]Scientific journal
- Lead, May 1999, ARTHRITIS AND RHEUMATISM, 42(5) (5), 954 - 962, English[Refereed]Scientific journal
- Oct. 1998, CLINICAL IMMUNOLOGY AND IMMUNOPATHOLOGY, 89(1) (1), 28 - 34, EnglishThe expression and localization of fibroblast growth factor-1 (FGF-1) and FGF receptor-1 (FGFR-1) in human breast cancer[Refereed]Scientific journal
- We report here a case of neuropsychiatric lupus erythematosus with organic brain syndrome and transverse myelitis which was successfully managed by plasmapheresis.The Japan Society for Clinical Immunology, Aug. 1998, Jpn. J. Clin. Immunol., 21(4) (4), 172 - 179, Japanese
A 27-year-old female with facial rash, arthralgia and fever was diagnosed as having SLE and treated with oral prednisolone (PSL) in June 1996. After 6 weeks she demonstrated muscle pain and a spiking temperature. The dose of PSL was increased but clinical symptoms did not improve. In August, pulse methyl-PSL was performed and she subsequentlydeveloped delirium, impairment of orientation, memory and perception, which were followed by paraplegia of the lower extremities and loss of sphincter control. Intravenous bolus cyclophosphamide was not effective, but liver dysfunction, bone marrow suppression and respiratory failure due to an infection of pneumocystis carinii were observed. We then performed plasmapheresis or immunoabsorption several times. After this treatment steady improvement was observed. High values of antiribosomal P protein antibodies in the serum and interleukin-6 in the cerebrospinal fluid decreased. Small foci of increased signal intensity detected on cranial magnetic resonance imaging and hypoperfused areas on singlephoton emission CT diminished.
The patient was maintained on low-dose PSL and no recurrence has been observed 15 months from the onset. - A 43-years-old female was admitted to our hospital because of facial erythema and photosensitivity in 1983 and was diagnosed as systemic lupus erythematosus (SLE). She was treated with betamethazone 2.5mg/day as an outpatient. Abdominal pain and diarrhea were developed in September, 1995. So she was admitted to our hospital and diagnosed as having paralytic ileus. Ultrasonography showed marked intestinal edema. Forbidden oral intake and given antibiotics, she was satisfactorily improved in a few days, but the symptoms got worse soon. We forbad oral intake again. We performed a pulse therapy with 1g of methylprednisolone and increased a dose of betamethasone 2.5 to 4.0mg/day, but the symptoms were not improved. Since October 6th, serum ceatinine level (s-CRE) increased to 8.1mg/dl at October, 20th. We suspected the worsening of SLE nephropathy or drug-induced nephropathy, so we stopped a medication of pravastatin and used 50 mg/day of azathioprine. Moreover, we did a pulse therapy of methylprednisolone and a plasmapheresis. By these treatments, s-CRE level returned to normal range and paralytic ileus was completely improved.The Japan Society for Clinical Immunology, Feb. 1998, Jpn. J. Clin. Immunol., 21(1) (1), 48 - 56, Japanese
The cause of hypercreatininemia was suspected to be rhabdomyolysis due to pravastatin. The main cause of paralytic ileus with intestinal edema was suspected to be vascular disturbance of superior mesenteric arteries.
We consider that pulse therapy and plasmapheresis are useful for a patient of SLE with marked intestinal edema and paralytic ileus. - 1998, Biotherapy, 12(5) (5), 905 - 907, JapaneseTh1 type cytokine production and induction of antitumor activity by bacterial superantigen SEA-activated lymph node cellsInternational conference proceedings
- 1998, Biotherapy, 12(5) (5), 867 - 869, JapaneseIL-12 enhances anti-tumor effects of adoptive immunotherapy using IVS cellsInternational conference proceedings
- 1997, Biotherapy, 11(3) (3), 361 - 363, JapaneseAdoptive immunotherapy with bacterial superantigen SEA activated T cellsInternational conference proceedings
- 1996, Biotherapy, 10(2) (2), 165 - 171, JapaneseEffects of M-CSF or GM-CSF and role of monocytes on LAK cell activityScientific journal
- 1996, Biotherapy, 10(3) (3), 444 - 446, JapaneseInduction of iNOSmRNA as biological response modifiers (BRMs) is murine peritoneal neutrophilScientific journal
- 1996, Biotherapy, 10(3) (3), 440 - 443, JapaneseMorphological study on adhesion between PSK-induced polymorphonuclear leukocytes (PMNs) and tumor cellsScientific journal
- 1996, BIOTHERAPY, 9(4) (4), 229 - 239, EnglishMorphological study of cytotoxicity produced by PSK-induced polymorphonuclear leukocytes (PMNs) and Nocardia rubra cell wall skeleton[Refereed]Scientific journal
- Sep. 1995, CANCER RESEARCH, 55(17) (17), 3785 - 3789, EnglishEXPRESSION OF CYCLOOXYGENASE-1 AND CYCLOOXYGENASE-2 IN HUMAN COLORECTAL-CANCER[Refereed]Scientific journal
- Oct. 2019, ARTHRITIS & RHEUMATOLOGY, 71, EnglishRoles of Histone Acetyltransferases CBP/p300 and Transcriptional Factor ROR alpha/REV-ERB alpha Against TNF alpha-induced CCL2 Expression in RA-FLSsSummary international conference
- Oct. 2019, ARTHRITIS & RHEUMATOLOGY, 71, EnglishChronotherapy Using Baricitinib Attenuates Collagen-induced Arthritis in MiceSummary international conference
- Lead, Oct. 2019, Journal of the Japanese Society of Internal Medicine, 108(10) (10), 2116 - 2123, JapaneseSleep disordr in patients with rheumatoid arthritis.[Refereed][Invited]Introduction scientific journal
- Oct. 2017, ARTHRITIS & RHEUMATOLOGY, 69, EnglishIL-6 and TNF-a Cooperate to Modulate the Cell Cycle of RA-Fibroblast-like Synoviocytes Via Cyclin Dependent Kinase InhibitorsSummary international conference
- Oct. 2017, ARTHRITIS & RHEUMATOLOGY, 69, EnglishBik Plays an Important Role of Cell Proliferation Caused By Nitric Oxide in Rheumatoid Arthritis SynoviumSummary international conference
- Jun. 2017, ANNALS OF THE RHEUMATIC DISEASES, 76, 499 - 499, EnglishSummary international conference
- Oct. 2016, ARTHRITIS & RHEUMATOLOGY, 68, EnglishTCZ Modulates the Production of Ccfdna Derived from RA Synovial CellsSummary international conference
- Oct. 2016, ARTHRITIS & RHEUMATOLOGY, 68, EnglishIL-6 and TNF-alpha Modulate Expressions of Cell Cycle Regulators of Rheumatoid Arthritis Fibroblast-like SynoviocytesSummary international conference
- Oct. 2016, ARTHRITIS & RHEUMATOLOGY, 68, EnglishA Novel Pharmacological Action of MTX on RA Fibroblast-like Synoviocytes Via Circadian Clock GenesSummary international conference
- Jul. 2016, リウマチ科, Japanese生物学的製剤使用中にみられるアレルギー反応への対処法[Refereed][Invited]Introduction scientific journal
- Jun. 2016, ANNALS OF THE RHEUMATIC DISEASES, 75, 983 - 983, EnglishSummary international conference
- Jun. 2016, ANNALS OF THE RHEUMATIC DISEASES, 75, 922 - 922, EnglishSummary international conference
- (一社)日本リウマチ学会, 18 Mar. 2016, 日本リウマチ学会総会・学術集会プログラム・抄録集, 60th, 627 - 627, JapaneseACPA陽性RA患者におけるDeath receptor 3(DR3)遺伝子変異
- Oct. 2015, ARTHRITIS & RHEUMATOLOGY, 67, EnglishEnhancement of Mitochondrial Biogenesis Inhibits Cell Proliferation and MMP-3/RANKL Secretion in Rheumatoid Arthritis Fibroblast-like Synovial Cells and Joint Destruction in Arthritis Model MiceSummary international conference
- Oct. 2014, ARTHRITIS & RHEUMATOLOGY, 66, S457 - S458, EnglishTNF-a Modulates the Expression of Circadian Clock Genes Via Calcium Signaling in Rheumatoid Synovial CellsSummary international conference
- Oct. 2013, ARTHRITIS AND RHEUMATISM, 65, S895 - S895, EnglishThe Effect Of a Novel System Of Insoles Using Styrene Foam Beads On Foot Deformities In RA PatientsSummary international conference
- Jul. 2013, 内科, 112(1) (1), 107 - 111, Japaneseリウマチ性疾患のバイオマーカーIntroduction scientific journal
- Jun. 2013, 実験治療, (710) (710), 74 - 79, Japanese睡眠障害と関節リウマチ 概日リズムの乱れIntroduction commerce magazine
- Oct. 2012, ARTHRITIS AND RHEUMATISM, 64(10) (10), S836 - S836, EnglishEffect of Adalimumab On the Serum Level of Undercarboxylated Osteocalcin (ucOC), Bone Biochemical Markers and Bone Mineral DensitySummary international conference
- Oct. 2012, リウマチ科, 48(4号) (4号), 458 - 464, Japanese関節リウマチにおけるhypoxiaと血管新生[Invited]Introduction scientific journal
- (一社)日本リウマチ学会, 19 Mar. 2012, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 56th-21st, 486 - 486, JapaneseTNFαが関節リウマチ患者滑膜細胞の時計遺伝子に及ぼす影響
- (一社)日本リウマチ学会, 19 Mar. 2012, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 56th-21st, 534 - 534, Japaneseアダリムマブ使用下における血清低カルボキシル化オステオカルシン濃度の変化について
