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YOSHIDA KohsukeGraduate School of Health Sciences / Faculty of Health SciencesAssociate Professor
Research activity information
■ Award- 2022 令和4年度前之園記念若手優秀論文賞
- 2020 兵庫県社会福祉事業団, 令和2年度職員表彰(理事長賞)
- 2009 日本リウマチ学会, JCR2009 International Workshop Award
- Objectives: The aim of this study was to determine the cause of elevated serum potassium levels when blood collection tubes containing separating gel are stored under refrigeration. Methods: Fifty-seven hospitalized patients and 11 healthy volunteers were recruited. Venous blood samples were obtained using Insepac II, Neotube, and Venoject® II, without anticoagulant. After centrifugation under different processing conditions, the capped tubes were stored at 4°C without aliquoting, and serum potassium levels were measured for up to 14 days. Correlation between the increase in potassium levels and blood cell counts was assessed. Furthermore, serum was replaced with a saline solution and potassium levels were determined after refrigeration. Results: Refrigerated samples stored in Insepac II tubes had significantly higher serum potassium levels on day 14 than on the day of blood collection. The increase in serum potassium levels was positively correlated with the number of red blood cells, but not white blood cells and platelets in venous blood. Furthermore, potassium levels were elevated when serum was replaced with a saline solution. Using Venoject II, which has a larger tube diameter and thicker separating gel than those of Insepac II and Neotube, did not increase serum potassium levels after storage. Increase in the serum potassium level was markedly suppressed by centrifugation at 2330 g for 15 minutes relative to other processing conditions. Conclusions: Potassium levels increase when serum is refrigerated in collection tubes containing separating gel. This can be attributed to contamination of the serum layer by blood cell components beyond the separating gel.Jun. 2024, Biopreservation and biobanking, 22(3) (3), 235 - 241, English, International magazineScientific journal
- 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.Jan. 2024, Biochemical and biophysical research communications, 691, 149315 - 149315, English, International magazineScientific journal
- 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 magazine[Refereed]Scientific journal
- Nov. 2021, Parkinsonism & Related Disorders[Refereed]Scientific journal
- Endogenous DNA derived from the nuclei or mitochondria is released into the bloodstream following cell damage or death. Extracellular DNA, called cell-free DNA (cfDNA), is associated with various pathological conditions. Recently, multiple aspects of cfDNA have been assessed, including cfDNA levels, integrity, methylation, and mutations. Rheumatoid arthritis (RA) is the most common form of autoimmune arthritis, and treatment of RA has highly varied outcomes. cfDNA in patients with RA is elevated in peripheral blood and synovial fluid and is associated with disease activity. Profiling of cfDNA in patients with RA may then be utilized in various aspects of clinical practice, such as the prediction of prognosis and treatment responses; monitoring disease state; and as a diagnostic marker. In this review, we discuss cfDNA in patients with RA, particularly the sources of cfDNA and the correlation of cfDNA with RA pathogenesis. We also highlight the potential of analyzing cfDNA profiles to guide individualized treatment approaches for RA.MDPI AG, Aug. 2021, International Journal of Molecular Sciences, 22(16) (16), 8941 - 8941, English[Refereed]Scientific journal
- OBJECTIVE: Diurnal variation of symptoms are observed in rheumatoid arthritis, especially in productions of cytokines that show peak concentrations during mid night. In contrast, cytokines of collagen-induced arthritis (CIA) mice increase in daytimes under Mid-light condition. By using chronotherapy, differences in drug efficacies according to administration time of Baricitinib, a wide ranged cytokine blocker, were examined in CIA mice. METHODS: CIA mice were administered a dose of 3 mg/kg of Baricitinib once a day at zeitgeber time (ZT) 0 or ZT12 for 21 days. Arthritis scores, histopathology and factors related to joint destruction in sera were examined. Phosphorylation of STAT3 in liver, expressions of cytokines in spleen, and Interleukin (IL)-6 and tumor necrosis factor (TNF)-α in sera were measured. RESULTS: In CIA mice, diurnal variations were observed both in expressions of cytokines and phosphorylation of STAT3. Arthritis scores of ZT0/12 group decreased from day3 as compared to untreated mice, and those of ZT0 group significantly decreased as compared to ZT12 group from day12. Pathological findings, immunohistochemistry of cytokines and Receptor activator