徳島大学 / 教育研究者総覧 --- 清水宗

専門分野

研究テーマ

著書・論文

学術論文(審査論文):

1.	Emiko Nakaue, Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa, Takeshi Harada, Asuka Oda, Yusuke Inoue, Sou Shimizu, Yoshiki Higa, Kimiko Sogabe, Masahiro Oura, Tomoyo Hara, Ryohei Sumitani, Tomoko Maruhashi, Hiroki Yamagami, Itsuro Endo, Eiji Tanaka and Masahiro Abe : Mechanisms of preferential bone formation in myeloma bone lesions by proteasome inhibitors., International Journal of Hematology, 2023. (要約) Proteasome inhibitors (PIs) can preferentially restore bone in bone-defective lesions of patients with multiple myeloma (MM) who respond favorably to these drugs. Most prior in vitro studies on PIs used continuous exposure to low PI concentrations, although pharmacokinetic analysis in patients has shown that serum concentrations of PIs change in a pulsatile manner. In the present study, we explored the effects of pulsatile treatment with PIs on bone metabolism to simulate in vivo PI pharmacokinetics. Pulsatile treatment with bortezomib, carfilzomib, or ixazomib induced MM cell death but only marginally affected the viability of osteoclasts (OCs) with F-actin ring formation. Pulsatile PI treatment suppressed osteoclastogenesis in OC precursors and bone resorption by mature OCs. OCs robustly enhanced osteoblastogenesis in cocultures with OCs and MC3T3-E1 pre-osteoblastic cells, indicating OC-mediated coupling to osteoblastogenesis. Importantly, pulsatile PI treatment did not impair robust OC-mediated osteoblastogenesis. These results suggest that PIs might sufficiently reduce MM cell-derived osteoblastogenesis inhibitors to permit OC-driven bone formation coupling while suppressing OC differentiation and activity in good responders to PIs. OC-mediated coupling to osteoblastogenesis appears to be a predominant mechanism for preferential occurrence of bone regeneration at sites of osteoclastic bone destruction in good responders. (徳島大学機関リポジトリ) ● Metadata: 118380 (出版サイトへのリンク) ● Publication site (DOI): 10.1007/s12185-023-03601-2 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 37039914 ● Search Scopus @ Elsevier (PMID): 37039914 ● Search Scopus @ Elsevier (DOI): 10.1007/s12185-023-03601-2 (徳島大学機関リポジトリ: 118380, DOI: 10.1007/s12185-023-03601-2, PubMed: 37039914)
2.	Yoshiki Higa, Masahiro Hiasa, Hirofumi Tenshin, Emiko Nakaue, Mariko Tanaka, Sooha Kim, Motosumi Nakagawa, Sou Shimizu, Kotaro Tanimoto, Jumpei Teramachi, Takeshi Harada, Asuka Oda, Masahiro Oura, Kimiko Sogabe, Tomoyo Hara, Ryohei Sumitani, Tomoko Maruhashi, Hiroki Yamagami, Itsuro Endo, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe : The Xanthine Oxidase Inhibitor Febuxostat Suppresses Adipogenesis and Activates Nrf2., Antioxidants, Vol.12, No.1, 2023. (要約) Xanthine oxidoreductase (XOR) is a rate-limiting enzyme in purine catabolism that acts as a novel regulator of adipogenesis. In pathological states, xanthine oxidoreductase activity increases to produce excess reactive oxygen species (ROS). The nuclear factor erythroid 2-related factor 2 (Nrf2) is a critical inducer of antioxidants, which is bound and repressed by a kelch-like ECH-associated protein 1 (Keap1) in the cytoplasm. The Keap1-Nrf2 axis appears to be a major mechanism for robust inducible antioxidant defenses. Here, we demonstrate that febuxostat, a xanthine oxidase inhibitor, alleviates