- (一社)日本リウマチ学会, 19 Mar. 2012, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 56th-21st, 579 - 579, Japanese関節リウマチ患者に対するトシリズマブの治療成績
- (一社)日本リウマチ学会, 19 Mar. 2012, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 56th-21st, 433 - 433, Japanese抗U1RNP抗体と炎症性サイトカインによるヒト肺動脈平滑筋細胞におけるTie‐2スプライスバリアントの誘導
- 2012, 日本臨床リウマチ学会プログラム・抄録集, 27th, 126, Japanese関節リウマチ寛解達成のための最適なトシリズマブ導入時期の検討
- 科学評論社, Jul. 2011, Clinical immunology & allergology, 56(1) (1), 72 - 77, JapaneseA novel regulation between circadian clock gene and TNF-α
- (一社)日本リウマチ学会, 20 Jun. 2011, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 55th-20th, 456 - 456, Japaneseリウマチ膠原病領域におけるB型肝炎再活性化に関する検討
- (一社)日本リウマチ学会, 20 Jun. 2011, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 55th-20th, 270 - 270, Japaneseコラーゲン関節炎におけるサイトカインの発現及びc‐Fos/AP‐1阻害剤T‐5224の抑制効果
- (一社)日本リウマチ学会, 20 Jun. 2011, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 55th-20th, 471 - 471, JapaneseTNFaは関節リウマチ患者滑膜細胞の時計遺伝子発現を変化させる
- (一社)日本リウマチ学会, 20 Jun. 2011, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 55th-20th, 490 - 490, Japaneseスプライシング調節蛋白質が変異型ヒトDR3遺伝子のイントロン5に結合する
- (一社)日本リウマチ学会, 20 Jun. 2011, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 55th-20th, 641 - 641, Japanese当センターにおける関節リウマチ患者に対するトシリズマブの治療成績
- (一社)日本リウマチ学会, 20 Jun. 2011, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 55th-20th, 140 - 140, Japanese関節炎・関節破壊の病態機序と転写因子c‐Fos/AP‐1
- (一社)日本リウマチ学会, 20 Jun. 2011, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 55th-20th, 535 - 535, Japanese悪性骨軟部腫瘍との鑑別が必要であった関節リウマチの3例
- (一社)日本リウマチ学会, 20 Jun. 2011, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 55th-20th, 564 - 564, Japanese当センターにおける新規関節リウマチ患者に対する治療成績
- (一社)日本リウマチ学会, 20 Jun. 2011, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 55th-20th, 343 - 343, JapaneseSLE発症における活性化T細胞の関与の検討
- (一社)日本リウマチ学会, 20 Jun. 2011, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 55th-20th, 469 - 469, Japanese抗U1RNP抗体の細胞内導入における炎症性サイトカインの影響
- (一社)日本リウマチ学会, 20 Jun. 2011, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 55th-20th, 283 - 283, Japanese抗U1RNP抗体によるMCTD疾患関連Ang‐1バリアント誘導における炎症性サイトカインの関与
- 2011, 日本臨床リウマチ学会プログラム・抄録集, 26th, 138, Japanese関節リウマチ患者に対するトシリズマブの治療成績―寛解導入に関わる因子の検討―
- Clinical squeal of the treatment of rheumatoid arthritis (RA) patients with adalimumab (ADA) was evaluated. A total of 159 patients with active RA were enrolled at Konan Kakogawa Hospital and Kobe University Hospital. The patients' profile at the start of study was age 57.8±12.8, women/men 129/30, Class 2.1±0.6 and X-ray stage 2.9±1.0. Of 159 patients, 115 (72.3%) were naïve biologics (naïve group) and 44 (27.7%) experienced more than one another biologics (switch group). Both naïve and switch groups showed significant improvements in disease activity including CRP, ESR and MMP-3 at 12-month periods, whereas it was relatively lesser in the switch group. At 6-month period, the drug adherence rate was approximately 80% both in naïve group and the switch group switched from infliximab. Instead, the drug adherence rate was 38% in the switch group switched from etanercept and 62% in the switch group switched from more than 2 biologics. In our facilities, 51 (32.1%) were treated with ADA, and 108 (67.9%) were treated with ADA and methotrexate (MTX). At 3 to 9-month periods, patients treated with ADA and MTX showed better improvement in CRP than those of treated with ADA solely. Of 46 patients, 14 (30.4%) patients treated with ADA for1year showed no progression in joint destruction as judged by X-ray study.The Japanese Society for Clinical Rheumatology and Related Research, 2011, Clinical Rheumatology and Related Research, 23(1) (1), 37 - 47, Japanese
- 日本医事新報社, 20 Nov. 2010, 週刊日本医事新報, (4517) (4517), 38 - 41, Japanese生体の日内リズムと関節炎
- 20 Oct. 2010, 脳21, 13(4) (4), 390-395,366, Japanese体内時計と身近な病気 時計遺伝子と関節リウマチ
- 日本臨床社, 20 May 2010, 日本臨床, 68, 430 - 439, Japanese関節リウマチの治療 薬物療法―有用性と副作用対策を中心に―分子標的治療薬 新規開発薬 関節炎・関節破壊の病態機序と新しい転写因子 c‐Fos/AP‐1阻害薬
- (一社)日本リウマチ学会, 19 Mar. 2010, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 54th-19th, 500 - 500, Japanese自己免疫性組織傷害の誘導におけるT細胞と免疫複合体の寄与の検討
- (一社)日本リウマチ学会, 19 Mar. 2010, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 54th-19th, 699 - 699, Japanese当センターにおける新規関節リウマチ患者に対する治療成績
- (一社)日本リウマチ学会, 19 Mar. 2010, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 54th-19th, 616 - 616, Japaneseインターフェロン治療中断後に,ポリニューロパチーにて発症したクリオグロブリン血症の一例
- (一社)日本リウマチ学会, 19 Mar. 2010, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 54th-19th, 499 - 499, JapaneseDeath Receptor3ノックアウトマウスにおける細胞死誘導とNF‐kBシグナル活性化の検討
- (一社)日本リウマチ学会, 19 Mar. 2010, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 54th-19th, 587 - 587, Japanese当センターにおける関節リウマチ患者に対するアダリムマブの使用成績
- (一社)日本リウマチ学会, 19 Mar. 2010, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 54th-19th, 515 - 515, Japanese新規低分子c‐Fos/AP‐1阻害剤T‐5224の破骨細胞分化・骨吸収に対する作用
- (一社)日本リウマチ学会, 19 Mar. 2010, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 54th-19th, 548 - 548, Japanese関節リウマチ患者の疾患活動性に対するハーブ足浴の効果
- (一社)日本リウマチ学会, 19 Mar. 2010, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 54th-19th, 549 - 549, Japanese関節リウマチ患者の血液学的マーカーに対するハーブ足浴の効果
- (一社)日本リウマチ学会, 19 Mar. 2010, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 54th-19th, 549 - 549, Japaneseハーブ足浴が関節リウマチ患者のc‐fos,wee1kinase発現に及ぼす影響
- (一社)日本リウマチ学会, 19 Mar. 2010, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 54th-19th, 666 - 666, Japanese関節リウマチ患者の睡眠障害に対するハーブ足浴の効果~アクチグラフを用いた検討~
- (一社)日本リウマチ学会, 19 Mar. 2010, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 54th-19th, 540 - 540, Japanese関節リウマチ患者の睡眠の質―睡眠ポリグラフィーを用いて測定―
- (一社)日本リウマチ学会, 19 Mar. 2010, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 54th-19th, 533 - 533, Japanese関節リウマチの疾患遺伝子変異型DR3のイントロン5にスプライシング調節蛋白が結合する
- (一社)日本リウマチ学会, 19 Mar. 2010, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 54th-19th, 548 - 666, Japanese関節リウマチ患者の睡眠障害に対するハーブ足浴の効果
- (一社)日本リウマチ学会, 19 Mar. 2010, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 54th-19th, 469 - 469, JapaneseRA患者における血清低カルボキシル化オステオカルシン(ucOC)濃度の検討(第2報)
- (一社)日本リウマチ学会, 19 Mar. 2010, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 54th-19th, 540 - 540, Japanese関節リウマチ患者における睡眠障害
- (一社)日本リウマチ学会, 19 Mar. 2010, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 54th-19th, 576 - 576, Japanese抗U1RNP抗体及び炎症性サイトカインによるMCTD疾患関連Ang‐1スプライスバリアント誘導
- (一社)日本リウマチ学会, 19 Mar. 2010, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 54th-19th, 453 - 453, JapaneseMICA129Met/A9アレルはSLEに強く関与する
- (一社)日本リウマチ学会, 19 Mar. 2010, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 54th-19th, 706 - 706, JapaneseMCTD患者におけるAng‐1スプライスバリアント誘導関連抗U1RNP抗体のエピトープ分析
- (一社)日本リウマチ学会, 19 Mar. 2010, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 54th-19th, 573 - 573, JapaneseAngiopoietin‐1(Ang‐1)バリアントの肺高血圧症への寄与の検討
- 2010, 日本臨床リウマチ学会プログラム・抄録集, 25th, 172, Japanese全身性エリテマトーデス治療中に発症し,閉塞性水頭症をきたしたクリプトコッカス髄膜脳炎の一例
- Oct. 2009, ARTHRITIS AND RHEUMATISM, 60Immune complex is required but insufficient for autoimmune tissue injury: essential role of effector CD8+ T cell[Refereed]
- (公社)日本生化学会, 25 Sep. 2009, 生化学, 82回, ROMBUNNO.3P-705 - 705, Japanese抗U1RNP自己抗体による血管新生因子Angiopoietin‐1(Ang‐1)スプライシング撹乱作用
- (一社)日本リウマチ学会, 19 Mar. 2009, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 53rd-18th, 372 - 372, Japanese抗原の繰り返し投与により成立したRAG発現自己応答性CD4+T細胞が自己抗体産生を誘導する
- (一社)日本リウマチ学会, 19 Mar. 2009, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 53rd-18th, 373 - 373, Japanese抗原のクロスプレゼンテーションにより活性化したCD8+T細胞が自己免疫性組織傷害を誘導する
- 19 Mar. 2009, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 53rd-18th, 213, Japanese変異型MICAはNK細胞のIFNγ産生を強く誘導する
- 19 Mar. 2009, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 53rd-18th, 374, Japanese抗TNFα抗体はCry欠損マウスの実験的関節炎を抑制する
- 19 Mar. 2009, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 53rd-18th, 310, JapaneseバリアントAngiopoietin‐1(Ang‐1)の肺動脈血管内皮および平滑筋細胞におけるERKシグナル伝達増強を介する肺高血圧症への寄与の研究
- 19 Mar. 2009, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 53rd-18th, 443, JapaneseSLE患者における抗Sm抗体と血管新生因子Angiopoietin‐1(Ang‐1)スプライシングバリアントの相関解析
- 19 Mar. 2009, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 53rd-18th, 443, JapaneseMCTD患者血清中抗U1RNP自己抗体による血管新生因子Angiopoietin‐1(Ang‐1)スプライシング干渉
- 19 Mar. 2009, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 53rd-18th, 268, JapaneseMCTD患者における血管新生因子Angiopoietin‐1(Ang‐1)mRNAスプライシング干渉要因としての抗U1RNP抗体
- 2009, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 53rd-18thMutant MICA enhances IFNγ production from NK cells as compared with wild type MICA
