Tokushima University / Educator and Researcher Directory --- Kanai, Mai

Field of Study

Subject of Study

Book / Paper

Academic Paper (Judged Full Paper):

1.	Sarina Takeuchi, Mayuko Shimizu, Satoshi Sumida, Koichi Tsuneyama, Mai Kanai, Watanabe Shunsuke, Kasai Takahiko and Michiko Yamashita : Clinico-laboratory and histological characteristics in patients with gelatinous transformation of bone marrow, Laboratory Medicine International, 4, 1, 34-45, 2025. (Keyword) gelatinous transformation / serum creatinine / bone marrow (Link to Publication Site) ● Publication site (DOI): 10.51041/lmi.4.1_34 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.51041/lmi.4.1_34 (DOI: 10.51041/lmi.4.1_34)
2.	Mai Kanai, Byambasuren Ganbaatar, Itsuro Endo, Yukiyo Ohnishi, Jumpei Teramachi, Hirofumi Tenshin, Yoshiki Higa, Masahiro Hiasa, Yukari Mitsui, Tomoyo Hara, Shiho Masuda, Hiroki Yamagami, Yuki Yamaguchi, Ken-ichi Aihara, Mayu Sebe, Rie Tsutsumi, Hiroshi Sakaue, Toshio Matsumoto and Masahiro Abe : Inflammatory Cytokine-Induced Muscle Atrophy and Weakness Can Be Ameliorated by an Inhibition of TGF-β-Activated Kinase-1, International Journal of Molecular Sciences, 25, 11, 5715, 2024. (Summary) Chronic inflammation causes muscle wasting. Because most inflammatory cytokine signals are mediated via TGF-β-activated kinase-1 (TAK1) activation, inflammatory cytokine-induced muscle wasting may be ameliorated by the inhibition of TAK1 activity. The present study was undertaken to clarify whether TAK1 inhibition can ameliorate inflammation-induced muscle wasting. SKG/Jcl mice as an autoimmune arthritis animal model were treated with a small amount of mannan as an adjuvant to enhance the production of TNF-α and IL-1β. The increase in these inflammatory cytokines caused a reduction in muscle mass and strength along with an induction of arthritis in SKG/Jcl mice. Those changes in muscle fibers were mediated via the phosphorylation of TAK1, which activated the downstream signaling cascade via NF-κB, p38 MAPK, and ERK pathways, resulting in an increase in myostatin expression. Myostatin then reduced the expression of muscle proteins not only via a reduction in MyoD1 expression but also via an enhancement of Atrogin-1 and Murf1 expression. TAK1 inhibitor, LL-Z1640-2, prevented all the cytokine-induced changes in muscle wasting. Thus, TAK1 inhibition can be a new therapeutic target of not only joint destruction but also muscle wasting induced by inflammatory cytokines. (Keyword) Animals / MAP Kinase Kinase Kinases / Muscular Atrophy / Mice / cytokinesis / Muscle Weakness / Myostatin / Muscle Proteins / Tumor Necrosis Factor-alpha / NF-kappa B / inflammation / signal transduction / Tripartite Motif Proteins / Disease Models, Animal / Interleukin-1beta / phosphorylation / Muscle, Skeletal / Zearalenone (Link to Publication Site) ● Publication site (DOI): 10.3390/ijms25115715 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 38891908 ● Summary page in Scopus @ Elsevier: 2-s2.0-85195855255 (DOI: 10.3390/ijms25115715, PubMed: 38891908, Elsevier: Scopus)
3.	Yukari Mitsui, Yuto Iizuka, Tomoaki Tanaka, Tomoyo Hara, Shiho Masuda, Yukiyo Ohnishi, Mai Kanai, Kiyoe Kurahashi, Sumiko Yoshida, Takeshi Kondo, Toshiko Kanezaki, Yasumi Shintani, Hiroki Yamagami, Hiroyuki Yamaguchi, Yuichi Fujinaka, Kana Morimoto, Atsuhisa Shirakami, Ken-ichi Aihara, Seiji Fukumoto, Masahiro Abe and Itsuro Endo : An attempt to create a treatment algorithm of central adrenal insufficiency using CRH test, DHEA-S and clinical evaluation., The Journal of Medical Investigation : JMI, 69, 3.4, 287-293, 2022. (Summary) Objective : To examine diagnostic performance of corticotropin-releasing hormone (CRH) test combined with baseline dehydroepiandrosterone sulfate (DHEA-S) in patients with a suspect of central adrenal insufficiency. Methods : Patients (n=215) requiring daily or intermittent hydrocortisone replacement, or no replacement were retrospectively checked with their peak cortisol after CRH test and baseline DHEA-S. Results : None of 106 patients with the peak cortisol · 17.5 g /L after CRH test required replacement, and all 64 patients with the peak cortisol < 10.0 g /L required daily replacement. Among 