教員紹介

和田哲幸

和田哲幸: 准教授

所属	薬学部医療薬学科薬学研究科原子力研究所
学位	博士（薬学）
専門	電気生理学
ジャンル	医療・健康/薬と社会
コメント	電気生理学的手法と蛍光色素を用いてイオンチャネルの性質について研究を行っています。また、初年時教育としてのリメディアル教育の充実を図り、専門教育への橋渡しを行っています。
リサーチマップ	https://researchmap.jp/read0066148
メールアドレス	tetsu@phar.kindai.ac.jp

教育専門部門

学歴/経歴

学歴

近畿大学薬学部
近畿大学薬学研究科
Kinki University Graduate School, Division of Pharmaceutical Sciences

研究活動情報

研究分野

ライフサイエンス, 薬理学
ライフサイエンス, 薬系衛生、生物化学

論文

Sodium influx through cerebral sodium-glucose transporter type 1 exacerbates the development of cerebral ischemic neuronal damage
Yui Yamazaki; Shinichi Harada; Tetsuyuki Wada; Teruki Hagiwara; Shigeru Yoshida; Shogo Tokuyama
EUROPEAN JOURNAL OF PHARMACOLOGY 799 103-110 2017年3月 [査読有り]
Sodium transport through the cerebral sodium-glucose transporter exacerbates neuron damage during cerebral ischaemia
Yui Yamazaki; Shinichi Harada; Tetsuyuki Wada; Shigeru Yoshida; Shogo Tokuyama
JOURNAL OF PHARMACY AND PHARMACOLOGY 68 (7) 922-931 2016年7月 [査読有り]
Ouabain exerts cytoprotection by diminishing the intracellular K+ concentration increase caused by distinct stimuli in human leukemic cells
Masayuki Takechi; Tetsuyuki Wada; Hideki Yagi; Takashi Masuko; Atsufumi Kawabata
JOURNAL OF PHARMACY AND PHARMACOLOGY 67 (1) 126-132 2015年1月 [査読有り]

ミネルヴァ書房, 『ケアマネジメント用語辞典（改訂版）』 , 南武志; 吉田繁; 巽純子; 辻内俊文; 和田哲幸; 今西孝至 , 2007年
ミネルヴァ書房, 『ケアマネジメント用語辞典』 , 南武志; 吉田繁; 巽純子; 辻内俊文; 和田哲幸; 今西孝至 , 2005年

講演・口頭発表等

医薬品の適正使用に関わる薬剤師の責務～薬学部教員からの視点～ , 和田哲幸; 片岡大士; 伊内秋夫; 志熊理史; 伊内智; 秋本義雄 , 第60回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会 , 2021年10月
GPR120を介した性腺刺激ホルモン合成および分泌調節メカニズムについて , 森山隆太郎; 池田隼也; 原尚輝; 萩原央記; 和田哲幸 , 第114回日本繁殖生物学会大会 , 2021年9月
患者のための医療サービスと薬局薬剤師業務負担に関する予備的意識調査 , 和田哲幸; 片岡大士; 瀧一洋; 米島貴夢; 伊内智; 伊内秋夫 , 第54回日本薬剤師会学術大会（福岡） , 2021年9月

