Updated on 2025/06/27

写真a

 
MURAKAMI Shingo
 
Organization
Faculty of Science and Engineering Professor
Other responsible organization
Electrical, Electronic, and Communication Engineering Course of Graduate School of Science and Engineering, Master's Program
Electrical Engineering and Information Systems Course of Graduate School of Science and Engineering, Doctoral Program
Contact information
The inquiry by e-mail is 《here
External link

Degree

  • 博士(工学) ( 東京大学 )

  • 修士(工学) ( 東京大学 )

Education

  • 2001.3
     

    The University of Tokyo   Graduate School, Division of Engineering   doctor course   completed

  • 1998.3
     

    The University of Tokyo   Graduate School, Division of Engineering   master course   completed

  • 1996.3
     

    Kyoto University   Faculty of Engineering   graduated

Research History

  • 2019.4 - 2022.3

    自然科学研究機構岡崎共通研究施設計算科学研究センター   外部運営委員

  • 2018.4 -  

    東邦大学理学部生理学講座統合生理学分野   非常勤講師

  • 2018.4 -  

    中央大学理工学部   教授

  • 2016.4 - 2018.3

    東邦大学医学部生理学講座統合生理分野   講師

  • 2007.4 - 2016.3

    大阪大学臨床医工学融合研究教育センター   助教(兼任)

  • 2006.4 - 2016.3

    大阪大学大学院医学系研究科薬理学講座(分子・細胞薬理学)   助手(現・助教)

  • 2006.4 - 2016.3

    大阪大学大学院医学系研究科薬理学講座(分子・細胞薬理学) 助手(現・助教)

  • 2005.1 - 2006.3

    ニューメキシコ大学医学部神経内科   Research Assistant Professor

  • 2002.12 - 2005.1

    ニューメキシコ大学医学部神経内科   Research Scientist

  • 2001.4 - 2002.12

    ニューメキシコ大学医学部神経内科   Post-Doctorial Scientist

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Professional Memberships

  • 応用物理学会

  • 日本生体医工学会

  • 日本神経回路学会

  • 日本循環薬理学会

  • 日本薬理学会

  • 日本生理学会

  • 日本不整脈心電学会

  • Asia-Pacific Neural Network Society

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Research Interests

  • Physiology

  • Systemis Biology

  • 医工学

  • Pharmacology

Research Areas

  • Life Science / Biomaterials  / Biomedical engineering/Biomaterial science and engineering

  • Life Science / Neuroscience-general  / Neurophysiology/General neuroscience

  • Life Science / Clinical pharmacy  / 生理学一般

  • Informatics / Life, health and medical informatics  / 生命・健康・医療情報学

  • Life Science / Basic brain sciences  / Brain biometrics

  • Life Science / Biomedical engineering  / Biomedical engineering/Biomaterial science and engineering

  • Life Science / Pharmacology  / 薬理学一般

  • Life Science / Physiology  / 生理学一般

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Papers

  • Quantitative evaluation of virtual reality-related attention allocation through somatic P300 response Reviewed

    Kaito Kageyama, Rintaro Maki, Yasushi Nakatani, Yumie Ono, Shingo Murakami

    Advanced Biomedical Engineering   13   116 - 122   2024.4

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    Authorship:Last author, Corresponding author   Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.14326/abe.13.116

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  • 光音響イメージングによるカルシウム濃度計測のための吸光試薬のスクリーニングシステム Reviewed

    山本 勇志, 興野 大輝, 五味 涼太, 庄司 一郎, 村上 慎吾

    電子情報通信学会論文誌 D   J107-D ( 4 )   265 - 272   2024.4

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  • Measuring the Permittivity of Liposome and Yeast Using a 3D-printed Electrode-replaceable Measuring Cell Reviewed

    Yuji KAGEYAMA, Haruna SUEOKA, Akira KIMURA, Masaki SATO, Akira ITO, Tetsuro HORIE, Genki OGATA, Yasuaki EINAGA, Hiroaki SUZUKI, Shingo MURAKAMI