8 patients with 10.0 g /L the peak cortisol < 17.5 g /L and baseline DHEA-S below the reference range, 6 patients required daily replacement and 1 patient was under intermittent replacement. Among 37 patients with 10.0 g /L the peak cortisol < 17.5 g /L and baseline DHEA-S within the reference range, 10 and 6 patients were under intermittent and daily replacement, respectively. Conclusions : No patients with the peak cortisol · 17.5 g /L required hydrocortisone replacement, and all patients with the peak cortisol below 10.0 g /L required daily replacement. Careful clinical evaluation was required to determine requirement for replacement in patients with 10.0 g /L the peak cortisol < 17.5 g /L even in combination with baseline DHEA-S. J. Med. Invest. 69 : 287-293, August, 2022. (Keyword) Adrenal Insufficiency / Adrenocorticotropic Hormone / Algorithms / Corticotropin-Releasing Hormone / Dehydroepiandrosterone Sulfate / Humans / Hydrocortisone / Retrospective Studies (Tokushima University Institutional Repository) ● Metadata: 2010535 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.69.287 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 36244782 ● CiNii @ National Institute of Informatics (CRID): 1390575263318485248 ● Summary page in Scopus @ Elsevier: 2-s2.0-85139886801 (Tokushima University Institutional Repository: 2010535, DOI: 10.2152/jmi.69.287, PubMed: 36244782, CiNii: 1390575263318485248, Elsevier: Scopus)
4.	Dong Bingzi, Itsuro Endo, Ohnishi Yukoyo, Mitsui Yukari, Kiyoe Kurahashi, Mai Kanai, Masahiro Hiasa, Jumpei Teramachi, Hirofumi Tenshin, Seiji Fukumoto, Masahiro Abe and Toshio Matsumoto : Persistent Activation of Calcium-Sensing Receptor Suppresses Bone Turnover, Increases Microcracks, and Decreases Bone Strength., JBMR Plus, 3, 7, e10182, 2019. (Summary) Activating mutations of calcium-sensing receptor (CaSR) cause autosomal dominant hypocalcemia type 1 (ADH1). Patients with ADH1 exhibit similar features to patients with hypoparathyroidism, including reduced serum parathyroid hormone (PTH) and Ca with low bone turnover. Although persistent suppression of bone turnover may increase bone fragility, bone strength in ADH1 patients has been unclear. We created knock-in mice harboring the A843E activating mutation of CaSR, mimicking severe features of ADH1 patients. The severe form of ADH1 model mice showed smaller body and bone size with lower bone mineral density (BMD) and cortical area of the femur compared with age-matched wild-type (WT) mice. Bone strength in the femur was lower in ADH1 mice even after correction by bone geometry and/or BMD. Microcracks were markedly increased in ADH1 mice, but were rarely detected in WT mice. There was a negative correlation between bone strength corrected by bone geometry and/or BMD and microcrack number or density in ADH1 and WT mice. Among ADH1 mice, negative correlation was still observed between bone strength and microcrack number or density. Microcracks increased with age in ADH1 mice, and were negatively correlated with bone strength. Treatment with PTH(1-34) or a calcilytic, JTT-305, increased bone turnover, reduced microcracks, and increased bone strength to similar levels to those in WT mice. The increase in microcracks was associated with a reduction in bone strength in ADH1 mice, and aging aggravates these changes. These results demonstrate that activating mutation of CaSR causes reduction in PTH secretion with suppressed bone turnover, that reduced bone turnover is associated with an age-dependent increase in microcracks with a reduction in bone strength, and that both PTH(1-34) and calcilytic ameliorate all these changes in bone turnover and strength. It is suggested that fracture susceptibility may be increased in severe types of ADH1 patients especially in the elderly. © 2019 The Authors. published by Wiley Periodicals, Inc. on behalf of American Society for Bone and Mineral Research. (Link to Publication Site) ● Publication site (DOI): 10.1002/jbm4.10182 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 31372589 ● Search Scopus @ Elsevier (PMID): 31372589 ● Search Scopus @ Elsevier (DOI): 10.1002/jbm4.10182 (DOI: 10.1002/jbm4.10182, PubMed: 31372589)