Inhibitory effects of tetrahydroisoquinoline derivatives on Ca2+ and Na+ channels in crude nerve endings , Y Zhang; J Abe; T Wada; S Ichida; GY Xu , BIOLOGICAL & PHARMACEUTICAL BULLETIN , 23 , 3 , 375 , 378 , 2000年3月
概要：Semi-synthetic tetrahydroisoquinoline derivatives prepared from natural alkaloids, possess Ca2+ antagonistic properties. These derivatives significantly blocked KCl-stimulated Ca2+ uptake (In chick and rat crude nerve endings) which fan be partially inhibited by the selective N-type Ca2+ channel blocker omega-conotoxin GVIA or the selective P-type Ca2+ channel blocker omega-agatoxin IVA. Moreover, PX42 (10 mu M; for the tetrahydroisoquinoline compounds in this study) could inhibit the activity of calmodulin-dependent phosphodiesterase and block veratridine-induced (or tetrodotoxin-sensitive) Na+ uptake. The possible mechanism(s) of non-selective inhibition of ion channels of PX42 is discussed.
Calcium/calmodulin inhibits the binding of specific [I-125]omega-conotoxin GVIA to chick brain membranes , S Ichida; J Abe; YA Zhang; K Sugihara; K Imoto; T Wada; H Sohma , NEUROCHEMICAL RESEARCH , 25 , 3 , 335 , 340 , 2000年3月
概要：The effect of Ca2+/calmodulin (CaM) on the specific binding of [I-125]omega-conotoxin GVIA (I-125-omega-CTX) to crude membranes from chick brain was investigated. When we examined the effects of the activation of various endogenous protein kinases on specific [I-125]omega-CTX binding to crude membranes, we observed that Ca2+/CaM had an inhibitory effect regardless of whether or not the standard medium contained ATP (0.5 mM). Ca2+/CaM also had an inhibitory effect in a simple binding-assay medium containing HEPES-HCl buffer, BSA, Ca2+ and CaM,and this effect was dependent on the concentration of Ca2+. The effect of Ca2+/CaM was attenuated by the CaM antagonists W-7 and CaM-kinase II fragment (290-309). An experiment with modified ELISA using purified anti omega-CTX antibody indicated that Ca2+/CaM did not affect the direct binding of [I-125]omega-CTX and CaM. These results suggest that Ca2+/CaM either directly or indirectly affects specific [I-125]omega-CTX binding sites, probably N-type Ca2+ channels in crude membranes from chick whole brain.
Proportions of Ca2+ channel subtypes in chick or rat P2 fraction and NG108-15 cells using various Ca2+ blockers , Zhang Yu-an; Takashi Imanishi; Tetsuyuki Wada; Seiji Ichida , Neurochemical Research , 24 , 8 , 1059 , 1066 , 1999年
概要：The proportions of calcium (Ca2+) channel subtypes in chick or rat P2 fraction and NG 108-15 cells were investigated using selective L-, N-, P- and P/Q- type Ca2+ channel blockers. KCl-stimulated 45Ca2+ uptake by chick P2 fraction was blocked by 40~50% using N-type Ca2+ channel blockers [ω- conotoxin GVIA, aminoglycoside antibiotics and dynorphin A(1-13)], but was not inhibited by P- or P/Q-type blockers (ω-agatoxin IVA or ω-conotoxin MVIIC). On the other hand, KCl-stimulated 45Ca2+ uptake by rat P2 fraction was blocked by 30~40% using P- or P/Q-type Ca2+ channel blockers, but was not inhibited by N-type Ca2+ channel blockers. The L-type Ca2+ channel blockers 1,4-dihydropyridines, diltiazem and verapamil, but not calciseptine (CaS), inhibited both KCl-stimulated 45Ca2+ uptake and veratridine-induced 22Na+ uptake by chick or rat P2 fraction with similar IC50 values. CaS did not have any effect on 45Ca2+ uptake by either chick or rat P2 fraction. In NG 108-15 cells, CaS, ω-agatoxin IVA and ω- conotoxin MVIIC, but not ω-conotoxin GVIA, inhibited KCl-stimulated 45Ca2+ uptake by 30-40%. Various combinations of these Ca2+ channel blockers had no significant additional effects in chick or rat P2 fraction or NG 108-15 cells. These findings suggest that KCl-stimulated 45Ca2+ uptake by chick or rat P2 fraction and NG 108-15 cells is a convenient and useful model for screening whether or not natural or synthetic substances have selective effects as L-, N-, P-, or P/Q- type Ca2+ channel antagonists or agonists.