    Advanced Biomedical Engineering   13   90 - 99   2024

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    Authorship:Last author, Corresponding author   Language:English   Publishing type:Research paper (scientific journal)   Publisher:Japanese Society for Medical and Biological Engineering  

    DOI: 10.14326/abe.13.90

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  • Event-related Potentials based Evaluation of attention allocation while watching VR Reviewed

    Advanced Biomedical Engineering   11   1 - 9   2022.1

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  • Different voltage dependence of ICaL blockade in nonselective IKr blockers causes their opposite effects on early afterdepolarization in drug-induced arrhythmia Reviewed

    Akira Kimura, Shingo Murakami

    Journal of Pharmacological Sciences   147 ( 1 )   95 - 103   2021.9

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    Authorship:Last author, Corresponding author   Language:English   Publishing type:Research paper (scientific journal)   Publisher:September 2021,  

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  • Computer modeling defines the system driving a constant current crucial for homeostasis in the mammalian cochlea by integrating unique ion transports Reviewed International journal

    Fumiaki Nin, Takamasa Yoshida, Shingo Murakami, Genki Ogata, Satoru Uetsuka, Samuel Choi, Katsumi Doi, Seishiro Sawamura, Hidenori Inohara, Shizuo Komune, Yoshihisa Kurachi, Hiroshi Hibino

    npj Systems Biology and Applications   3 ( 24 )   1 - 10   2017.8

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Nature Publishing  

    The cochlear lateral wall-an epithelial-like tissue comprising inner and outer layers-maintains +80 mV in endolymph. This endocochlear potential supports hearing and represents the sum of all membrane potentials across apical and basolateral surfaces of both layers. The apical surfaces are governed by K+ equilibrium potentials. Underlying extracellular and intracellular [K+] is likely controlled by the "circulation current," which crosses the two layers and unidirectionally flows throughout the cochlea. This idea was conceptually reinforced by our computational model integrating ion channels and transporters; however, contribution of the outer layer's basolateral surface remains unclear. Recent experiments showed that this basolateral surface transports K+ using Na+, K+-ATPases and an unusual characteristic of greater permeability to Na+ than to other ions. To determine whether and how these machineries are involved in the circulation current, we used an in silico approach. In our updated model, the outer layer's basolateral surface was provided with only Na+, K+-ATPases, Na+ conductance, and leak conductance. Under normal conditions, the circulation current was assumed to consist of K+ and be driven predominantly by Na+, K+-ATPases. The model replicated the experimentally measured electrochemical properties in all compartments of the lateral wall, and endocochlear potential, under normal conditions and during blocking of Na+, K+-ATPases. Therefore, the circulation current across the outer layer's basolateral surface depends primarily on the three ion transport mechanisms. During the blockage, the reduced circulation current partially consisted of transiently evoked Na+ flow via the two conductances. This work defines the comprehensive system driving the circulation current.

    DOI: 10.1038/s41540-017-0025-0

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  • アセチルコリン感受性カリウム電流における短期脱感作のシミュレーション解析 Reviewed

    村上慎吾, 稲野辺厚, 倉智嘉久

    心電図   35 ( 4 )   245 - 257   2016.10

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    Authorship:Lead author   Language:Japanese   Publishing type:Research paper (scientific journal)   Publisher:日本心電学会  