the increase in adipose tissue mass in obese mouse models with a high-fat diet or ovariectomy. Febuxostat disrupts in vitro adipocytic differentiation in adipogenic media. Adipocytes appeared at day 7 in absence or presence of febuxostat were 160.8 ± 21.2 vs. 52.5 ± 12.7 (p < 0.01) in 3T3L1 cells, and 126.0 ± 18.7 vs. 55.3 ± 13.4 (p < 0.01) in 10T1/2 cells, respectively. Adipocyte differentiation was further enhanced by the addition of hydrogen peroxide, which was also suppressed by febuxostat. Interestingly, febuxostat, but not allopurinol (another xanthine oxidase inhibitor), rapidly induced the nuclear translocation of Nrf2 and facilitated the degradation of Keap1, similar to the electrophilic Nrf2 activator omaveloxolone. These results suggest that febuxostat alleviates adipogenesis under oxidative conditions, at least in part by suppressing ROS production and Nrf2 activation. Regulation of adipocytic differentiation by febuxostat is expected to inhibit obesity due to menopause or overeating. (徳島大学機関リポジトリ) ● Metadata: 118313 (出版サイトへのリンク) ● Publication site (DOI): 10.3390/antiox12010133 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36670994 ● Search Scopus @ Elsevier (PMID): 36670994 ● Search Scopus @ Elsevier (DOI): 10.3390/antiox12010133 (徳島大学機関リポジトリ: 118313, DOI: 10.3390/antiox12010133, PubMed: 36670994)
3.	Sou Shimizu, Jumpei Teramachi, Takeshi Harada, Masahiro Hiasa, Hirofumi Tenshin, A Oda, A Seki, Y Inoue, Kotaro Tanimoto, Yoshiki Higa, M Oura, K Sogabe, Takeshi Harada, Ryohei Sumitani, T Maruhashi, H Yamagami, Y Sawa, Itsuro Endo, K Tsuneyama, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe : Aberrant upregulation of the endogenous PP2A inhibitor CIP2A is vital for myeloma cell growth and survival, International Journal of Myeloma, Vol.12, No.2, 14-23, 2022. (要約) <p>The serine/threonine kinase TAK1 is constitutively overexpressed and auto-phosphorylated in multiple myeloma (MM) cells. Protein phosphatase 2A (PP2A) is a major serine/threonine phosphatase which dephosphorylates proteins phosphorylated by various serine/threonine kinases to regulate multiple cellular functions. We recently reported that the serine/threonine kinase TGF-β-activated kinase-1 (TAK1) is highly expressed and auto-phosphorylated to mediate critical growth and survival signaling in MM cells. We demonstrate here that regulation of PP2A activity inversely affects the phosphorylation levels of TAK1 in MM cells, and that MM cells aberrantly overexpress cancerous inhibitor of PP2A (CIP2A), an endogenous inhibitor for PP2A. <i>CIP2A</i> gene silencing as well as treatment with the CIP2A inhibitor TD52 potently induced MM cell death along with suppression of TAK1 expression in MM cells. These results suggest the critical role of PP2A inactivation via CIP2A upregulation in TAK1 phosphorylation and its protein expression and thereby MM cell growth and survival, posing the CIP2A-PP2A axis as an important therapeutic target.</p> (キーワード) multiple myeloma / TAK1 / CIP2A / PP2A (PP2A) (徳島大学機関リポジトリ) ● Metadata: 117150 (出版サイトへのリンク) ● Publication site (DOI): 10.57352/ijm.12.2_14 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1390573947533793024 ● Search Scopus @ Elsevier (DOI): 10.57352/ijm.12.2_14 (徳島大学機関リポジトリ: 117150, DOI: 10.57352/ijm.12.2_14, CiNii: 1390573947533793024)