Proceeding of International Conference:

1.	Michiko Yamashita, Sarina Takeuchi, Mizuki Fujii, Hikaru Nishizoe, Mai Kanai, Yuko Matsuda, Nobuyuki Sei, Mitsuho Watanabe and Takahiko Kasai : Biochemical Markers Correlated to Gelationous Degeneration of Bone Marrow: An Autopsy Study, ANNALS OF LABORATORY MEDICINE, Supplement, 42, S63, Seoul, Oct. 2022. (Keyword) Gelatinous degeneration / Serous atrophy / Bone marrow / cachexia / Protein-Energy Malnutrition
2.	Mai Kanai, Itsuro Endo, Yasuko Takahashi, Jumpei Teramachi, Hirofumi Tenshin, Masahiro Hiasa, Seiji Fukumoto, Masahiro Abe and Toshio Matsumoto : Establishment of model mice of FGF23-related hypophosphatemia induced by iron solution administration, ASBMR 2019, Orlando, Sep. 2019.

Proceeding of Domestic Conference:

1.	Sho Tanaka, Takumi Hari, Kazuki Fujiwara, Yuka Nomura, MATSUDA Wako, NAGAI Teruyuki, 大西幸代, Tomoyo Hara, Kiyoe Kurahashi, Ganbaatar Byambasuren, Mai Kanai and Itsuro Endo : ミトコンドリア移植による乳癌新規治療法開発の試み, 第45回徳島県医学検査学会, Dec. 2021.
2.	NAGAI Teruyuki, MATSUDA Wako, 大西幸代, Tomoyo Hara, Kiyoe Kurahashi, Ganbaatar Byambasuren, Mai Kanai and Itsuro Endo : 健常ミトコンドリア産生工場としての間葉系幹細胞, 第45回徳島県医学検査学会, Dec. 2021.
3.	Mai Kanai, Itsuro Endo, 平田有紀奈, 西尾進 and Kenya Kusunose : イバブラジン投与における心機能への効果について~心エコー図検査を用いた短期間パイロット研究~, 第45回徳島県医学検査学会, Dec. 2021.
4.	Mai Kanai, 大西幸代, Tomoyo Hara, Itsuro Endo, Masahiro Abe, Seiji Fukumoto and Toshio Matsumoto : TAK1 阻害による炎症性サイトカイン誘導性筋萎縮の改善, 第94回日本内分泌学会学術総会, Apr. 2021.
5.	Mai Kanai, 長井輝幸, Itsuro Endo, 大西幸代, 原倫世, 三井由加里, Kiyoe Kurahashi, Sumiko Yoshida, 瀬部真由, Hiroshi Sakaue, Seiji Fukumoto, 松本俊夫 and 安倍正博 : TAK1阻害による炎症性サイトカイン誘導性骨格筋萎縮の改善, Folia endocrinologica Japonica, 97, 1, 365, Apr. 2021. (Keyword) cytokinesis / 筋萎縮症(遺伝学,病理学,実験的) / 骨格筋(病理学) / 腫瘍壊死因子アルファ / 核内受容体NR2C2(拮抗物質・阻害物質) / マウス / animal
6.	Chihiro Yoshimoto, Sonoka Aibara, Teruyuki Nagai, Wako Matsuda, 大西幸代, Tomoyo Hara, 中村信元, Kumiko Kagawa, Hirokazu Miki, Masahiro Abe, Akiko Sakurai, Mai Kanai and Itsuro Endo : 血液悪性腫瘍化学療法入院中の骨格筋量の減少ビタミンD充足との関連, 第44回徳島県医学検査学会, Dec. 2020.
7.	Sonoka Aibara, Teruyuki Nagai, Wako Matsuda, Chihiro Yoshimoto, 大西幸代, Tomoyo Hara, Mai Kanai, Itsuro Endo, Hirokazu Miki and Akiko Sakurai : 多発性骨髄腫に対するゾレドロン酸の治療経験, 第44回徳島県医学検査学会, Dec. 2020.
8.	Teruyuki Nagai, Chihiro Yoshimoto, Wako Matsuda, Sonoka Aibara, 大西幸代, Tomoyo Hara, Kiyoe Kurahashi, Masahiro Abe, Mai Kanai and Itsuro Endo : TAK1阻害による炎症性サイトカイン誘導性筋萎縮の改善, 第44回徳島県医学検査学会, Dec. 2020.
9.	Wako Matsuda, Sonoka Aibara, Teruyuki Nagai, Chihiro Yoshimoto, 金島慶太, 大西幸代, Tomoyo Hara, Akiko Sakurai, Mai Kanai and Itsuro Endo : 原発性骨粗鬆症におけるビタミンD充足の検討, 第44回徳島県医学検査学会, Dec. 2020.