    Acetylcholine (ACh) increases the amplitude of cardiac K+ current (IK.ACh) through activation of the muscarinic K+ (KACh) channel, but the amplitude gradually decreases to a quasi-steady-state level within seconds. This phenomenon, known as short-term desensitization, is believed to play a role in cellular adaptation to external input. However, the precise mechanism and physiological role of short-term desensitization is still unclear. In the present review, we introduced our experimental and theoretical studies on the mechanisms underlying short-term desensitization of IK.ACh. In atrial myocytes, short-term desensitization features the unique dose responses of the transient and quasi-steady state IK.ACh, effects of ACh preperfusion and recovery from short-term desensitization. In simulation analysis, two conditions are required for the mathematical IK.ACh model to reconstitute short-term desensitization. The first condition is distinct muscarinic receptors (M2Rs) with different affinities for ACh, which conferred an IK.ACh response over a wide range of ACh concentrations. The second condition is 2 distinct KACh channels with different affinities for the G-proteinβγsubunit, which contributes to reconstitution of the temporal behavior of IK.ACh. Under these conditions, the model quantitatively reproduced the unique properties of short-term desensitization observed in experiments. Furthermore, the present model conferred vagal escape on the mathematical action potential models of sinus node cells. Therefore, 2 different populations of KACh channels and M2Rs may be responsible for short-term desensitization and vagal escape at nodal cells.

    DOI: 10.5105/jse.35.245

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    Other Link: http://search.jamas.or.jp/link/ui/2016139097

  • The unique electrical properties in an extracellular fluid of the mammalian cochlea; their functional roles, homeostatic processes, and pathological significance Reviewed

    Fumiaki Nin, Takamasa Yoshida, Seishiro Sawamura, Genki Ogata, Takeru Ota, Taiga Higuchi, Shingo Murakami, Katsumi Doi, Yoshihisa Kurachi, Hiroshi Hibino

    PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY   468 ( 10 )   1637 - 1649   2016.10

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    DOI: 10.1007/s00424-016-1871-0

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  • The unique ion permeability profile of cochlear fibrocytes and its contribution to establishing their positive resting membrane potential Reviewed

    Takamasa Yoshida, Fumiaki Nin, Shingo Murakami, Genki Ogata, Satoru Uetsuka, Samuel Choi, Takashi Nakagawa, Hidenori Inohara, Shizuo Komune, Yoshihisa Kurachi, Hiroshi Hibino

    PFLUGERS ARCHIV-EUROPEAN JOURNAL OF PHYSIOLOGY   468 ( 9 )   1609 - 1619   2016.9

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    DOI: 10.1007/s00424-016-1853-2

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  • Mechanisms of astrocytic K+ clearance and swelling under high extracellular K+ concentrations Reviewed

    Shingo Murakami, Yoshihisa Kurachi

    JOURNAL OF PHYSIOLOGICAL SCIENCES   66 ( 2 )   127 - 142   2016.3

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    DOI: 10.1007/s12576-015-0404-5

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  • Invariance in current dipole moment density across brain structures and species: Physiological constraint for neuroimaging Reviewed

    Shingo Murakami, Yoshio Okada

    NEUROIMAGE   111   49 - 58   2015.5

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    DOI: 10.1016/j.neuroimage.2015.02.003

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  • Short-term desensitization of muscarinic K+ current in the heart Reviewed

    Shingo Murakami, Atsushi Inanobe, Yoshihisa Kurachi

    Biophysical Journal   105 ( 6 )   1515 - 1525   2013.11

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  • 内耳内リンパ液の特殊電位環境の成立機構の理解

    日比野浩, 任書晃, 村上慎吾, 土井勝美, 鈴木敏弘, 久育男, 倉智嘉久

    日本耳鼻咽喉科学会会報   116 ( 2 )   60 - 68   2013.2

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    Language:Japanese   Publisher:日本耳鼻咽喉科学会  

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  • Computational model of a circulation current that controls electrochemical properties in the mammalian cochlea Reviewed

    Fumiaki Nin, Hiroshi Hibino, Shingo Murakami, Toshihiro Suzuki, Yasuo Hisa, Yoshihisa Kurachi

    PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA   109 ( 23 )   9191 - 9196   2012.6

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    DOI: 10.1073/pnas.1120067109

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  • Transmural dispersion of repolarization determines scroll wave behavior during ventricular tachyarrhythmias - a simulation study - Reviewed