4.	Toyoaki Takagi, Sou Shimizu and Eiji Tanaka : Alveolar corticotomy for extrusion of an ankylosed lower first molar., Journal of Clinical Orthodontics, Vol.56, No.5, 299-307, 2022. (キーワード) Humans / Molar / Tooth Ankylosis / Tooth Movement Techniques (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35767859 ● Search Scopus @ Elsevier (PMID): 35767859 (PubMed: 35767859)
5.	Hirofumi Tenshin, Jumpei Teramachi, Mohannad Ashtar, Masahiro Hiasa, Yusuke Inoue, Asuka Oda, Kotaro Tanimoto, Sou Shimizu, Yoshiki Higa, Takeshi Harada, Masahiro Oura, Kimiko Sogabe, Tomoyo Hara, Ryohei Sumitani, Tomoko Maruhashi, Mayu Sebe, Rie Tsutsumi, Hiroshi Sakaue, Itsuro Endo, Toshio Matsumoto, Eiji Tanaka and Masahiro Abe : TGF-β-activated kinase-1 inhibitor LL-Z1640-2 reduces joint inflammation and bone destruction in mouse models of rheumatoid arthritis by inhibiting NLRP3 inflammasome, TACE, TNF-α and RANKL expression., Clinical & translational immunology, Vol.11, No.1, 2022. (要約) TAK1 inhibition with LLZ may become a novel treatment strategy to effectively alleviate inflammasome-mediated inflammation and RANKL-induced osteoclastic bone destruction in joints alongside its potent suppression of TNF-α and IL-6 production and proteinase-mediated pathological processes in RA. (徳島大学機関リポジトリ) ● Metadata: 117260 (出版サイトへのリンク) ● Publication site (DOI): 10.1002/cti2.1371 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 35079379 ● Search Scopus @ Elsevier (PMID): 35079379 ● Search Scopus @ Elsevier (DOI): 10.1002/cti2.1371 (徳島大学機関リポジトリ: 117260, DOI: 10.1002/cti2.1371, PubMed: 35079379)
6.	Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa, Asuka Oda, Ariunzaya Bat-Erdene, Takeshi Harada, Shingen Nakamura, Mohannad Ashtar, Sou Shimizu, Masami Iwasa, Kimiko Sogabe, Masahiro Oura, Shiroh Fujii, Kumiko Kagawa, Hirokazu Miki, Itsuro Endo, Tatsuji Haneji, Toshio Matsumoto and Masahiro Abe : TAK1 is a pivotal therapeutic target for tumor progression and bone destruction in myeloma, Haematologica, Vol.106, No.5, 1401-1413, 2021. (要約) Along with the tumor progression, the bone marrow microenvironment is skewed in multiple myeloma (MM), which underlies the unique pathophysiology of MM and confers aggressiveness and drug resistance in MM cells. TGF-β-activated kinase-1 (TAK1) mediates a wide range of intracellular signaling pathways. We demonstrate here that TAK1 is constitutively overexpressed and phosphorylated in MM cells, and that TAK1 inhibition suppresses the activation of NF-κB, p38MAPK, ERK and STAT3 to decrease the expression of critical mediators for MM growth and survival, including PIM2, MYC, Mcl-1, IRF4, and Sp1, along with a substantial reduction in the angiogenic factor VEGF in MM cells. Intriguingly, TAK1 phosphorylation was also induced along with upregulation of vascular cell adhesion molecule-1 (VCAM-1) in bone marrow stromal cells (BMSCs) in cocultures with MM cells, which facilitated MM cell-BMSC adhesion while inducing IL-6 production and receptor activator of nuclear factor κ-Β ligand (RANKL) expression by BMSCs. TAK1 inhibition effectively impaired MM cell adhesion to BMSCs to disrupt the support of MM cell growth and survival by BMSCs. Furthermore, TAK1 inhibition suppressed osteoclastogenesis enhanced by RANKL in cocultures of bone marrow cells with MM cells, and restored osteoblastic differentiation