- 2009, 日本臨床リウマチ学会プログラム・抄録集, 24th, 111, Japanese関節リウマチ患者に発症したNSAIDs起因性多発小腸潰瘍の1例
- (株)金芳堂, 20 Oct. 2008, 脳21, 11(4) (4), 465 - 470, Japanese睡眠・リズム障害の臨床 関節リウマチ患者の睡眠障害
- Sep. 2008, ARTHRITIS AND RHEUMATISM, 58(9) (9), S705 - S706Full maturation of CD8+ T cell via antigen cross presentation into IFNγ-producing effector is prerequisite to the induction of autoimmune tissue injury[Refereed]
- 最新医学社, Sep. 2008, 最新医学, 63, 1956 - 1963, JapaneseDisease susceptible gene for rheumatoid arthritis
- メディカルレビュー社, 10 Aug. 2008, Front Rheumatol Clin Immunol, 2(3) (3), 150 - 154, JapaneseRAとAngiopoietin‐1遺伝子
- 南江堂, 15 Jul. 2008, 整形外科, 59(8) (8), 916 - 921, Japanese
- (一社)日本リウマチ学会, 2008, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 52nd-17th, 402 - 402, Japanese当科におけるレフルノミドの長期成績と中止事象の検討
- 2008, 日本臨床リウマチ学会プログラム・抄録集, 23rd, 106, Japanese多発性関節炎で急速に発症した成人Still病の一例
- (一社)日本リウマチ学会, 2008, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 52nd-17th, 360 - 360, Japanese関節リウマチ患者に対するインフリキシマブ時間短縮投与の試み
- (一社)日本リウマチ学会, 2008, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 52nd-17th, 384 - 384, Japanese抗原の繰り返し投与による自己免疫誘導の際のクロスプレゼンテーションに関与する分子
- (一社)日本リウマチ学会, 2008, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 52nd-17th, 273 - 273, Japanese新規低分子c‐Fos/AP‐1阻害剤T‐5224の滑膜細胞伸展及び破骨細胞活性化に対する作用
- (一社)日本リウマチ学会, 2008, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 52nd-17th, 491 - 491, Japanese滑膜細胞遊走能に関するintegrin‐linked kinase(ILK)の役割の検討
- (一社)日本リウマチ学会, 2008, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 52nd-17th, 384 - 384, JapaneseCD8+T細胞欠損マウスへの抗原の繰り返し投与による自己免疫疾患の解析
- (一社)日本リウマチ学会, 2008, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 52nd-17th, 384 - 384, Japanese抗原の繰り返し投与によるCD8+T細胞の活性化と腎炎の関与の検討
- (一社)日本リウマチ学会, 2008, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 52nd-17th, 270 - 270, Japanese関節リウマチ患者を対象としたMTX治療効果に関するProspective Study
- (一社)日本リウマチ学会, 2008, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 52nd-17th, 383 - 383, JapaneseSEBの繰り返し投与によるT細胞アネルギーの破綻を誘導するエフェクター分子の同定
- (一社)日本リウマチ学会, 2008, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 52nd-17th, 253 - 253, Japanese実験的関節炎誘導による概日リズムの障害
- (一社)日本リウマチ学会, 2008, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 52nd-17th, 253 - 253, Japanese時計遺伝子欠損マウスにおける実験的関節炎の増悪には炎症性サイトカインTNFαが関与する
- 2008, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 52nd-17th, 254, Japanese時計遺伝子CryとNKG2Dレセプター/NKG2Dリガンド相互作用
- (一社)日本リウマチ学会, 2008, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 52nd-17th, 292 - 292, Japaneseリウマチ滑膜細胞上のVLA‐5(α5β1インテグリン)はAngiopoietin‐1のシグナル伝達に関与する
- (一社)日本リウマチ学会, 2008, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 52nd-17th, 487 - 487, Japanese269Gly(+)型Angiopoietin‐1(Ang‐1)は肺動脈血管内皮と平滑筋の共培養においてERKのリン酸化を強く引き起こす
- Nov. 2007, ARTHRITIS AND RHEUMATISM, 56Repeated priming with exogenous antigen inhibits autoimmunity in MRL/lpr mice via reduction of double negative lpr T cell[Refereed]
- Nov. 2007, ARTHRITIS AND RHEUMATISM, 56Variant Death Receptor 3 (DR3) gene, genetically associated with Rheumatoid arthritis, inhibits TL1A-induced splenocyte signaling and CD4-8- T cell subset in thymus[Refereed]
- Jul. 2007, ANNALS OF THE RHEUMATIC DISEASES, 66, 316 - 316, EnglishRepeated priming with SEB suppresses LPR T cell proliferation to improve survival of MRL/LPR miceSummary international conference
- (一社)日本リウマチ学会, Apr. 2007, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 51st-16th, 402 - 402, Japanese関節炎と概日リズム~時計遺伝子欠損マウスで実験的関節炎は増悪する~
- 28 Mar. 2007, 月刊リウマチ科, 37(3) (3), 197 - 202, Japaneseリウマチ性疾患・膠原病における疾患感受性遺伝子 関節リウマチ
- 2007, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 51st-16th関節リウマチ患者における変異型death receptor 3(DR3)遺伝子の頻度:日本人・韓国人2およびコーカシアンにおける遺伝調査
- (一社)日本リウマチ学会, 2007, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 51st-16th, 404 - 404, JapaneseMRL/lprへのSEB繰り返し投与はlpr T細胞増殖を抑制して生存率を改善する
- (一社)日本リウマチ学会, 2007, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 51st-16th, 328 - 328, Japanese新規低分子c‐Fos/AP‐1阻害剤T‐5224のマウスII型コラーゲン誘発関節炎(CIA)に対する予防効果
- (一社)日本リウマチ学会, 2007, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 51st-16th, 383 - 383, Japanese関節リウマチ疾患遺伝子変異型DR3トランスジェニックマウス脾細胞ではNFκB活性化が抑制される
- (一社)日本リウマチ学会, 2007, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 51st-16th, 414 - 414, JapaneseHeat schock protein 90はインテグリンを介して関節リウマチ滑膜細胞のシグナル伝達に作用する
- (一社)日本リウマチ学会, 2007, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 51st-16th, 263 - 263, JapaneseAngiopoietin‐1は滑膜細胞上のVLA‐5(α5β1インテグリン)を介してシグナル伝達する
- (一社)日本リウマチ学会, 2007, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 51st-16th, 327 - 327, Japanese新規低分子c‐Fos/AP‐1阻害剤T‐5224の治療的投与によるマウスII型コラーゲン誘発関節炎(CIA)の抑制
- (一社)日本リウマチ学会, 2007, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 51st-16th, 405 - 405, Japanese抗原の繰り返し投与による自己抗体産生と腎炎発症におけるT細胞の関与
- (一社)日本リウマチ学会, 2007, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 51st-16th, 382 - 382, Japanese新規低分子c‐Fos/AP‐1阻害剤T‐5224はIL‐1β及びMMPを阻害し,関節炎を抑制する
- (一社)日本リウマチ学会, 2007, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 51st-16th, 242 - 242, Japanese当院における関節リウマチのエタネルセプト単独治療とMTX併用治療の比較検討
- 2007, 生化学, 4P-1083, Japanese各種免疫刺激物質による関節リウマチ(RA)疾患感受性遺伝子候補Dblプロトオンコジーンスプライシングバリアント生成の誘起
- Dec. 2006, 日本免疫学会総会・学術集会記録, 36Experimental induction of SLE-like autoimmune disease in mice after repeated priming with antigen: Expansion of effecter and memory IFN-γ-producing CD8+ T cell
- Sep. 2006, ARTHRITIS AND RHEUMATISM, 54(9) (9), S180 - S181, EnglishMutant type human death receptor 3 acts on the onset of collagen-induced arthritis.Summary international conference
- Sep. 2006, ARTHRITIS AND RHEUMATISM, 54(9) (9), S640Natural killer T cell is sine qua non for the reactivation of once-anergized T cell after repeated priming with antigen and induction of autoimmunity.[Refereed]
- Sep. 2006, ARTHRITIS AND RHEUMATISM, 54(9) (9), S194 - S194, EnglishAnti-CCP2 assay accurately predicts future development of rheumatoid arthritis as early as 3 months from onset of arthritic symptoms.[Refereed]Summary international conference
- Sep. 2006, ARTHRITIS AND RHEUMATISM, 54(9) (9), S176 - S176, EnglishDisruption of circadian rhythm aggravates experimental arthritis: Study in cry gene-knockout mice.[Refereed]Summary international conference
- (一社)日本リウマチ学会, 23 Mar. 2006, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 50th-15th, 157 - 157, Japanese抗原の繰り返し刺激によるアネルギーの破綻が自己抗体産生へ及ぼす影響
- (一社)日本リウマチ学会, 23 Mar. 2006, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 50th-15th, 158 - 158, Japanese睡眠障害Cry遺伝子欠損マウスでは実験的関節炎が増悪する
- (一社)日本リウマチ学会, 23 Mar. 2006, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 50th-15th, 159 - 159, Japanese変異型ヒトDR3トランスジェニックマウスにおける免疫応答
- (一社)日本リウマチ学会, 23 Mar. 2006, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 50th-15th, 95 - 95, Japanese変異型ヒトDR3のTGマウスを用いた細胞死制御機構の検討
- (一社)日本リウマチ学会, 23 Mar. 2006, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 50th-15th, 123 - 123, Japanese初診時の抗CCP抗体価が関節リウマチのその後の臨床経過と関節破壊に及ぼす影響:前向き研究
- (一社)日本リウマチ学会, 23 Mar. 2006, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 50th-15th, 223 - 223, Japaneseインフリキシマブ中止例の検討
- (一社)日本リウマチ学会, 23 Mar. 2006, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 50th-15th, 159 - 159, JapaneseNKT細胞への繰り返し刺激によるT細胞のアネルギー破綻とRF産生の検討
- (一社)日本リウマチ学会, 23 Mar. 2006, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 50th-15th, 158 - 158, Japanese抗原の繰り返し投与による自己抗体産生誘導とCD8+T細胞の解析
- (一社)日本リウマチ学会, 23 Mar. 2006, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 50th-15th, 104 - 104, Japanese関節リウマチにおけるMTXの治療効果に関するProspective Study
- (一社)日本リウマチ学会, 23 Mar. 2006, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 50th-15th, 166 - 166, Japaneseインフリキシマブの治療効果―関節破壊の抑制―
- (一社)日本リウマチ学会, 23 Mar. 2006, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 50th-15th, 237 - 237, Japanese関節リウマチにおける初診時血中MMP‐3値が臨床経過に及ぼす影響の前向き研究
- (一社)日本リウマチ学会, 23 Mar. 2006, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 50th-15th, 126 - 126, Japanese変異型ヒトDR3TGマウスは関節炎を悪化させる
- (一社)日本リウマチ学会, 23 Mar. 2006, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 50th-15th, 105 - 105, Japaneseメトトレキサート2mgカプセル週3回投与時の日本人リウマチ患者の薬物血中濃度
- (一社)日本リウマチ学会, 23 Mar. 2006, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 50th-15th, 308 - 308, JapaneseRivedo reticularis with summer ulcerationの3例とそのジアフェニルスルホンによる治療
- 2006, 日本免疫学会総会・学術集会記録, 36Angiopoietin-1 activates MAP kinases via VLA-5 (α5β1 integrin) in rheumatoid fibroblast-like synoviocytes.