of nuclear factor kappa-Β ligand (RANKL)/osteoprotegerin ratio in sera well reflected results of arthritis scores. Diurnal variation of STAT3 phosphorylation was suppressed in ZT0 group. At ZT2, expressions of IL-6/Interferon-γ/TNF/granulocyte-macrophage colony-stimulating factor in ZT0 group were significantly decreased as compared to untreated mice, though not in ZT12 group. In ZT0 group, IL-6 and TNF-α in sera were decreased for longer time than that in ZT12 group. CONCLUSION: Chronotherapy using Baricitinib targeting cytokine secretions is effective in CIA mice. Clinical applications of chronotherapy can be expected to enhance the drug efficacy.Jul. 2020, International immunopharmacology, 84, 106549 - 106549, English, International magazine[Refereed]Scientific journal
- 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
- Objectives: Rheumatoid Arthritis (RA) is the autoimmune disease representing the circadian variations of symptoms such as morning stiffness of joints or increased production of cytokines around midnight. Clock genes have been reported to affect on the pathogenesis of RA, however, the detailed relation between clock genes and disease activities of RA has remained unclear.Methods: In this study, 15 RA patients treated with biological disease modifying anti-rheumatic drugs (bDMARDs) were enrolled (TNF inhibitor, 5; IL-6 inhibitor, 5; CTLA4-IgG, 5). Blood samples were collected from RA patients before treatment and at the study end-point fulfilling DAS28-ESR < 3.2. Total RNA was extracted from leukocytes to examine the expressions of the clock genes. We then evaluated the correlation of the clock gene expression with disease activity and the diagnostic values of the clock genes.Results: The expressions of the clock genes were significantly modulated by bDMARDs treatments. Disease activities were significantly correlated with the clock genes expressions, and disease remission/low disease activity could be distinguished from moderate/high disease activity due to the sensitivities, the specificities and the areas under the curves of that.Conclusion: The expressions of the clock genes in leukocytes could be useful as novel biomarkers predicting disease activities and therapeutic efficacies for bDMARDs in RA treatments.May 2019, Modern Rheumatology, 30(2) (2), 293 - 300, English, International magazine[Refereed]Scientific journal
- Lead, (一社)日本臨床衛生検査技師会, May 2018, Japanese Journal of Medical Technology, 67(3) (3), 289 - 293, English, Domestic magazine[Refereed]Scientific journal
- BioMed Central Ltd., Mar. 2018, Arthritis Research and Therapy, 20(1) (1), 55 - 55, English[Refereed]Scientific journal
- Lead, Elsevier B.V., Jan. 2018, Biochemical and Biophysical Research Communications, 495(2) (2), 1675 - 1680, English[Refereed]Scientific journal
- 2018, Journal of Translational Science, 4(4) (4), 1, English[Refereed]Scientific journal
- American Society for Biochemistry and Molecular Biology Inc., 2018, Journal of Biological Chemistry, 293(6) (6), 1933 - 1943, English[Refereed]Scientific journal
- Jun. 2017, INTERNATIONAL JOURNAL OF RHEUMATIC DISEASES, 20(6) (6), 722 - 730, English[Refereed]Scientific journal
- Lead, 2015, International Journal of Clinical Rheumatology, 10(5) (5), 335 - 344, English[Refereed]Scientific journal
- Lead, 2014, JOURNAL OF IMMUNOLOGY RESEARCH, 2014, 282495, English[Refereed]Scientific journal
- Lead, 2013, Advances in Neuroimmune Biology, 4(1) (1), 7 - 11, English[Refereed]Scientific journal
- Lead, 2013, Scandinavian Journal of Rheumatology, 42(4) (4), 276 - 280, English[Refereed]Scientific journal
- Lead, Jan. 2013, TISSUE ANTIGENS, 81(1) (1), 44 - 45, English[Refereed]Scientific journal
- Lead, Oct. 2011, ARTHRITIS AND RHEUMATISM, 63(10) (10), 3058 - 3066, English[Refereed]Scientific journal
- May 2011, RHEUMATOLOGY, 50(5) (5), 852 - 861, English[Refereed]Scientific journal
- Apr. 2011, ARCHIVUM IMMUNOLOGIAE ET THERAPIAE EXPERIMENTALIS, 59(2) (2), 89 - 95, English[Refereed]Scientific journal
- Feb. 2010, JOURNAL OF IMMUNOLOGY, 184(3) (3), 1560 - 1565, English[Refereed]Scientific journal
- Jul. 2007, ARTHRITIS AND RHEUMATISM, 56(7) (7), 2170 - 2179, English[Refereed]Scientific journal
- Nov. 2024, American college of Rheumatology, Annual Scientific Meeting 2024Clock Gene Bmal1 Contributes to Inflammation via Phosphorylation of NF-κB/p65 in RA-FLS
- (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
- Jun. 2024, European league against Rheumatism, annual European congress of Rheumatology 2024IL-6 interferes with apoptosis-induction of Rheumatoid Arthritis fibroblast-like synovial cells by affecting Bcl-2 family of proteins
- (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
- Nov. 2023, ACR convergence2023(米国リウマチ学会)Clock Gene Bmal1 Promotes Transcriptional Activity of NF-κB to Regulate Production of Inflammatory Mediators in RA-FLS