    Ryo Haraguchi, Takashi Ashihara, Tsunetoyo Namba, Kunichika Tsumoto, Shingo Murakami, Yoshihisa Kurachi, Takanori Ikeda, Kazuo Nakazawa

    Circulation Journal   75 ( 1 )   80 - 88   2011

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Japanese Ciruculation Society  

    DOI: 10.1253/circj.CJ-10-0071

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  • フィジオームとシステムバイオロジー

    村上慎吾, 倉智嘉久

    生体の科学   61 ( 4 )   364 - 371   2010.8

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  • Cellular modelling: experiments and simulation to develop the physiological model for G-protein control of cardiac muscarinic K+ channels Reviewed

    Shingo Murakami, Shingo Suzuki, Masaru Ishii, Atsushi Inanobe, Yoshihisa Kurachi

    Philosophical Transactions of the Royal Society A   368 ( 1921 )   2983 - 3000   2010.1

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  • 薬物誘発性不整脈の発生危険度予測システムの開発 Reviewed

    村上慎吾, 鈴木慎悟, 上島豊, 野村泰伸, 倉智嘉久

    生体医工学   48 ( 1 )   106 - 114   2010.1

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  • Inwardly rectifying potassium channels: their structure, function and physiological roles Reviewed International journal

    Hiroshi Hibino, Atsushi Inanobe, Kazuharu Furutani, Shingo Murakami, Ian Findlay, Yoshihisa Kurachi

    Physiological Review   90 ( 1 )   291 - 366   2010.1

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:American Physiological Scoiety  

    Inwardly rectifying K(+) (Kir) channels allow K(+) to move more easily into rather than out of the cell. They have diverse physiological functions depending on their type and their location. There are seven Kir channel subfamilies that can be classified into four functional groups: classical Kir channels (Kir2.x) are constitutively active, G protein-gated Kir channels (Kir3.x) are regulated by G protein-coupled receptors, ATP-sensitive K(+) channels (Kir6.x) are tightly linked to cellular metabolism, and K(+) transport channels (Kir1.x, Kir4.x, Kir5.x, and Kir7.x). Inward rectification results from pore block by intracellular substances such as Mg(2+) and polyamines. Kir channel activity can be modulated by ions, phospholipids, and binding proteins. The basic building block of a Kir channel is made up of two transmembrane helices with cytoplasmic NH(2) and COOH termini and an extracellular loop which folds back to form the pore-lining ion selectivity filter. In vivo, functional Kir channels are composed of four such subunits which are either homo- or heterotetramers. Gene targeting and genetic analysis have linked Kir channel dysfunction to diverse pathologies. The crystal structure of different Kir channels is opening the way to understanding the structure-function relationships of this simple but diverse ion channel family.

    DOI: 10.1152/physrev.00021.2009

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  • Development of drug-induced arrhythmia prediction system

    Shingo Murakami, Shingo Suzuki, Yutaka Ueshima, Taishin Nomura, Yoshihisa Kurachi

    Transactions of Japanese Society for Medical and Biological Engineering   48 ( 1 )   106 - 114   2010

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  • In silico study on the effects of I_<Kr> and I_<Kur> block kinetics on prolongation of human action potential

    MURAKAMI Shingo, TSUJIMAE Kenji, SUZUKI Shingo, KURACHI Yoshihisa

    Japanese Journal of Electrocardiology   29 ( 2 )   126 - 132   2009.4

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    Language:Japanese   Publisher:The Japanese Society of Electrocardiology  

    DOI: 10.5105/jse.29.126

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    Other Link: http://search.jamas.or.jp/link/ui/2009199477

  • 貫壁性再分極時間の差が増悪すると3次元スパイラルリエントリーの分裂が促進される シミュレーションモデルによる検討

    原口 亮, 芦原 貴司, 八尾 武憲, 難波 経豊, 藤堂 貴弘, 村上 慎吾, 倉智 嘉久, 池田 隆徳, 中沢 一雄

    心電図   29 ( Suppl.1 )   S - 86   2009.3

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  • In silico risk assessment for drug-induction of cardiac arrhythmia Reviewed