- 28 Dec. 2005, 日本臨床, 63, 228 - 231, JapaneseA.遺伝子診断(genetic diagnosis)(遺伝学的検査genetic testing,遺伝子検査gene‐based testing,核酸検査nucleic acid‐based testing)III.疾患群の遺伝学的検査(genetic testing)と遺伝子検査(gene‐based testing)リウマチ・こう原病
- (株)日本臨床社, Dec. 2005, 日本臨床, 63巻, 増刊12, pp.228-231(増刊12 遺伝子診療学) (増刊12 遺伝子診療学), 228 - 231, JapaneseIntroduction scientific journal
- 25 Nov. 2005, 日本分子生物学会年会講演要旨集, 28th, 290, Japanese抗原の繰り返し投与による自己免疫疾患誘導とCD8+T細胞の解析
- Sep. 2005, ARTHRITIS AND RHEUMATISM, 52(9) (9), S579 - S580, EnglishBiological functions of angiopoietin-1 on cartilage destruction in Rheumatoid Arthritis.Summary international conference
- Sep. 2005, ARTHRITIS AND RHEUMATISM, 52(9) (9), S421 - S421, EnglishVariant haplotype of death receptor 3 (DR3) gene encoding DR3 molecule lacking death domain is prevalent in rheumatoid arthritis patients in Japan and Korea and predisposes to rheumatoid joint destruction.Summary international conference
- Sep. 2005, ARTHRITIS AND RHEUMATISM, 52(9) (9), S156 - S157, EnglishThe truncated DR3 molecule lacking death domain and transmembrane domain negatively regulates TL1A-induced apoptosis signalingSummary international conference
- Sep. 2005, ARTHRITIS AND RHEUMATISM, 52(9) (9), S283 - S283, EnglishContribution of mutation in angiopoietin-1 (ANG1) gene to the clinical presentation of patients with mixed connective tissue disease (MCTD) and systemic sclerosis (SSC): Genetic association with pulmonary hypertension.Summary international conference
- (一社)日本臨床リウマチ学会, Sep. 2005, 臨床リウマチ, 17巻, 3号, pp.155-159(3) (3), 155 - 159, JapaneseRAの疾患遺伝子DR3の遺伝子重複Introduction scientific journal
- Jul. 2005, ANNALS OF THE RHEUMATIC DISEASES, 64, 128 - 128, EnglishDeath receptor 3 is specially expressed in rheumatoid synovium and TL1A, a physiological ligand for DR3, efficiently induces apoptosis in rheumatoid synovial fibroblastsSummary international conference
- Jul. 2005, ANNALS OF THE RHEUMATIC DISEASES, 64, 124 - +, EnglishBiological functions of angiopoietin-1/TIE-2 signaling in rheumatoid synovial cellSummary international conference
- May 2005, The 1st East Asia group of RheumatologyThe contribution of CD8+ T cells for the induction of autoimmune disease upon repeated priming with antigen[Refereed]
- (一社)日本リウマチ学会, Apr. 2005, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 49回・14回, 213 - 213, Japanese抗原の繰り返し投与による自己抗体産生誘導とCD8+T細胞の解析
- (一社)日本リウマチ学会, Apr. 2005, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 49回・14回, 119 - 119, JapaneseRAの早期診断 RA早期診断における抗CCP抗体の有用性に関するprospective study
- (一社)日本リウマチ学会, Apr. 2005, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 49回・14回, 124 - 124, Japanese発症早期RA患者における血清抗CCP抗体価とMMP-3値について
- (一社)日本リウマチ学会, Apr. 2005, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 49回・14回, 163 - 163, Japaneseリウマトイド因子(RF)及び抗Sm抗体は抗原の繰り返し刺激によって生成する
- (一社)日本リウマチ学会, Apr. 2005, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 49回・14回, 213 - 213, Japanese抗原の繰り返し投与による自己免疫誘導 NKT細胞の役割
- (一社)日本リウマチ学会, Apr. 2005, 日本リウマチ学会総会・学術集会・国際リウマチシンポジウムプログラム・抄録集, 49回・14回, 277 - 277, Japanese抗原の繰り返し投与によるRF産生誘導 CD4+T細胞の機能解析
- (有)科学評論社, Apr. 2005, リウマチ科, 33巻, 4号, pp.426-434(4) (4), 426 - 434, Japanese関節リウマチの遺伝子解析Introduction scientific journal
- Apr. 2005, ゲノム医学, 5巻, 2号, pp.185-190(2) (2), JapaneseHLAと疾病 HLAと膠原病Introduction scientific journal
- メディカルレビュー社, Feb. 2005, ゲノム医学, 5巻, 1号, pp. 33-38(1) (1), 33 - 38, Japanese【関節リウマチとゲノム】 Linkage解析によるRA関連遺伝子 疾患候補遺伝子としてのAngiopoietin-1Introduction scientific journal
- (株)日本臨床社, Jan. 2005, 日本臨床, 63巻, 増刊1, pp. 122-126(増刊1 関節リウマチ) (増刊1 関節リウマチ), 122 - 126, JapaneseIntroduction scientific journal
- (NPO)日本免疫学会, 05 Nov. 2004, 日本免疫学会総会・学術集会記録, 34, 158 - 158, Japanese関節リウマチ(RA)患者末梢血リンパ球(PBMC)におけるDeath Receptor 3(DR3)陽性細胞の解析
- (NPO)日本免疫学会, 05 Nov. 2004, 日本免疫学会総会・学術集会記録, 34, 160 - 160, Japanese滑膜細胞における関節リウマチ疾患遺伝子Dblプロトオンコジーンの下流シグナルの解析
- Sep. 2004, ARTHRITIS AND RHEUMATISM, 50(9) (9), S567 - S567, EnglishGeldanamycin induces apoptosis in rheumatoid synovial cells by down-regulating MAPK and PI3-K pathway.Summary international conference
- Sep. 2004, ARTHRITIS AND RHEUMATISM, 50(9) (9), S545 - S546, EnglishTransgenic expression of mutant type human DR3 gene lacking death domain affords to resistance against apoptosis induction in mice.Summary international conference
- Sep. 2004, ARTHRITIS AND RHEUMATISM, 50(9) (9), S569 - S569, EnglishTL1A, a specific ligand for death receptor 3 and agonistic anti-DR3 antibody, inhibit type II collagen-induced arthritis in mice.Summary international conference
- Sep. 2004, ARTHRITIS AND RHEUMATISM, 50(9) (9), S671 - S671, EnglishThe promoter region of death receptor 3 (DR3) gene is specifically hypermethylated in rheumatoid synovial cellsSummary international conference
- Sep. 2004, ARTHRITIS AND RHEUMATISM, 50(9) (9), S354 - S354, EnglishDeath receptor 3 is specially expressed in rheumatoid Synovium and TL1A, a physiological ligand for DR3, efficiently induces apoptosis in rheumatoid synovial fibroblasts that express DR3.Summary international conference
- Sep. 2004, ARTHRITIS AND RHEUMATISM, 50(9) (9), S152 - S152, EnglishIdentification of new effector proteins of Cdc42 that was specifically down-regulated by exon-skipped phenotype of Dbl proto-oncogene with genetic association with rheumatoid arthritis (RA)Summary international conference
- Sep. 2004, ARTHRITIS AND RHEUMATISM, 50(9) (9), S655 - S656, EnglishAngiopoietin-1/Tie-2 signaling protects synovial cells from apoptosis by potentiating MAPK and P13'-kinase pathway.Summary international conference
- (有)科学評論社, Sep. 2004, リウマチ科, 32巻, 3号, pp. 229-236(3) (3), 229 - 236, Japanese【メトトレキサート(MTX)の臨床と問題点】 関節リウマチに対するMTXの治療効果Introduction scientific journal
- (株)メジカルビュー社, Aug. 2004, 関節外科, 23巻, 8号, pp. 1008-1013(8) (8), 1008 - 1013, Japanese【RAの早期診断とガイドライン】 RAの疾患遺伝子DR3遺伝子変異についてIntroduction scientific journal
- 医歯薬出版(株), Jul. 2004, 医学のあゆみ, 210巻, 4号, pp. 308-310(4) (4), 308 - 310, JapaneseIntroduction scientific journal
- Apr. 2004, 日本リウマチ学会総会・学術集会抄録集, 48th, 280, JapaneseヒトDR3トランスジェニック(TG)マウスの関節炎に対する影響の検討
- (有)科学評論社, Mar. 2004, 臨床免疫, 41巻, 3号, pp. 291-296(3) (3), 291 - 296, Japanese【関節炎をめぐる新知見】 分子遺伝学アプローチによる関節リウマチ(RA)遺伝素因探索 血管新生因子Angiopoietin-1のRA病態形成機構への関与Introduction scientific journal
- 2004, 臨床リウマチ, 16巻, , pp. 181-87, Japanese関節リウマチと分子シャロンーHSP90を介した滑膜細胞のシグナル伝達系ーIntroduction scientific journal
- (株)メジカルビュー社, 2004, 関節外科, 23巻, 8, pp. 28-33(8) (8), 1008 - 1013, JapaneseRAの疾患遺伝子DR3遺伝子変異についてIntroduction scientific journal
- 26 Dec. 2003, 日本医学会総会総会会誌, 26th(2) (2), 194, Japanese疾患遺伝子のこう原病発症における役割
- (株)医薬ジャーナル社, Dec. 2003, 医薬ジャーナル, 39巻, 12号, pp. 3251-3261(12) (12), 3251 - 3261, Japanese【膠原病薬物療法の最前線】 膠原病薬物治療の実際 多発性筋炎・皮膚筋炎(polymyositis/dermatomyositis)Introduction scientific journal
- 中山書店, Dec. 2003, Molecular Medicine, 40巻, 臨増, pp. 336-342, 336 - 342, Japanese【免疫2004】 病気と免疫 マイクロサテライトマーカーによる家系解析 関節リウマチの疾患遺伝子についてIntroduction scientific journal
- (NPO)日本免疫学会, 05 Nov. 2003, 日本免疫学会総会・学術集会記録, 33, 219 - 219, Japanese関節リウマチ滑膜細胞のシグナル伝達におけるHSP90の関与
- Oct. 2003, ONCOGENE, 22(44) (44), 6839 - 6844, EnglishIntroduction scientific journal
- Sep. 2003, ARTHRITIS AND RHEUMATISM, 48(9) (9), S458 - S458, EnglishExpression of the soluble form of human DR3 in the peripheral blood mononuclear cells of patients with rheumatoid arthritis.Summary international conference
- Sep. 2003, ARTHRITIS AND RHEUMATISM, 48(9) (9), S44 - S44, EnglishInteraction of fibronectin and V-LA-5(alpha5beta1 integrin) protects rheumatoid synovial cells from Fas mediated apoptosisSummary international conference
- Jun. 2003, DIABETES, 52, A315 - A315, EnglishEnhanced insulin sensitivity in mice lacking ganglioside GM3Summary international conference
- Jun. 2003, DIABETES, 52, A337 - A337, EnglishThe G-protein coupled receptor, S1P1, is required for proper beta-cell function.Summary international conference
- Apr. 2003, リウマチ, 43(2) (2), 329, JapaneseSDSおよびSTAIを用いた関節リウマチ患者のうつ傾向と不安心理の検討
- Apr. 2003, リウマチ, 43(2) (2), 302, Japanese関節リウマチ(RA)の疾患遺伝子Dbl proto‐oncogene下流のシグナル伝達異常
- (一社)日本リウマチ学会, Mar. 2003, リウマチ, 43(2) (2), 316 - 316, Japanese関節リウマチに対するMTXの治療効果
- 2003, ARTHRITIS RESEARCH & THERAPY, 5, S36 - S36, EnglishSummary international conference
- 2003, 関節外科22, pp. 87-96, JapaneseRAのaggressive therpyとはIntroduction scientific journal
- Mar. 2002, FASEB JOURNAL, 16(5) (5), A881 - A881, EnglishThe mutation causing osteopetrosis in tl rats maps to a 2.5 cM interval on rat chromosome 2.Summary international conference
- Sep. 2001, ARTHRITIS AND RHEUMATISM, 44(9) (9), S41 - S41, EnglishLocalization of the gene responsible for osteopetrosis in the op rat to a 0.51 cm region on rat chromosome 10.Summary international conference
- Sep. 2001, ARTHRITIS AND RHEUMATISM, 44(9) (9), S218 - S218, EnglishInhibitory effect of T-614, N-(3-formylamino-1-oxo-6-phenoxy-4H-chromen-Z-yl)methanesulfonamide, on tumor necrosis factor-alpha-induced cytokine production and NF-kappa B activation in cultures synovial cells.Summary international conference
- Sep. 2001, ARTHRITIS AND RHEUMATISM, 44(9) (9), S85 - S85, EnglishPolymorphisms of the tumor necrosis factor alpha and tumor necrosis factor receptors type I locus among autoimmune disease susceptible and resistant inbred rat strainsSummary international conference
- Sep. 2001, ARTHRITIS AND RHEUMATISM, 44(9) (9), S178 - S178, EnglishCollagen-induced arthritis quantitative trait loci (QTLs) isolated in congenic rats modulate experimental arthritis: Non-MHC QTL effects differ in males and females.Summary international conference
- Mar. 2001, FASEB JOURNAL, 15(4) (4), A486 - A486, EnglishAn improved radiation hybrid map of the proximal region of rat chromosome 10 which contains the mutation responsible for osteopetrosis in the op rat.Summary international conference
- Sep. 1999, ARTHRITIS AND RHEUMATISM, 42(9) (9), S86 - S86, EnglishPeroxisome proliferator-activated receptors (PPARs) expresson in synovial tissues from rheumatoid arthritis and induction of syoviocyte apoptosis through PPAR-gamma ligands.Summary international conference
- Sep. 1998, ARTHRITIS AND RHEUMATISM, 41(9) (9), S161 - S161, EnglishTreatment of rheumatoid arthritis and rat adjuvant-induced arthritis by cyclooxygenase-2 antisense through induction of apoptosis.Summary international conference
- We investigated the immunosuppressive effect of FK 506 on adjuvant arthritis in rats as an experimental model of rheumatoid arthritis.The Japanese Society of Inflammation and Regeneration, 1998, Ensho Saisei, 18(1), 25-30(1) (1), 25 - 30, Japanese
FK 506 was intramuscularly administered at a dose of 0.32 mg/kg/day from day 0 to day 28 after adjuvant injection. The severity of arthritis was evaluated by macroscopic score graded from 0 to 4 for each limb and histopathological examination of joints stained with hematoxylin and eosin. We also examined the expression of fibroblast growth factor (FGF) -1 and tyrosine phosphorylated proteins (phosphotyrosine, P-Tyr) in the inflamed synovia by immunoperoxidase staining.