suppressed by MM cells or inhibitory factors for osteoblastogenesis overproduced in MM. Finally, treatment with the TAK1 inhibitor LLZ1640-2 markedly suppressed MM tumor growth and prevented bone destruction and loss in mouse MM models. Therefore, TAK1 inhibition may be a promising therapeutic option targeting not only MM cells but also the skewed bone marrow microenvironment in MM. (キーワード) Animals / Bone Marrow Cells / MAP Kinase Kinase Kinases / Mice / Multiple Myeloma / NF-kappa B / Osteoclasts / Osteolysis / RANK Ligand / Tumor Microenvironment (徳島大学機関リポジトリ) ● Metadata: 116529 (出版サイトへのリンク) ● Publication site (DOI): 10.3324/haematol.2019.234476 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32273474 ● Search Scopus @ Elsevier (PMID): 32273474 ● Search Scopus @ Elsevier (DOI): 10.3324/haematol.2019.234476 (徳島大学機関リポジトリ: 116529, DOI: 10.3324/haematol.2019.234476, PubMed: 32273474)
7.	Toyoaki Takagi, Sou Shimizu and Eiji Tanaka : Surgical orthodontic treatment of skeletal mandibular protrusion with multiple impacted ankylosed teeth treated with alveolar corticotomy, The Journal of Contemporary Dental Practice, Vol.22, No.4, 412-421, 2021. (要約) To present a case of skeletal mandibular protrusion with multiple impacted ankylosed teeth, which were treated with conventional orthognathic surgery and alveolar corticotomy, respectively. Tooth ankylosis is characterized by the fusion of a root surface with the surrounding alveolar bone. Various treatment modalities for tooth ankylosis have been developed and are used commonly in the clinic. Corticotomy is defined as the application of intentional surgical injury to the cortical bone to mobilize a tooth with the adjacent bone and soft tissues. The corticotomy technique has been improved in recent years to avoid possible risks such as periodontal damage, tooth devitalization, and osseous necrosis due to an inadequate blood supply. A female patient aged 16 years and 3 months was diagnosed with anterior crossbite and the impaction and ankylosis of multiple canines. After the confirmation of ankylosis, alveolar corticotomy was performed on the maxillary left and mandibular right canines. After 6 months of traction (patient age, 19 years and 7 months), both canines had extruded successfully. After the completion of preoperative treatment, bilateral intraoral vertical ramus osteotomy was performed to correct the anterior crossbite involving a skeletal mandibular protrusion. The amounts of mandibular setback on the right and left sides were approximately 7 and 5 mm, respectively. The total treatment period was 55 months. Acceptable occlusion with a balanced profile was maintained over a 5-year retention period, indicating the long-term stability and success of the treatment. Our results indicate that alveolar corticotomy should be considered to facilitate the treatment of multiple impacted ankylosed teeth. This report proposes an efficacy of alveolar corticotomy for extrusion of impacted ankylosed teeth. (キーワード) 成人 (adult) / Alveolar Process / Cuspid / 女性 (female) / Humans / Mandible / Tooth Ankylosis / Tooth Movement Techniques / Tooth, Impacted / Young Adult (徳島大学機関リポジトリ) ● Metadata: 117252 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 34267012 ● Search Scopus @ Elsevier (PMID): 34267012 (徳島大学機関リポジトリ: 117252, PubMed: 34267012)