    Shingo Suzuki, Shingo Murakami, Kenji Tsujimae, Ian Findlay, Yoshihisa Kurachi

    Progress in Biophysics & Molecular Biology   98 ( 1 )   52 - 60   2008.11

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  • 3次元心室壁モデルにおけるスパイラルリエントリーのin silicoフィラメント動態解析~致死的不整脈防御機構としての心室較差の電気生理学的意義~ Reviewed

    芦原貴司, 藤堂貴弘, 難波経豊, 村上慎吾, 倉智嘉久, 中沢一雄

    生体医工学   46 ( 6 )   660 - 666   2008.11

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  • In silico prediction of the chemical block of human Ether-a-go-go-Related Gene (hERG) K+ current Reviewed

    Atsushi Inanobe, Narutoshi Kamiya, Shingo Murakami, Yoshifumi Fukunishi, Haruki Nakamura, Yoshihisa Kurachi

    Journal of Physiological Sciences   58 ( 7 )   459 - 470   2008.11

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  • 貫壁性再分極時間の差が頻脈性不整脈の興奮伝播ダイナミクスに与える影響について

    原口 亮, 芦原 貴司, 鈴木 慎悟, 難波 経豊, 藤堂 貴弘, 八尾 武憲, 村上 慎吾, 倉智 嘉久, 池田 隆徳, 中沢 一雄

    心電図   28 ( 5 )   466 - 466   2008.10

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  • クレフト電位仮説による貫壁性心室較差の再現に関する理論的研究

    鈴木 慎悟, 芦原 貴司, 原口 亮, 村上 慎吾, 倉智 嘉久, 中沢 一雄

    心電図   28 ( 5 )   525 - 525   2008.10

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  • Scroll wave dynamics in tachyarrhythmia: Roles of transmural gradient. Reviewed

    Haraguchi R, Ashihara T, Yao T, Todo T, Namba T, Murakami S, Kurachi Y, Nakazawa K

    Transactions of the Japanese Society for Medical and Biological Engineering (JSMBE).   46   480 - 481   2008.7

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  • In silico study on the effects of I-Kur block kinetics on prolongation of human action potential after atrial fibrillation-induced electrical remodeling Reviewed

    Kenji Tsujimae, Shingo Murakami, Yoshihisa Kurachi

    AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY   294 ( 2 )   H793 - H800   2008.2

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    DOI: 10.1152/ajpheart.01229.2007

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  • Physiological modulation of voltage-dependent inactivation in the cardiac muscle L-type calcium channel: A modelling study Reviewed

    Ian Findlay, Shingo Suzuki, Shingo Murakami, Yoshihisa Kurachi

    PROGRESS IN BIOPHYSICS & MOLECULAR BIOLOGY   96 ( 1-3 )   482 - 498   2008.1

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    DOI: 10.1016/j.pbiomolbio.2007.07.002

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  • In silico study on the effects of I-kur block kinetics on prolongation of human action potential after atrial fibrillation-induced electrical-remodeling Reviewed

    Kenji Tsujimae, Shingo Muramami, Yoshihisa Kurachi

    JOURNAL OF PHARMACOLOGICAL SCIENCES   106 ( 2 )   261P - 261P   2008

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  • Microstructure-Based Monte Carlo Simulation of Ca2+ Dynamics Evoking Cardiac Calcium Channel Inactivation Reviewed

    Kawazu Toshihiro, Murakami Shingo, Adachi-Akahane Satomi, Findlay Ian, Ait-Haddou Rachid, Kurachi Yoshihisa, Nomura Taishin

    The Journal of Physiological Sciences   58 ( 7 )   471 - 480   2008

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:PHYSIOLOGICAL SOCIETY OF JAPAN  