FK 506 macroscopically prevented the development of arthritis and suppressed the proliferation of synovial tissues, the infiltration of inflammatory mononuclear cells and the destruction of bone and cartilage when compared with the control group. The expression of FGF-1 and P-Tyr of synovial sections was suppressed by treatment with FK 506. The intensity of immunostaining observed within synovial lining cells, sublining stromal fibroblast-like cells and cartilage chondrocytes decreased.
These findings suggest that FK 506 is a useful drug for the treatment of rheumatoid arthritis. - Sep. 1997, ARTHRITIS AND RHEUMATISM, 40(9) (9), 411 - 411, EnglishThe effects of cyclooxygenase (COX)-2 antisense on RA synoviocyte proliferation and adjuvant arthritis in Lewis rats.Summary international conference
- Joint work, フジメディカル出版, Apr. 2019, Japanese実臨床に活かす抗リウマチ薬ガイドブックGeneral book
- Joint work, 先端医療技術研究所, 2003, Japanese先端医療シリーズ19 アレルギー・リウマチ・膠原病の最新医療, 2003 / 関節リウマチのゲノム解析Scholarly book
- 第84回インターフェロンサイトカイン学会, Aug. 2019, Japanese, Domestic conferenceTNF阻害剤の基礎と臨床Public discourse
- 第40回日本炎症再生医学会, Jul. 2019, Japanese, 神戸国際会議場, Domestic conferenceJAK阻害剤が拓く最新リウマチ診療Public discourse
- 第63回日本リウマチ学会, Apr. 2019, Japanese, International conference生物学的製剤治療が関節リウマチ患者白血球における時計遺伝子発現を変動させるPublic symposium
- 第63回日本リウマチ学会, Apr. 2019, Japanese, 京都国際会議場, International conference関節リウマチモデルマウスにおけるJAK阻害剤を用いた時間治療の検討Public symposium
- 第63回日本リウマチ学会, Apr. 2019, Japanese, International conference滑膜細胞におけるTNFα誘導性CCL2発現増加に対するヒストンアセチル化酵素と転写因子RORα/REV-ERBαの役割Poster presentation
- 第63回日本リウマチ学会, Apr. 2019, Japanese, International conferenceIL-6は時計遺伝子を介して関節リウマチ滑膜細胞に細胞死抵抗性をもたらすPoster presentation
- 米国リウマチ学会, Nov. 2018, English, シカゴ, International conferenceIL-6 and TNF- cooperate to modulate Cell Cycle of RA-FLS via Cyclin Dependent Kinase 6.Poster presentation
- 日本リウマチ学会ベーシックリサーチカンファレンス, Sep. 2018, Japanese, Domestic conference生物学的製剤治療前後の関節リウマチ患者白血球における時計遺伝子発現Poster presentation
- 日本リウマチ学会ベーシックリサーチカンファレンス, Sep. 2018, Japanese, Domestic conferenceIL-6は時計遺伝子を介して関節リウマチ滑膜細胞に細胞死抵抗性をもたらすPoster presentation
- 第62回日本リウマチ学会, Apr. 2018, Japanese, 東京国際フォーラム, International conference時計遺伝子Bmal1は細胞周期調節因子を介して関節リウマチ滑膜細胞の増殖能を制御するPoster presentation
- 第62回日本リウマチ学会, Apr. 2018, Japanese, 東京国際フォーラム, International conferenceTNF-αはc-Mycを介してリウマチ滑膜細胞のp27Kip発現を変化させるPoster presentation
- 第62回日本リウマチ学会, Apr. 2018, Japanese, International conferenceIL-6は時計遺伝子を介して滑膜細胞に細胞死抵抗性をもたらすPoster presentation
- 第62回日本リウマチ学会, Apr. 2018, Japanese, 東京国際フォーラム, International conferenceIL-6とTNFαは細胞周期調節因子を介して協調的に滑膜細胞増殖に関与するPublic symposium
- 米国リウマチ学会, Nov. 2017, English, サンディエゴ, International conferenceNitric Oxide Accelerates Cell Proliferation by Preventing Bik Expression by NPAS2 in Rheumatoid Arthritis Synovium.Keynote oral presentation
- 米国リウマチ学会, Nov. 2017, English, サンディエゴ, International conferenceIL-6 and TNF-alpha cooperate to modulate The Cell Cycle of RA-FLS via Cyclin Dependent Kinase Inhibitors.Poster presentation
- 日本リウマチ学会近畿支部学術集会, Sep. 2017, Japanese, Domestic conferenceMTXの新しい薬理作用に基づく時間療法の検討Public symposium
- 日本リウマチ学会近畿支部学術集会, Sep. 2017, Japanese, Domestic conferenceIL-6とTNF-αはp27Kip1遺伝子発現を介して関節リウマチ滑膜細胞の細胞周期を調節するPoster presentation
- 欧州リウマチ会議, Jun. 2017, English, マドリード, International conferenceA Novel Pharmacological Action of MTX through circadian clock genes in RA Fibroblast-like Synovial Cells.Poster presentation
- 第61回日本リウマチ学会, Apr. 2017, Japanese, International conference転写因子群PAR bZIPを介したメトトレキサートの新しい薬理作用Public symposium
- 第61回日本リウマチ学会, Apr. 2017, Japanese, International conference時計遺伝子が滑膜細胞の細胞周期を調節するPoster presentation
- 第61回日本リウマチ学会, Apr. 2017, Japanese, International conferenceTNFαはヒストンアセチル化酵素を介してRA滑膜細胞内の時計遺伝子Bmal1発現を調節するPoster presentation
- 第61回日本リウマチ学会, Apr. 2017, Japanese, International conferenceIL-6とTNF-αが関節リウマチ滑膜細胞の細胞周期調節因子の発現を制御するPoster presentation
- 第61回日本リウマチ学会, Apr. 2017, Japanese, International conferenceDNA integrity indexを用いたTCZの新しい薬理効果の検証Poster presentation
- 米国リウマチ学会, Nov. 2016, English, ワシントンDC, International conferenceTCZ modulates the production of ccfDNA derived from RA synovial cells.Poster presentation
- 米国リウマチ学会, Nov. 2016, English, International conferenceIL-6 and TNF-α modulate expressions of Cell Cycle regulators of Rheumatoid ArthritisPoster presentation
- 米国リウマチ学会, Nov. 2016, English, International conferenceA Novel Pharmacological Action of MTX on RA Fibroblast-like Synoviocytes via Circadian Clock Genes.Poster presentation
- 第60回日本リウマチ学会, Apr. 2016, Japanese, International conference高齢者関節リウマチ(RA)患者に対するアバタセプトの使用経験Poster presentation
- 第60回日本リウマチ学会, Apr. 2016, Japanese, International conference関節リウマチ患者における血清遊離DNAの臨床的意義Public symposium
- 第60回日本リウマチ学会, Apr. 2016, Japanese, International conferenceメトトレキサートがRA-FLSの時計遺伝子に与える影響Poster presentation
- 第60回日本リウマチ学会, Apr. 2016, Japanese, International conferenceRA滑膜細胞由来の遊離DNA産生はTCZにより制御されるPoster presentation
- 第60回日本リウマチ学会, Apr. 2016, Japanese, International conferenceCa2+イオンによる時計遺伝子発現リズムの制御Poster presentation
- The 77th Annual Scientific Meeting of American College of Rheumatology, Oct. 2013, English, International conferenceThe Effect Of a Novel System Of Insoles Using Styrene Foam Beads On Foot Deformities In RA Patients.Poster presentation
- 第57回日本リウマチ学会総会・学術集会, Apr. 2013, Japanese, Domestic conference発泡スチロールビーズを使用した新開発インソールの、RA足部変形に対する効果Poster presentation
- 第57回日本リウマチ学会総会・学術集会, Apr. 2013, Japanese, Domestic conferenceトシリズマブにてバイオフリー寛解を試みた関節リウマチ患者7症例の検討Poster presentation
- 第57回日本リウマチ学会総会・学術集会, Apr. 2013, Japanese, Domestic conferenceTNFαは関節リウマチ滑膜細胞の時計遺伝子Per2発現量をD-box配列を介して抑制するPoster presentation
- American College of Rheumatology 73st Annual Scientific Meeting,, Oct. 2009, English, アメリカリウマチ学会, フィラデルフィア, アメリカ, International conferenceVariant angiopoientin-1 with 269Gly insertion contributes to the pathogenesis of pulmonary hypertension;a novel mechanism for stimulating pulmonary smooth muscle cell growth.Poster presentation
- American College of Rheumatology 73st Annual Scientific Meeting,, Oct. 2009, English, アメリカリウマチ学会, フィラデルフィア, アメリカ, International conferenceImmune complex is repuired but insufficient for autoimmune tissue injury:essential role of effector CD8+T Cell.Poster presentation
- 10th Annual Congress of the European League against Rheumatism, Jun. 2009, English, ヨーロッパリウマチ学会, コペンハーゲン, デンマーク, International conferenceMolecular clock modulates arthritis.Poster presentation
- 第53回日本リウマチ学会学術総会, Apr. 2009, Japanese, 日本リウマチ学会, 東京, Domestic conference変異型MICAはNK細胞のIFN産生を強く誘導するOral presentation
- 第53回日本リウマチ学会学術総会, Apr. 2009, Japanese, 日本リウマチ学会, 東京, Domestic conference新規低分子c-Fos/AP-1阻害剤T-5224のマウス抗II型コラーゲン抗体誘発関節炎(CAIA)に対する抑制作用Poster presentation
- 第53回日本リウマチ学会学術総会, Apr. 2009, Japanese, 日本リウマチ学会, 東京, Domestic conference抗原の繰り返し投与により成立したRAG発現自己応答性CD4+T細胞が自己抗体産生を誘導するPoster presentation
- 第53回日本リウマチ学会学術総会, Apr. 2009, Japanese, 日本リウマチ学会, 東京, Domestic conference抗原のクロスプレゼンテーションにより活性化したCD8+T細胞が自己免疫性組織傷害を誘導するPoster presentation
- 第53回日本リウマチ学会学術総会, Apr. 2009, Japanese, 日本リウマチ学会, 東京, Domestic conference抗TNF抗体はCry欠損マウスの実験的関節炎を抑制するPoster presentation
- 第53回日本リウマチ学会学術総会, Apr. 2009, Japanese, 日本リウマチ学会, 東京, Domestic conference関節リウマチ患者の睡眠障害の研究Poster presentation
- 第53回日本リウマチ学会学術総会, Apr. 2009, Japanese, 日本リウマチ学会, 東京, Domestic conference関節リウマチ患者における血清低カルボキシル化オステオカルシン(ucOC)濃度の検討Poster presentation