10.	Kiyoe Kurahashi, 村井純平, 堀太貴, Ryohei Sumitani, Takeshi Harada, Shingen Nakamura, Mai Kanai, Akiko Sakurai, 原倫世, 桝田志保, Sumiko Yoshida, Itsuro Endo, 松本俊夫, Masahiro Abe and Seiji Fukumoto : 高1,25(OH)2D血症による高Ca血症を来したホジキンリンパ腫の一例, The Annual Meeting of the Japanese Society for Bone and Mineral Research Program & Abstracts, 150, Oct. 2020. (Keyword) Calcitriol Dacarbazine(治療的利用) Doxorubicin(治療的利用) Hodgkin病(合併症,病理学,薬物療法) Vinblastine(治療的利用) *高カルシウム血症(病因,病理学,薬物療法) 免疫組織化学 Brentuximab Vedotin(治療的利用) ヒト高齢者(65~79) 男
11.	黒田大智, 水本健斗, Akiko Sakurai, Mai Kanai, 大西幸代, 松岡飛翔 and Itsuro Endo : 鉄剤投与によるFGF23関連低リン血症モデル作成の試み, 第43回徳島県医学検査学会, Dec. 2019.
12.	菊池結愛, 坂井ちか, Akiko Sakurai, Mai Kanai, 大西幸代, Masahiro Abe and Itsuro Endo : TAK1阻害による炎症性サイトカイン誘導性筋萎縮の改善, 第43回徳島県医学検査学会, Dec. 2019.
13.	水本健斗, 菊池結愛, Kiyoe Kurahashi, Akiko Sakurai, Mai Kanai, 大西幸代 and Itsuro Endo : カルシウム感知受容体活性型変異における耐糖能異常, 第43回徳島県医学検査学会, Dec. 2019.
14.	坂井ちか, 菊池結愛, 黒田大智, Akiko Sakurai, Mai Kanai, 大西幸代 and Itsuro Endo : 副腎皮質機能低下症・不全症のカットオフ値設定の試み, 第43回徳島県医学検査学会, Dec. 2019.
15.	Mai Kanai, 松岡飛翔, Itsuro Endo, 大西幸代, Yuichi Takashi, Kiyoe Kurahashi, Sumiko Yoshida, Ken-ichi Aihara, Masahiro Abe, Seiji Fukumoto and Toshio Matsumoto : 鉄製剤投与によるFGF23関連低リン血症モデル作成の試み, 第92回日本内分泌学会学術総会, 95, 1, 422, May 2019.
16.	木村優里, 高橋寛典, 松島滉海, Akiko Sakurai, Mai Kanai and Itsuro Endo : TAK1阻害による炎症性サイトカイン誘導性サルコペ二ア改善の可能性, 第42回徳島県医学検査学会, Dec. 2018.
17.	Hiromi Matsushima, Yuri Kimura, 高橋寛典, Akiko Sakurai, Mai Kanai, Takeshi Kondo, 桝田志保, Tomoteru Kishimoto and Itsuro Endo : hCG, FSH製剤の併用によりパートナーの妊娠，健常児正常出産が確認された低ゴナドトロピン性男背性性腺機能低下症の2例, 第42回徳島県医学検査学会, Dec. 2018.
18.	Ako Kakee, Mayu Nishikawa, Jin Furuike, Mai Kanai and Noriko Kagawa : 腎盂に発生した肉腫様がんの一例, 第41回徳島県臨床検査技師会, Dec. 2017.
19.	Jin Furuike, Ako Kakee, Mayu Nishikawa, Mai Kanai and Noriko Kagawa : 拡張型心筋症の病理学的検討-2 ー全周性切り出しによるー, 第41回徳島県臨床検査技師会, Dec. 2017.
20.	Mayu Nishikawa, Ako Kakee, Jin Furuike, Mai Kanai and Noriko Kagawa : 拡張型心筋症の病理学的検討-1 ー介在板間の測定ー, 第41回徳島県臨床検査技師会, Dec. 2017.
21.	岡諭紀, Mai Kanai, Akiko Sakurai and Itsuro Endo : 免疫チェックポイント阻害薬で中枢性副腎不全を来した2例, 第41回徳島県医学検査学会, Dec. 2017.
22.	野原圭一郎, 岡諭紀, 藤田幸那, Mai Kanai, Akiko Sakurai and Itsuro Endo : デノスマブによる対糖能改善, 第41回徳島県医学検査学会, Dec. 2017.

Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)

ステロイド骨粗鬆症へのSema3A, IL-11の関与と新規治療への応用 (Project/Area Number: 25K11823 )
Inflammatory cytokine-induced muscle atrophy and weakness can be ameliorated by an inhibition of TGF-beta-activated kinase-1 (Project/Area Number: 21K07339 )
Search by Researcher Number (90836470)

Assistant Professor : Kanai, Mai

Research

Field of Study

Subject of Study

Book / Paper

Academic Paper (Judged Full Paper):

Proceeding of International Conference:

Proceeding of Domestic Conference:

Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)