    Ca2+ dynamics underlying cardiac excitation-contraction coupling are essential for heart functions. In this study, we constructed microstructure-based models of Ca2+ dynamics to simulate Ca2+ influx through individual L-type calcium channels (LCCs), an effective Ca2+ diffusion within the cytoplasmic space and in the dyadic space, and the experimentally observed calcium-dependent inactivation (CDI) of the LCCs induced by local and global Ca2+ sensing. The models consisted of LCCs with distal and proximal Ca2+ (Calmodulin-Ca2+ complex) binding sites. In one model, the intracellular space was organelle-free cytoplasmic space, and the other was with a dyadic space including sarcoplasmic reticulum membrane. The Ca2+ dynamics and CDI of the LCCs in the model with and without the dyadic space were then simulated using the Monte Carlo method. We first showed that an appropriate set of parameter values of the models with effectively extra-slow Ca2+ diffusion enabled the models to reproduce major features of the CDI process induced by the local and global sensing of Ca2+ near LCCs as measured with single and two spatially separated LCCs by Imredy and Yue (Neuron. 1992;9:197-207). The effective slow Ca2+ diffusion might be due to association and dissociation of Ca2+ and Calmodulin (CaM). We then examined how the local and global CDIs were affected by the presence of the dyadic space. The results suggested that in microstructure modeling of Ca2+ dynamics in cardiac myocytes, the effective Ca2+ diffusion under CaM-Ca2+ interaction, the nanodomain structure of LCCs for detailed CDI, and the geometry of subcellular space for modeling dyadic space should be considered.<br>

    DOI: 10.2170/physiolsci.RP013208

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  • Mechanisms of action of antiarrhythmic drugs Reviewed

    Shingo Murakami, Yoshihisa Kurachi

    Electrical Diseases of the Heart: Genetics, Mechanisms, Treatment, Prevention   133 - 144   2008

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    Authorship:Lead author   Language:English   Publishing type:Part of collection (book)   Publisher:Springer London  

    DOI: 10.1007/978-1-84628-854-8_7

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  • Frequency dependent effects of various IKr blockers on cardiac action potential duration in a human atrial model Reviewed

    Kenji Tsujimae, Shingo Suzuki, Shingo Murakami, Yoshihisa Kurachi

    American Journal of Physiology - Heart and Circulatory Physiology   293 ( 1 )   H660 - H669   2007.1

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  • Contributions of principal neocortical neurons to magnetoencephalography (MEG) and electroencephalography (EEG) signals Reviewed

    Shingo Murakami, Yoshio Okada

    Journal of Physiology   575 ( 3 )   925 - 936   2006.11

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  • Contribution of ionic currents to magnetoencephalography (MEG) and electroencephalography (EEG) signals generated by guinea-pig CA3 slices Reviewed

    S Murakami, A Hirose, YC Okada

    JOURNAL OF PHYSIOLOGY-LONDON   553 ( 3 )   975 - 985   2003.12

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    Authorship:Lead author   Language:English   Publishing type:Research paper (scientific journal)  

    DOI: 10.1113/jphysiol.2003.051144

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  • Physiological origins of evoked magnetic fields and extracellular field potentials produced by guinea-pig CA3 hippocampal slices Reviewed

    S Murakami, TS Zhang, A Hirose, YC Okada

    JOURNAL OF PHYSIOLOGY-LONDON   544 ( 1 )   237 - 251   2002.10

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    DOI: 10.1113/jphysiol.2002.027094

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MISC

  • 不整脈の基質とトリガーによるリスク評価 Invited

    村上 慎吾

    BIO Clinica   35 ( 8 )   48 - 51   2020.7

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    Language:Japanese   Publishing type:Article, review, commentary, editorial, etc. (trade magazine, newspaper, online media)  

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  • 蝸牛らせん靱帯の持続的脱分極性膜電位に関するin silico解析