- 第53回日本リウマチ学会学術総会, Apr. 2009, Japanese, 日本リウマチ学会, 東京, Domestic conferenceバリアントAngiopoietin-1(Ang-1)の肺動脈血管内皮および平滑筋細胞におけるERKシグナル伝達増強を介する肺高血圧症への寄与の研究Poster presentation
- 第53回日本リウマチ学会学術総会, Apr. 2009, Japanese, 日本リウマチ学会, 東京, Domestic conferenceコクサッキーA7ウイルス感染症を契機に発症した成人スチル病の一例Poster presentation
- 第53回日本リウマチ学会学術総会, Apr. 2009, Japanese, 日本リウマチ学会, 東京, Domestic conferenceSLE患者における抗Sm抗体と血管新生因子Angiopoietin-1(Ang-1)スプライシングバリアントの相関解析Poster presentation
- 第53回日本リウマチ学会学術総会, Apr. 2009, Japanese, 日本リウマチ学会, 東京, Domestic conferenceMCTD患者血清中抗U1RNP自己抗体による血管新生因子Angiopoietin-1(Ang-1)スプライシング干渉Poster presentation
- 第53回日本リウマチ学会学術総会, Apr. 2009, Japanese, 日本リウマチ学会, 東京, Domestic conferenceMCTD患者における血管新生因子Angiopoietin-1(Ang-1)mRNAスプライシング干渉要因としての抗U1RNP抗体Oral presentation
- 第53回日本リウマチ学会学術総会, Apr. 2009, Japanese, 日本リウマチ学会, 東京, Domestic conferenceAngiopoietin-1(Ang-1)バリアントによるTie2活性化増強を介する肺高血圧症への寄与の検討Poster presentation
- 第52回日本リウマチ学会総会, Apr. 2008, Japanese, 日本リウマチ学会, 札幌, Domestic conference当科におけるレフルミドの長期成績と中止事象の検討Oral presentation
- 第52回日本リウマチ学会総会, Apr. 2008, Japanese, 日本リウマチ学会, 札幌, Domestic conference関節リウマチ患者に対するインフリキシマブ時間短縮投与の試みOral presentation
- 第30回日本分子生物学会年会・第80回日本生化学会大会合同大会, Dec. 2007, Japanese, 日本分子生物学会・日本生化学会, 横浜, Domestic conference各種免疫刺激物質による関節リウマチ(RA)疾患感受性遺伝子候補Dblプロトオンコジーンスプライシングバリアント生成の誘起Oral presentation
- AmericanCollegeofRheumatology71stAnnualScientificMeeting, Nov. 2007, English, American College of Rheumatology, ボストン, アメリカ, International conferenceVariant death receptor 3 (DR3) gene, genetically associated with rheumatoid arthritis, inhibits TL1A-induced splenocyte signaling and CD4-8- T cell subset in thymus.Oral presentation
- AmericanCollegeofRheumatology71stAnnualScientificMeeting, Nov. 2007, English, American College of Rheumatology, ボストン, アメリカ, International conferenceRepeated priming with exogenous antigen inhibits autoimmunity in MRL/lpr mice via reduction of double negative lpr T cell.Oral presentation
- AmericanCollegeofRheumatology71stAnnualScientificMeeting, Nov. 2007, English, American College of Rheumatology, ボストン, アメリカ, International conferenceInflammatory cytokines induce aberrant splicing of Dbl protooncogene as rheumatoid arthritis disease gene.Oral presentation
- AmericanCollegeofRheumatology71stAnnualScientificMeeting, Nov. 2007, English, American College of Rheumatology, ボストン, アメリカ, International conferenceCharacterization of anti-arthritic effect of a novel small molecule AP-1 inhibitor T-5224.Oral presentation
- The2007AnnualEuropeanCongressofRheumatologyEULAR., Jun. 2007, English, European Congress of Rheumatology, バルセロナ, スペイン, International conferenceRepeated priming with SEB suppresses lpr T cell proliferation to improve survival of MRL/lpr mice.Oral presentation
- 第2回東アジアリウマチ学会議, May 2007, English, 韓国リウマチ学会, ソウル, 韓国, International conferenceThe anxiety status and depressive symptoms were correlated with clinical conditions in Japanese patients with rheumatoid arthritisOral presentation
- 第51回日本リウマチ学会学術総会・学術集会, Apr. 2007, Japanese, 有限責任中間法人日本リウマチ学会, 横浜, Domestic conference新規低分子c-Fos/AP-1阻害剤T-5224はIL-1β及びMMPを阻害し、関節炎を抑制するOral presentation
- 第51回日本リウマチ学会学術総会・学術集会, Apr. 2007, Japanese, 有限責任中間法人日本リウマチ学会, 横浜, Domestic conference新規低分子c-Fos/AP-1阻害剤T-5224の治療的投与によるマウスII型コラーゲン誘発関節炎(CIA)の抑制Oral presentation
- 第51回日本リウマチ学会学術総会・学術集会, Apr. 2007, Japanese, 有限責任中間法人日本リウマチ学会, 横浜, Domestic conference新規低分子c-Fos/AP-1阻害剤T-5224のマウスII型コラーゲン誘発関節炎(CIA)に対する予防効果Oral presentation
- 第51日本リウマチ学会学術総会・学術集会, Apr. 2007, Japanese, 有限責任中間法人日本リウマチ学会, 横浜, Domestic conference関節リウマチ疾患遺伝子変異型DR3トランスジェニックマウス脾細胞ではNFκB活性化が抑制されるOral presentation
- 第51回日本リウマチ学会学術総会・学術集会, Apr. 2007, Japanese, 有限責任中間法人日本リウマチ学会, 横浜, Domestic conference関節リウマチ患者における変異型death receptor 3(DR3)遺伝子の頻度 日本人・韓国人2およびコーカシアンにおける遺伝調査Oral presentation
- 第51回日本リウマチ学会総会、学術集会, Apr. 2007, Japanese, 日本リウマチ学会, 横浜, Domestic conferenceレフルノミドとメソトレキサートを併用した関節リウマチ症例の検討Poster presentation
- 第51回日本リウマチ学会学術総会・学術集会, Apr. 2007, Japanese, 有限責任中間法人日本リウマチ学会, 横浜, Domestic conferenceMRL/lprへのSEB繰り返し投与はlpr T細胞増殖を抑制して生存率を改善するOral presentation
- 第51回日本リウマチ学会総会、学術集会, Apr. 2007, Japanese, 日本リウマチ学会, 横浜, Domestic conferenceHACA陽性となり減弱したインフリキシマブの効果がMTX増量により回復した関節リウマチの1症例Oral presentation
- 第51回日本リウマチ学会学術総会・学術集会, Apr. 2007, Japanese, 有限責任中間法人日本リウマチ学会, 横浜, Domestic conferenceAngiopoietin-1は滑膜細胞上のVLA-5(α5β1インテグリン)を介してシグナル伝達するOral presentation
- American College of Rheumatology 70th Annual Scientific Meeting, Nov. 2006, English, American College of Rheumatology, ワシントン, International conferenceOnce-anergized T cell in autoimmune-prone MRL/lpr mice cannot be reactivated from anergy and generate autoantibodies after repeated priming with exogenous antigen.Oral presentation
- American College of Rheumatology 70th Annual Scientific Meeting, Nov. 2006, English, American College of Rheumatology, ワシントン, International conferenceNatural killer T cell is Sine Qua Non for the reactivation of once-anergized T cell after repeated priming with antigen and induction of autoimmunity.Oral presentation
- American College of Rheumatology 70th Annual Scientific Meeting, Nov. 2006, English, American College of Rheumatology, ワシントン, International conferenceMutant type human death receptor 3 acts on the onset of collagen-induced arthritis.Oral presentation
- American College of Rheumatology 70th Annual Scientific Meeting, Nov. 2006, English, American College of Rheumatology, ワシントン, International conferenceDistribution of apoptosis-inducing death receptor 3 (DR3) and fas is significantly different among T cell subsets: DR3+ naive CD8+ T cell population is contracted in patients with rheumatoid arthritis.Oral presentation
- American College of Rheumatology 70th Annual Scientific Meeting, Nov. 2006, English, American College of Rheumatology, ワシントン, International conferenceDisruption of circadian rhythm aggravates experimental arthritis: study in cry gene-knockout mice.Oral presentation
- American College of Rheumatology 70th Annual Scientific Meeting, Nov. 2006, English, American College of Rheumatology, ワシントン, International conferenceAnti-CCP2 assay accurately predicts future development of rheumatoid arthritis as early as 3 months from onset of arthritic symptoms.Oral presentation
- American College of Rheumatology 70th Annual Scientific Meeting, Nov. 2006, English, American College of Rheumatology, ワシントン, International conferenceA novel small molecule AP-1 inhibitor T-5224 resolves mouse type Ⅱ collagen-induced arthritis in a c-Fos/AP-1-specific fashion.Oral presentation
- American College of Rheumatology 70th Annual Scientific Meeting, Nov. 2006, English, American College of Rheumatology, ワシントン, International conferenceAngiopoietin-1 acts onto (alpha)5(beta)1 integrin (VLA-5) to activate MAP kinases in rheumatoid synovial cells.Oral presentation
- 第50回日本リウマチ学会学術総会・学術集会, Apr. 2006, Japanese, 有限責任中間法人 日本リウマチ学会, 長崎, Domestic conference変異型ヒトDR3のTGマウスを用いた細胞死制御機構の検討Oral presentation
- 第50回日本リウマチ学会学術総会・学術集会, Apr. 2006, Japanese, 有限責任中間法人 日本リウマチ学会, 長崎, Domestic conference変異型ヒトDR3トランスジェニックマウスにおける免疫応答Oral presentation
- 第50回日本リウマチ学会学術総会・学術集会, Apr. 2006, Japanese, 有限責任中間法人 日本リウマチ学会, 長崎, Domestic conference当科におけるレフルノミドの使用成績と、中止後の治療方法の検討Oral presentation
- 第50回日本リウマチ学会学術総会・学術集会, Apr. 2006, Japanese, 有限責任中間法人 日本リウマチ学会, 長崎, Domestic conference睡眠障害Cry遺伝子欠損マウスでは実験的関節炎が増悪するOral presentation