- (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
- (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)日本臨床衛生検査技師会, May 2022, 日本医学検査学会抄録集, 71回, 171 - 171, Japanese血清カリウム値が冷蔵保管で増加する原因 血球層が「分離剤を超えて」血清層へ混入
- Lead, Apr. 2022, 医学のあゆみ, 281(2) (2), 180 - 185体内時計による関節リウマチの制御
- (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
- (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)日本臨床衛生検査技師会, Sep. 2020, 日本医学検査学会抄録集, 69回, 485 - 485, Japanese高齢者女性の低負荷運動の継続が血圧脈波・身体組成および呼吸機能に及ぼす影響
- (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
- 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
- (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
- (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
- 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
- Jun. 2017, ANNALS OF THE RHEUMATIC DISEASES, 76, 499 - 499, EnglishSummary international conference
- (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
- 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
- Jun. 2016, ANNALS OF THE RHEUMATIC DISEASES, 75, 983 - 983, EnglishSummary international conference
- (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. 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
- 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
- (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
- (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
- 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.Summary international conference
- (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
- Oct. 2011, ARTHRITIS AND RHEUMATISM, 63(10) (10), S141 - S142, EnglishTNF alpha Modulates the Expression of Circadian Clock Genes in Rheumatoid Synovial Cells.Summary international conference
- (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, 283 - 283, JapaneseMICA 129ValアリルはHLA‐DRB1と独立した日本人MCTD患者における遺伝素因である
- Nov. 2010, ARTHRITIS AND RHEUMATISM, 62Identification of a pathological TCR of autoantibody-inducing CD4+ T cell that induces autoantibodies and lupus-like immune tissue injury
- (株)金芳堂, 20 Oct. 2010, 脳21, 13(4) (4), 390-395,366 - 395, Japanese体内時計と身近な病気 時計遺伝子と関節リウマチ
- (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, 453 - 453, JapaneseMICA129Met/A9アレルはSLEに強く関与する
- 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
- 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
- The Japanese Society for Clinical Rheumatology and Related Research, 2009, Clinical Rheumatology and Related Research, 21(4) (4), 425 - 426, Japanese
- Sep. 2008, ARTHRITIS AND RHEUMATISM, 58(9) (9), S515Arthritis modulates biological clock: Cry directly regulates the transactivation, of TNF-alpha gene
- Sep. 2008, ARTHRITIS AND RHEUMATISM, 58(9) (9), S657Hsp 90 modulates actin filament rearrangement in rheumatoid synovial cell via IIk-dependent pathway
- Sep. 2008, ARTHRITIS AND RHEUMATISM, 58(9) (9), S815Genetic polymorphism of MHC class I chain-related gene A (MICA) in Japanese patients with systemic lupus erythematosus (SLE)
- (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
- (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, 254 - 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, 308 - 308, JapaneseMICA遺伝子多型によるSLE,RA疾患感受性の検討
- Jul. 2007, ANNALS OF THE RHEUMATIC DISEASES, 66, 138 - 139, EnglishAssociation of major histocompatibility complex class I chain-related gene A (MICA) A4/A5.1 and A5/A5.1 genotypes with Japanese patients with rheumatoid arthritis (RA)Summary international conference
- (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, 369 - 369, Japanese日本人関節リウマチ患者におけるMICA遺伝子多型解析
- (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
- 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, 369, Japanese日本人関節リウマチ患者におけるMICA遺伝子多型解析
- (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, 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, 193 - 193, Japanese滑膜細胞内シグナル伝達におけるAngiopoietin‐1とα5β1インテグリンの相互作用
- 日本認知症学会2023 - Present
- 日本認知症予防学会2020 - Present
- JAPANESE ASSOCIATION OF MEDICAL TECHNOLOGISTS2012 - Present
- JAPAN COLLEGE OF RHEUMATOLOGY2005 - Present
- 日本学術振興会, 科学研究費助成事業 基盤研究(C), 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~
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- 一般社団法人日本リウマチ学会, 関節リウマチの精密医療の推進に資する研究推進プログラム 研究助成金, Nov. 2023 - Mar. 2025, Principal investigator関節リウマチ治療反応性を早期に予測する循環細胞外遊離DNA検出システムの開発
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- 公益財団法人 ひょうご科学技術協会, 令和5年度学術研究助成, Apr. 2023 - Mar. 2024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~
- 黒住医学研究振興財団, 2021年度「第29回研究助成金」, Oct. 2021血清カリウム値が冷蔵保管で増加する原因 ~血球層が「分離剤を超えて」血清層へ混入~
- 日本学術振興会, 科学研究費補助金(若手研究B), Apr. 2017 - Mar. 2020, Principal investigatorCompetitive research funding
- 日本学術振興会, 科学研究費補助金(若手研究B), Apr. 2014 - Mar. 2016, Principal investigatorCompetitive research funding