8.	清水宗, 堀内信也, 森浩喜, 天眞寛文, 岩浅亮彦, 渡邉佳一郎, 高木豊明, 田中栄二 : 徳島大学病院矯正歯科における保険診療に関する実態調査-先天性疾患における裂奇形の併発について, 中·四国矯正歯科学会雑誌, Vol.32, No.1, 87-92, 2020年. (要約) 矯正歯科治療に健康保険が導入されて約40年が経過し，唇顎口蓋裂と顎変形症の他に2018年現在53項目が保険治療の対象になっている．今回，我々は当科における矯正歯科治療の保険適用患者の実態を調査し，特に唇顎口蓋裂と他の先天性疾患との関連性について臨床統計学的検討を行ったので報告する．徳島大学病院病院情報システム・データウェアハウスを用い，2008年1月から2018年12月までの11年間に当院矯正歯科を受診した患者から保険治療を受けている患者を抽出し，顎変形症単独症例を除く先天性疾患患者について，電子カルテ全文検索システムを用いて臨床統計学的検討を行った．研究対象期間に当科にて保険治療を受けた矯正患者は345人で，そのうち，本研究対象患者は，顎変形症単独症例を除く207人であった．患者の内訳は，裂奇形を主徴候とする症例が全体の5割を占め最も多く，次いで，6歯以上の先天性部分性無歯症，ゴールデンハー症候群(鰓弓異常症を含む)，ダウン症候群の順であった．また，症候性疾患の中で裂奇形の併発は，ピエール・ロバン症候群，ダウン症候群，ゴールデンハー症候群の順に多く，その裂型は，口蓋裂(軟口蓋裂を含む)，唇顎口蓋裂，唇裂の順に多かった．以上のことから，当病院は裂奇形を併発した先天性疾患への専門的な対応が不可欠であり，希少疾患にも柔軟に対応できるよう複数の診療科，職種による診療科の枠組みを超えたチーム医療体制の構築が必要であることが示唆された． (キーワード) 先天性疾患 / 口唇裂・口蓋裂 / 臨床統計学的調査 / 合併症 (徳島大学機関リポジトリ) ● Metadata: 116914 (文献検索サイトへのリンク) ● CiNii @ 国立情報学研究所 (CRID): 1050010457800163712 (徳島大学機関リポジトリ: 116914, CiNii: 1050010457800163712)
9.	Mohannad Ashtar, Hirofumi Tenshin, Jumpei Teramachi, Ariunzaya Bat-Erdene, Masahiro Hiasa, Asuka Oda, Kotaro Tanimoto, Sou Shimizu, Yoshiki Higa, Takeshi Harada, Masahiro Oura, Kimiko Sogabe, Shingen Nakamura, Shiroh Fujii, Ryohei Sumitani, Hirokazu Miki, Kengo Udaka, Mamiko Takahashi, Kumiko Kagawa, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : The Roles of ROS Generation in RANKL-Induced Osteoclastogenesis: Suppressive Effects of Febuxostat., Cancers, Vol.12, No.4, 2020. (要約) Receptor activator of NF-κB ligand (RANKL), a critical mediator of osteoclastogenesis, is upregulated in multiple myeloma (MM). The xanthine oxidase inhibitor febuxostat, clinically used for prevention of tumor lysis syndrome, has been demonstrated to effectively inhibit not only the generation of uric acid but also the formation of reactive oxygen species (ROS). ROS has been demonstrated to mediate RANKL-mediated osteoclastogenesis. In the present study, we therefore explored the role of cancer-treatment-induced ROS in RANKL-mediated osteoclastogenesis and the suppressive effects of febuxostat on ROS generation and osteoclastogenesis. RANKL dose-dependently induced ROS production in RAW264.7 preosteoclastic cells; however, febuxostat inhibited the RANKL-induced ROS production and osteoclast (OC) formation. Interestingly, doxorubicin (Dox) further enhanced RANKL-induced osteoclastogenesis through upregulation of ROS production, which was mostly abolished by addition of febuxostat. Febuxostat also inhibited osteoclastogenesis enhanced in cocultures of bone marrow cells with MM cells. Importantly, febuxostat rather suppressed MM cell viability and did not compromise Dox's anti-MM activity. In addition, febuxostat was able to alleviate pathological osteoclastic activity and bone loss in ovariectomized mice. Collectively, these results suggest that excessive ROS production by aberrant RANKL overexpression and/or anticancer treatment disadvantageously impacts bone, and that febuxostat can prevent the ROS-mediated osteoclastic bone damage. (徳島大学機関リポジトリ) ● Metadata: 115041 (出版サイトへのリンク) ● Publication site (DOI): 10.3390/cancers12040929 (文献検索サイトへのリンク) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 32283857 ● Search Scopus @ Elsevier (PMID): 32283857 ● Search Scopus @ Elsevier (DOI): 10.3390/cancers12040929 (徳島大学機関リポジトリ: 115041, DOI: 10.3390/cancers12040929, PubMed: 32283857)