- 第50回日本リウマチ学会学術総会・学術集会, Apr. 2006, Japanese, 有限責任中間法人 日本リウマチ学会, 長崎, Domestic conference初診時の抗CCP抗体が関節リウマチのその後の臨床経過と関節破壊に及ぼす影響:前向き研究Oral presentation
- 第50回日本リウマチ学会学術総会・学術集会, Apr. 2006, Japanese, 有限責任中間法人 日本リウマチ学会, 長崎, Domestic conference抗原の繰り返し投与による自己抗体産生誘導とCD8T細胞の解析Oral presentation
- 第50回日本リウマチ学会学術総会・学術集会, Apr. 2006, Japanese, 有限責任中間法人 日本リウマチ学会, 長崎, Domestic conference抗原の繰り返し刺激によるアネルギーの破綻が自己抗体産生へ及ぼす影響Oral presentation
- 第50回日本リウマチ学会学術集会, Apr. 2006, Japanese, 日本リウマチ学会, 長崎, Domestic conference関節リウマチ患者における変異型death receptor 3 (DR3)遺伝子の頻度:日本人および韓国人2,480例の遺伝調査Oral presentation
- 第50回日本リウマチ学会学術総会・学術集会, Apr. 2006, Japanese, 有限責任中間法人 日本リウマチ学会, 長崎, Domestic conference関節リウマチ滑膜細胞におけるdecoy receptor 3の機能解析Oral presentation
- 第50回日本リウマチ学会学術総会・学術集会, Apr. 2006, Japanese, 有限責任中間法人 日本リウマチ学会, 長崎, Domestic conference関節リウマチにおけるMTXの治療効果に関するProspective StudyOral presentation
- 第50回日本リウマチ学会学術総会・学術集会, Apr. 2006, Japanese, 有限責任中間法人 日本リウマチ学会, 長崎, Domestic conferenceメトトレキサート2mgカプセル週3回投与時の日本人リウマチ患者の薬物血中濃度Oral presentation
- 第50回日本リウマチ学会学術総会・学術集会, Apr. 2006, Japanese, 有限責任中間法人 日本リウマチ学会, 長崎, Domestic conferenceステロイドによる特発性大腿骨頭壊死症に及ぼすスタチンの作用についての前向き研究Poster presentation
- 第50回日本リウマチ学会学術総会・学術集会, Apr. 2006, Japanese, 有限責任中間法人 日本リウマチ学会, 長崎, Domestic conferenceインフリキシマブ中止例の検討Oral presentation
- 第50回日本リウマチ学会学術総会・学術集会, Apr. 2006, Japanese, 有限責任中間法人 日本リウマチ学会, 長崎, Domestic conferenceSLEにおけるDR3プロモーター領域DNAのメチル化Oral presentation
- 第50回日本リウマチ学会学術総会・学術集会, Apr. 2006, Japanese, 有限責任中間法人 日本リウマチ学会, 長崎, Domestic conferenceRivedo reticularis with summer ulcerationの3例とそのジアフェニルスルホンによる治療Poster presentation
- 第50回日本リウマチ学会学術総会・学術集会, Apr. 2006, Japanese, 有限責任中間法人 日本リウマチ学会, 長崎, Domestic conferenceNKT細胞への繰り返し刺激によるT細部のアネルギー破綻とRF産生の検討Oral presentation
- 第50回日本リウマチ学会学術集会, Apr. 2006, Japanese, 日本リウマチ学会, 長崎, Domestic conferenceAngiopoietin-1 (Ang-1)は関節リウマチの軟骨破壊を促進するPoster presentation
- American College of Rheumatology 69th annual scientific meeting, Oct. 2005, English, アメリカリウマチ学会, San Diego, International conferenceVariant Haplotype of Death Receptor 3 (dr3) Gene Encoding Dr3 Molecule Lacking Death Domain is Prevalent in Rheumatoid Arthritis Patients in Japan and Korea and Predisposes to Rheumatoid Joint DestructionPoster presentation
- American College of Rheumatology 69th annual scientific meeting, Oct. 2005, English, アメリカリウマチ学会, San Diego, International conferenceContribution of Mutation in Angiopoietin-1 (ang1) Gene to the Clinical Presentation of Patients with Mixed Connective Tissue Disease (mctd) and Systemic Sclerosis (ssc): Genetic Association with Pulmonary HypertensionOral presentation
- American College of Rheumatology 69th annual scientific meeting, Oct. 2005, English, アメリカリウマチ学会, San Diego, International conferenceBiological Functions of Angiopoietin-1 on Cartilage Destruction in Rheumatoid ArthritisPoster presentation
- Annual European Congress of Rheumatology 2005, Jun. 2005, English, ヨーロッパリウマチ会議, Vienna, International conferenceBiological functions of Angiopoietin-1/Tie-2 signaling in rheumatoid synovial cell.Poster presentation
- The 1st East Asian Group of Rheumatology meeting, May 2005, English, アジア太平洋リウマチ会議, 東京, International conferenceContribution of Mutation in Angiopoietin-1 Gene (ANG1) to Clinical Manifestation of Patients with Mixed Connective Tissue (MCTD) and Systemic Screrosis (SSc): A Possible Genetic Association with Pulmonary Hypertension.Poster presentation
- The 1st East Asian Group of Rheumatology meeting, May 2005, English, アジア太平洋リウマチ会議, 東京, International conferenceBiological functions of Angiopoietin-1 in rheumatoid synovial cellsPoster presentation
- 第49回日本リウマチ学会学術集会, Apr. 2005, Japanese, 日本リウマチ学会, 横浜, Domestic conference混合性結合織病(MCTD)および強皮症(SSc)におけるANG-1遺伝子変異と臨床所見の関連Poster presentation
- 第49回日本リウマチ学会総会・学術集会, Apr. 2005, Japanese, 日本リウマチ学会, 横浜, Domestic conference関節リウマチ滑膜細胞におけるDR3プロモータ領域DNAの高度メチル化Poster presentation
- 第49回日本リウマチ学会学術集会, Apr. 2005, Japanese, 日本リウマチ学会, 横浜, Domestic conference関節リウマチ滑膜細胞におけるDR3プロモータ領域DNAの高度メチル化Poster presentation
- 第49回日本リウマチ学会学術集会, Apr. 2005, Japanese, 日本リウマチ学会, 横浜, Domestic conference関節リウマチの疾患遺伝子候補Angiopoietin-1変異体の機能解析Poster presentation
- 第49回日本リウマチ学会学術集会, Apr. 2005, Japanese, 日本リウマチ学会, 横浜, Domestic conference関節リウマチ(RA)の疾患候補遺伝子Angiopoietin-1(Ang-1)の機能解析Poster presentation
- 第49回日本リウマチ学会総会・学術集会, Apr. 2005, Japanese, 日本リウマチ学会, 横浜, Domestic conference関節リウマチ(RA)の滑膜細胞におけるRA疾患遺伝子Dblプロトオンコジーンエクソン23,24欠失型の機能異常Poster presentation
- 第49回日本リウマチ学会学術集会, Apr. 2005, Japanese, 日本リウマチ学会, 横浜, Domestic conference関節リウマチ(RA)の滑膜細胞におけるRA疾患遺伝子Dblプロトオンコジーンエクソン23,24欠失型の機能異常Poster presentation
- 第27回日本分子生物学会年会, Dec. 2004, Japanese, 日本分子生物学会, 神戸, Domestic conference関節リウマチ滑膜細胞におけるDR3プロモーター領域DNAの高度メチル化.Poster presentation
- 第34回日本免疫学会学術集会, Dec. 2004, Japanese, 日本免疫学会, 札幌, Domestic conference関節リウマチ(RA)の疾患候補遺伝子Angiopoietin-1(Ang-1)の機能解析Poster presentation
- 第34回日本免疫学会総会・学術集会, Dec. 2004, Japanese, 日本免疫学会, 札幌, Domestic conference滑膜細胞における関節リウマチ疾患遺伝子Dblプロトオンコジーンの下流シグナルの解析Poster presentation
- 第34回日本免疫学会学術集会, Dec. 2004, Japanese, 日本免疫学会, 札幌, Domestic conference同左Poster presentation
- 第68回米国リウマチ学会, Oct. 2004, English, 米国リウマチ学会, サンアントニオ, International conferenceThe Promoter region of Death receptor 3 (DR3) gene is specifically hypermethylated in rheumatoid synovial cellsOral presentation
- American College of Rheumatology 68th annual scientific meeting, Oct. 2004, English, アメリカリウマチ学会, San Antonio, International conferenceIdentification of New Effector Proteins of Cdc42 That Was Specifically Down-Regulated by Exon-Skipped Phenotype of Dbl Proto-Oncogene with Genetic Association with Rheumatoid Arthritis (RA)Poster presentation
- 第77回日本生化学会大会, Oct. 2004, Japanese, 日本生化学会大会, 横浜, Domestic conference同左Poster presentation
- American College of Rheumatology 68th annual scientific meeting, Oct. 2004, English, アメリカリウマチ学会, San Antonio, International conferenceAngiopoietin-1/Tie-2 Signaling Protects Synovial Cells from Apoptosis by Potentiating MAPK and PI3'-Kinase PathwayOral presentation
- 第11回APLAR総会・学術集会, Sep. 2004, English, アジア太平洋リウマチ会議, 済州島, International conferenceThe Promoter region of Death receptor 3 (DR3) gene is specifically hypermethylated in rheumatoid synovial cells.Oral presentation
- 11th Asia Pacific League of Associations for Rheumatology Congress, Sep. 2004, English, アジア太平洋リウマチ会議, 済州島, International conferenceFunctional Defect of Splicing Variant of Dbl proto-oncogene with genetic association with rheumatoid arthritis (RA)Oral presentation
- 11th Asia Pacific League of Associations for Rheumatology Congress, Sep. 2004, English, アジア太平洋リウマチ会議, 済州島, International conferenceAngiopoietin-1/Tie-2 Signaling Protects Synovial Cells from Apoptosis by Potentiating MAPK and PI3'-Kinase PathwayOral presentation
- 第48回日本リウマチ学会総会・学術集会, Apr. 2004, Japanese, 日本リウマチ学会, 岡山, Domestic conference早期関節リウマチの診断と治療 関節リウマチ 疾患遺伝子DR3からみた早期診断と臨床経過の予知Oral presentation
- 第48回日本リウマチ学会学術集会, Apr. 2004, Japanese, 日本リウマチ学会, 岡山, Domestic conference好中球のアクチン重合に影響を及ぼす関節リウマチ(RA)の疾患遺伝子DBL proto-oncogenePoster presentation
- 第48回日本リウマチ学会学術集会, Apr. 2004, Japanese, 日本リウマチ学会, 岡山, Domestic conference滑膜細胞におけるRA疾患遺伝子Dblプロトオンコジーンエフェクター分子の同定Poster presentation
- 臨床リウマチ学会, Oct. 2003, Japanese, 日本臨床リウマチ学会, 札幌, Domestic conference標準治療としてのMTXOral presentation
- 第14回 神戸免疫・膠原病懇話会, Oct. 2003, Japanese, 日本リウマチ財団, 神戸, Domestic conferenceAnti-nuclear envelope antibodies (ANEA) 陽性例の臨床的検討Oral presentation
- 第40回日本臨床分子医学会, Apr. 2003, Japanese, 日本臨床分子医学会, 東京, Domestic conference関節リウマチ(RA)疾患遺伝子候補アンジオポエチン-1Poster presentation
- 第40回日本臨床分子医学会, Apr. 2003, Japanese, 日本臨床分子医学会, 東京, Domestic conference関節リウマチ(RA)疾患遺伝子DBLの遺伝生化学的解析Poster presentation
- 第47回日本リウマチ学会学術集会, Apr. 2003, Japanese, 日本リウマチ学会, 東京, Domestic conference関節リウマチ (RA) の疾患遺伝子 Dbl proto-oncogene 下流のシグナル伝達異常Poster presentation
- 第26回日本医学会総会, Apr. 2003, Japanese, 日本医学会, 福岡, Domestic conference医学・医療の進歩を世界へ向けて ゲノム医科学 ゲノム時代からポストゲノム時代へ 疾患遺伝子の膠原病発症における役割[Invited]Invited oral presentation
- 12th International Rheumatology Symposium, Apr. 2003, English, 日本リウマチ学会他, 東京, International conferenceMolecular Genetics and Biochemistry of the Rheumatoid Arthritis Disease Genes, Death Receptor 3 (DR3), Angiopoietin-1 (Ang-1) and Dbl Containing Nucleotide PolymorphismOral presentation
- 日本学術振興会, 科学研究費助成事業, 基盤研究(C), 神戸大学, 01 Apr. 2023 - 31 Mar. 2026認知症における新規血中バイオマーカーの探索 ~炎症誘導性マイクロRNAの意義~現在、認知症の診断、特にアルツハイマー型認知症を診断するにあたり、保険適用となる唯一の検体は髄液材料である。髄液採取は腰椎穿刺によって実施されるが、侵襲性が高く、被検者の負担が非常に大きいことから、経過観察のために受診毎に実施する検査材料ではない。今回、炎症と関わりのあるmiRNAを対象とし、認知症を診断できる、および認知症の進行や治療効果を評価できるバイオマーカーの探索研究を開始した。 [R5年度の研究実績]・脳脊髄液中と血漿中のmiRNA発現量の比較:まず、炎症に関連する3種類のmiRNA(Candidate (Cand) miRNA-A, -B, -C)に焦点を当て、軽度認知障害(以下MCI)患者を対象として脳脊髄液と血漿中のmiRNA発現量を定量した。その結果、miRNAの種類によって、脳脊髄液と血漿における発現量(分布)が異なることが明らかとなった。具体的には、Cand miRNA-Aは脳脊髄液において、Cand miRNA-B, -Cは血漿中において有意に発現していた。 ・脳脊髄液中ADマーカーと脳脊髄液/血漿中miRNA発現の相関:次に、脳脊髄液中のADマーカー(アミロイドβ42/40比、リン酸化タウ、総タウ)と脳脊髄液/血漿中miRNA発現の相関を調べた。脳脊髄液中ADマーカーとの相関係数がもっとも高かったのは血漿中Cand miRNA-Cであり、脳脊髄液中アミロイドβ42/40比と正の相関、脳脊髄液中リン酸化タウ、総タウと負の相関を示した。 ・血漿中miRNAにより認知機能低下を予測できるかの評価:さらに、MCI患者の初診時と2回目の受診結果から、認知機能の低下を示した群と認知機能が維持されていた群に分け、初診時の血漿中miRNA発現量を解析した。その結果、認知機能が低下した群は初診時の血漿中Cand miRNA-Aが低下していた。
- 日本学術振興会, 科学研究費助成事業, 基盤研究(C), 神戸大学, 01 Apr. 2022 - 31 Mar. 2025Tef 遺伝子改変マウスを用いた関節リウマチ病態解析と創薬へのアプローチ
- 学術研究助成基金助成金/基盤研究(C), Apr. 2018 - Mar. 2021, Principal investigatorCompetitive research funding
- Japan Society for the Promotion of Science, Grants-in-Aid for Scientific Research, Grant-in-Aid for Young Scientists (B), Kobe University, 01 Apr. 2014 - 31 Mar. 2016Role of the clock genes in rheumatoid arthritisI found a novel mechanism between inflammation and circadian rhythm in rheumatoid synovial cells as follows; ① A pro-inflammatory cytokine, Tumor necrosis factor-alpha (TNF-α) reduced the mRNA expression of a circadian core clock gene, Per2, and induced those of Bmal1. However, TNF-α did not affect the oscillation of Bmal1 gene expression.② Up-regulation of Bmal1 gene, induced by TNF-α, was associated with ROR alpha, an activator of Bmal1 gene expression. ③These results were cancelled by an intracellular calcium chelator, BAPTA-AM but not a calcineurin inhibitor FK-506, suggesting that TNF-α-induced up-regulation of Bmal1 gene is independent of a transcriptional factor NFAT.
- 科学研究費補助金/基盤研究(C), 2010, Principal investigatorCompetitive research funding
- 科学研究費補助金/基盤研究(C), 2006, Principal investigatorCompetitive research funding
- 科学研究費補助金/基盤研究(C), 2005Competitive research funding
- Japan Society for the Promotion of Science, Grants-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research (C), Kobe University, 2003 - 2004Research of rheumatoid arthritis using Dbl knock-out miceRheumatoid arthritis (RA) is a chronic polyarthritis finally leading to joint destruction. While the ratio of the risk for siblings of patients with a disease was much greater in familial RA, suggesting that genetic factors may be important as a cause of familial clustering, we have previously reported in Japanese familial RA with 3 principal chromosomal regions of linkage, D1S253/214, D8S556 and DXS1232. Komai et al. have subsequently identified DBL proto-oncogene (wild type DBL; GenBank/EMBL/DDBJ Accession No.AB085902) located on DXS1232/984 as a candidate for RA disease gene : a mutant DBL cDNA lacking exons 23 and 24 (deleted type DBL ; GenBank/EMBL/DDBJ Accession No. AB085901) was associated with familial RA. The DBL proto-oncogene is a prototype guanine nucleotide exchange factor (GEF) that modulates activity of small G proteins, including Rho family GTPases, RhoA and Cdc42 and possibly Rac1. Dbl converts the client proteins from the GDP-bound (inactive) form to the GTP-bound (active) form, allowing its effector domain to interact with downstream signaling molecules. Previous studies have shown that the Rho family GTPases control actin cytoskeleton organization and modulate movement, proliferation, and apoptosis of the cell. In humans, Rho family GEFs play important roles in the maturation and organization of skeletal muscles or nerves, also in the maturation and cytokine production of lymphoid cells. The mutation in some of the GEF family genes has been implicated in the human disease such as faciogenital dysplasia ^<15)>. It have been reported that deleted form of Dbl showed a weaker GEF activity toward Cdc42, and that infiltration and NADPH oxidase activity of neutrophils were significantly decreased in rheumatoid patients with this deleted mutant DBL. In the present study, we established mouse embryonic fibroblast(MEF) cell lines from Dbl knock-out mice and evaluated the activity of Rho family proteins and the intracellular localization and mobility of Dbl protein in mutant or wild type MEFs. The result showed that Dbl proto-oncogene affect the activation of Rho family proteins in MEFs through the decrease of intracellular mobility. We are now going to back-cross Dbl knock-out mice with DBIJ mice to examine the effects of Dbl gene-deletion on collagen-induced arthritis in mice.
- Japan Society for the Promotion of Science, Grants-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research on Priority Areas, Kobe University, 2000 - 2004Studies on the causative disease gene in autoimmunity and rheumatoid arthritisBACKGROUND while the defect in apoptosis causes characteristic systemic autoimmunity in mice, the contribution of apoptosis to human systemic autoimmunity is unclear. The present study was designed to elucidate the contribution of death receptor 3 (DR3) gene, a member of apoptosis-inducing TNF receptor gene family including Fas, to the pathogenesis of RA. METHODS Mutation was identified by sequencing death receptor 3(DR3) genome and assessed in relation to gene expression, molecular assembly, apoptosis induction and the prevalence of RA in 2,480 patients with RA and 1,270 healthy controls in Japan and Korea. RESULTS We identified a variant of DR3 gene, a family of apoptosis-inducing Fas gene, containing 4 single nucleotide polymorphisms (SNPs) and one locus of a 14 nucleotide deletion within exon 5 and intron 5 in patients with rheumatoid arthritis (RA), in which g.2590 A>T mutation resulted in insertion of a portion of intron 5 into the coding sequence to generate premature stop codon. Truncated product DR3 molecule lacking death domain assembled with authentic DR3 to inhibit ligand-induced apoptosis in the lymphocytes of patients with mutation. The variant existed in 3.19% of patients with RA among Japanese oriental genealogy with odds ratio 13.9 (p=1.2x10^<-10>). CONCLUSIONS Variant DR3 of relatively low frequency generates truncated DR3 molecule lacking death domain, which assembled with authentic DR3 molecule to inhibit apoptosis and predisposes to RA.