国際会議:

1.	Hirofumi Tenshin, Takeshi Harada, Yusuke Inoue, Jumpei Teramachi, Masahiro Hiasa, Sou Shimizu, Emiko Nakaue, Kotaro Tanimoto, Yoshiki Higa, Masahiro Oura, Kimiko Sogabe, Tomoyo Hara, Ryohei Sumitani, Tomoko Maruhashi, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : Targeting SLAMF7 to disrupt myeloma-osteoclast interaction: elotuzumabs ADCC activity with Th1-like gamma delta T cells towards osteoclasts and myeloma cells., Cancer and bone society young investigator symposium, Feb. 2022.
2.	Hirofumi Tenshin, Takeshi Harada, 井上雄介, Jumpei Teramachi, Masahiro Hiasa, 小田明日香, Kotaro Tanimoto, Sou Shimizu, Yoshiki Higa, Masahiro Oura, Kimiko Sogabe, Tomoyo Hara, Tomoko Maruhashi, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : The anti-SLAMF7 elotuzumab enhances ADCC activity with Th1-like γδT cells towards osteoclasts and myeloma cells., The European Calcified Tissue Society 2021 Digital Congress 2021, web, Mar. 2021.
3.	Hirofumi Tenshin, Jumpei Teramachi, Masahiro Hiasa, Takeshi Harada, Eiji Tanaka, Kotaro Tanimoto, Sou Shimizu, Masahiro Oura, Kimiko Sogabe, Masahiro Abe, Toshio Matsumoto and Itsuro Endo : The novel therapeutic approaches with TAK1 inhibition against the aberrant NLRP3 inflammasome activation in rheumatoid arthritis, ECTS 2020 Digital Congress, Oct. 2020.
4.	Toyoaki Takagi, Sou Shimizu and Eiji Tanaka : Mandibular deviation and unilateral posterior crossbite treated with minicrew-assisted radid palatal expander., 9th IOC, Yokohama, Oct. 2020.

国内講演発表:

1.	西田真衣, 堀内信也, 清水宗, 田中茉里子, 和田涼平, 谷本幸多朗, 渡邉佳一郎, 田中栄二 : 徳島大学病院矯正歯科における成長ホルモン投与矯正患者に関する実態調査, 中·四国矯正歯科学会雑誌, Vol.35, No.1, 115, 2023年8月. (キーワード) 成長ホルモン(治療的利用) 外来患者歯科矯正治療 *病院歯科診療部門実態調査ヒト男女歯学
2.	比嘉佳基, 日浅雅博, 金秀河, 田中茉里子, 中上絵美子, 清水宗, 谷本幸多朗, 天眞寛文, 田中栄二, 安倍正博 : キサンチンオキシダーゼ阻害薬febuxostatはKEAP1-NRF2軸を介し脂肪細胞分化と骨芽細胞分化を制御する, 第81回日本矯正歯科学会学術大会, 2022年10月.
3.	清水宗, 寺町順平, 日浅雅博, 天眞寛文, 比嘉佳基, 中上絵美子, 安倍正博, 田中栄二 : 骨髄腫細胞の生存・増殖におけるTAK1-CIP2A経路の重要な役割, 第81回日本矯正歯科学会学術大会, 2022年10月.
4.	岩浅亮彦, 比嘉佳基, 中上絵美子, 吉永薫, 清水宗, 松木佑太, 谷本幸多朗, 渡邉佳一郎, 日浅雅博, 堀内信也, 田中栄二 : 特発性下顎頭吸収を呈する矯正患者の下顎頭の形態学的特徴, 第81回日本矯正歯科学会学術大会, 2022年10月.
5.	中上絵美子, 天眞寛文, 日浅雅博, 寺町順平, 原田武志, 井上雄介, 谷本幸多朗, 清水宗, 比嘉佳基, 遠藤逸朗, 田中栄二, 松本俊夫, 安倍正博 : プロテアソーム阻害薬による骨髄腫骨病変部選択的骨形成誘導活性の検討, 第40回日本骨代謝学会学術集会, 141, 2022年7月.
6.	田中茉里子, 日浅雅博, 谷本幸多朗, 天眞寛文, 清水宗, 比嘉佳基, 中上絵美子, 金秀河, 寺町順平, 原田武志, 中村信元, 遠藤逸朗, 田中栄二, 松本俊夫, 安倍正博 : 不動は骨髄腫骨病変部DPP-4発現増加と骨髄腫の腫瘍進展・髄外播種を加速させる, 第40回日本骨代謝学会学術集会, 2022年7月.
7.	岩浅亮彦, 比嘉佳基, 中上絵美子, 清水宗, 中村竜也, 藤原慎視, 堀内信也, 田中栄二 : 上顎埋伏犬歯に対して開窓牽引を行った叢生症例-長期保定観察例-, 中·四国矯正歯科学会雑誌, 2022年7月. (キーワード) 臨床矯正歯科学 (clinical orthodontics)
8.	寺町順平, 天眞寛文, 日浅雅博, 小田明日香, 清水宗, 住谷龍平, 大浦雅博, 曽我部公子, 丸橋朋子, 藤井志朗, 中村信元, 三木浩和, 遠藤逸朗, 原田武志, 安倍正博 : TAK1 阻害は骨髄腫の細胞間相互作用による骨破壊と薬剤耐性を改善する, 第47回日本骨髄腫学会学術集会, 2022年5月.
9.	比嘉佳基, 日浅雅博, 天眞寛文, 谷本幸多朗, 清水宗, 寺町順平, 原田武志, 小田明日香, 遠藤逸朗, 松本俊夫, 田中栄二, 安倍正博 : 骨髄腫骨髄微小環境の変容におけるキサンチンオキシダーゼ-ROS経路の重要な役割, International Journal of Myeloma, Vol.12, No.3, 149, 2022年5月.
10.	中上絵美子, 天眞寛文, 寺町順平, 日浅雅博, 原田武志, 谷本幸多朗, 清水宗, 比嘉佳基, 住谷龍平, 丸橋朋子, 大浦雅博, 曽我部公子, 中村信元, 三木浩和, 遠藤逸朗, 田中栄二, 安倍正博 : プロテアソーム阻害薬のパルス投与の骨代謝への影響, International Journal of Myeloma, Vol.12, No.3, 152, 2022年5月. (キーワード) 骨髄腫-多発性(薬物療法,病理学) / 骨組織リモデリング / パルス療法(薬物療法) / Proteasome Inhibitors(治療的利用,薬理学) / ヒト (Homo sapiens)
11.	Sou Shimizu, Jumpei Teramachi, Takeshi Harada, 小田明日香, Hirofumi Tenshin, Masahiro Hiasa, Kotaro Tanimoto, Yoshiki Higa, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : The critical roles of the TAK1-CIP2A axis in MM cell growth and survival and osteoclastogensis, 第83回日本血液学会学術集会, BPA-3-3, Sep. 2021.
12.	Hirofumi Tenshin, 寺町順平日浅雅博小田明日香原田武志, Masahiro Hiasa, 小田明日香, Takeshi Harada, Masahiro Oura, Kimiko Sogabe, Kotaro Tanimoto, Sou Shimizu, Yoshiki Higa, Eiji Tanaka, Itsuro Endo, Toshio Matsumoto and Masahiro Abe : NLRP3 inflammasome aggravates osteoclastic bone destruction in myeloma, 日本血液学会学術集会83回 Page 83回 Page OS2-4B-4(2021.09), Sep. 2021.
13.	佐藤博子, 堀内信也, 清水宗, 田中栄二 : 埋伏した巨大な上顎中切歯を伴う上顎前突症例, 中·四国矯正歯科学会雑誌, Vol.33, No.1, 86-87, 2021年8月. (キーワード) 顎前突症(合併症,治療,予後) 過剰歯(合併症,外科的療法,予後) 上顎骨切歯抜歯埋伏歯(合併症,外科的療法,予後) 歯科矯正用ブラケットヘッドギアヒト小児(6∼12) 男歯学
14.	清水宗, 寺町順平, 原田武志, 小田明日香, 天眞寛文, 日浅雅博, 谷本幸多朗, 比嘉佳基, 田中栄二, 松本俊夫, 安倍正博 : 骨髄腫細胞のPP2A阻害因子CIP2A発現誘導を介するTAK1活性化増強機構, 日本骨代謝学会学術集会プログラム抄録集, 149, 2020年10月.
15.	谷本幸多朗, 日浅雅博, 天眞寛文, ASHTAR MOHANNAD, 清水宗, 比嘉佳基, 寺町順平, 原田武志, 中村信元, 三木浩和, 遠藤逸朗, 田中栄二, 松本俊夫, 安倍正博 : 不動は骨吸収と骨髄腫進展を促進させる, 日本骨代謝学会学術集会プログラム抄録集, 149, 2020年10月.
16.	天眞寛文, ASHTAR MOHANNAD, 寺町順平, 日浅雅博, 谷本幸多朗, 清水宗, 比嘉佳基, 原田武志, 大浦雅博, 曽我部公子, 中村信元, 三木浩和, 遠藤逸朗, 田中栄二, 松本俊夫, 安倍正博 : 抗腫瘍薬が誘導するROSは破骨細胞分化を促進する:Xanthine oxidase阻害剤febuxostatの治療効果．, 日本骨代謝学会学術集会プログラム抄録集, 148, 2020年10月.
17.	Hirofumi Tenshin, アシテルモハナッド, Jumpei Teramachi, Masahiro Hiasa, Kotaro Tanimoto, Sou Shimizu, 比嘉佳基, Takeshi Harada, Masahiro Oura, Kimiko Sogabe, Shingen Nakamura, Hirokazu Miki, Itsuro Endo, Eiji Tanaka, Toshio Matsumoto and Masahiro Abe : 抗腫瘍薬が誘導するROSは破骨細胞分化を促進する Xanthine oxidase阻害剤febuxostatの治療効果, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, 148, Oct. 2020. (キーワード) Xanthine Oxidase(拮抗物質・阻害物質) / 活性酸素 (reactive oxygen species) / 抗腫瘍剤(毒性・副作用) / 骨吸収(化学的誘発,薬物療法,実験的) / 細胞分化 (cell differentiation) / 破骨細胞 (osteoclast) / 破骨細胞分化因子 / Febuxostat(治療的利用) / RAW264.7細胞 / マウス / 動物 (animal)
18.	比嘉佳基, 泰江章博, 坂巻拓馬, 清水宗, 渡邊正彦, 荒井大志, 堀内信也, 田中栄二 : Temporary Anchorage Device (TAD)を用いた非抜歯遠心移動治療の長期保定2症例．, 第63回中・四国矯正歯科学会大会, 2020年7月.
19.	原田武志, 天眞寛文, 谷本幸多朗, 清水宗, 安倍正博 : 骨髄腫細胞はHDAC1とIRF4を介しSLAMF7を過剰発現する, 第24回日本がん分子標的治療学会学術集会, 2020年6月.
20.	清水宗, 堀内信也, 天眞寛文, 岩浅亮彦, 渡邉佳一郎, 日浅雅博, 岩本勉, 田中栄二 : 徳島大学病院矯正歯科における口唇裂・口蓋裂患者の合併先天異常に関する実態調査．, 日本口蓋裂学会雑誌, 2019年5月.

科学研究費補助金 (KAKEN Grants Database @ NII.ac.jp)

ELK1を標的とした骨破壊抑制を併せ持つ新規抗腫瘍療法の開発 (研究課題/領域番号: 23K15975 )
研究者番号（20963755）による検索

助教 : 清水宗

研究活動

専門分野

研究テーマ

著書・論文

学術論文(審査論文):

国際会議:

国内講演発表:

科学研究費補助金 (KAKEN Grants Database @ NII.ac.jp)

助教 : 清水 宗

研究活動

専門分野

研究テーマ

著書・論文

学術論文(審査論文):

国際会議:

国内講演発表:

科学研究費補助金 (KAKEN Grants Database @ NII.ac.jp)

助教 : 清水宗