    任 書晃, 吉田 崇正, 村上 慎吾, 緒方 元気, 上塚 学, 小宗 静男, 倉智 嘉久, 日比野 浩

    日本生理学雑誌   78 ( 2 )   46 - 47   2016.3

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    Language:Japanese   Publisher:(一社)日本生理学会  

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  • 内耳蝸牛側壁のK+輸送システムに立脚した内リンパ液高電位の成立機構

    任 書晃, 吉田 崇正, 村上 慎吾, 倉智 嘉久, 日比野 浩

    Audiology Japan   59 ( 2 )   109 - 118   2016

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    Language:Japanese   Publisher:Japan Audiological Society  

    <p> Endolymph, a unique extracellular fluid in the cochlea of the inner ear, exhibits a highly positive potential of +80 mV. This so-called endocochlear potential (EP), which is indispensable for hearing, originates from the lateral cochlear wall. The lateral wall, which comprises the stria vascularis and its neighboring spiral ligament, is likely made up of two epithelial layers. By using electrophysiological and theoretical approaches, we have shown that the EP depends on the K+ dynamics in the extra/intracellular compartments of the lateral wall. Of importance, the K+ environment seems to be controlled by the unidirectional K+ transport throughout the cochlea. Moreover, the results of our recent study suggest that of the several K+-transport molecules expressed in the lateral wall, only Na+, K+-ATPase is likely to be involved in driving the unidirectional K+ transport. These findings will contribute not only to elucidation of the mechanism underlying hearing, but also that of the pathophysiological processes involved in deafness caused by impairment of the EP.</p>

    DOI: 10.4295/audiology.59.109

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  • Theoretical and experimental analysis of ototoxic mechanism in the spiral ligament fibrocytes by multi-level simulation with ion transports in the cochlea

    任書晃, 吉田崇正, 吉田崇正, 村上慎吾, 上塚学, 上塚学, 緒方元気, 倉智嘉久, 日比野浩

    日本薬理学雑誌   147 ( 2 )   80-83 (J-STAGE) - 83   2016

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    Language:Japanese   Publisher:公益社団法人 日本薬理学会  

    空気の振動である音は,内耳蝸牛に存在する音の感覚細胞である有毛細胞を振動させる.この時,有毛細胞の毛に存在するイオンチャネルが開口し,常時+80 mVを示す特殊な内リンパ液からイオンが流入する.この「内リンパ液高電位」は,有毛細胞の興奮に不可欠であり,蝸牛側壁の血管条が成立させる.Na&lt;sup&gt;+&lt;/sup&gt;,K&lt;sup&gt;+&lt;/sup&gt;,2Cl&lt;sup&gt;-&lt;/sup&gt;共輸送体(NKCC)やNa&lt;sup&gt;+&lt;/sup&gt;,K&lt;sup&gt;+&lt;/sup&gt;-ATPaseの阻害薬は,内リンパ液高電位を低下させることで,薬剤性難聴を惹起することが報告されているが,その電位低下のメカニズムは明らかにされていなかった.我々はこれまでに,血管条に発現するNKCCとNa&lt;sup&gt;+&lt;/sup&gt;,K&lt;sup&gt;+&lt;/sup&gt;-ATPaseが制御する内リンパ液高電位成立機構を電気生理学的手法により示し,さらに蝸牛内の多階層イオン輸送モデル「Nin-Hibino-Kurachi(NHK)model」の構築とコンピュータシミュレーションによって,阻害薬を経動脈的に投与した時に起こる内リンパ液高電位低下のメカニズムを説明した.血管条に隣接し,その一部と一体化しているらせん靭帯を構成する線維細胞にも,NKCCとNa&lt;sup&gt;+&lt;/sup&gt;,K&lt;sup&gt;+&lt;/sup&gt;-ATPaseが発現していることが知られているが,薬剤性難聴時のこれらの関与は不明である.近年我々は,らせん靭帯ではおもにNa&lt;sup&gt;+&lt;/sup&gt;,K&lt;sup&gt;+&lt;/sup&gt;-ATPaseが,K&lt;sup&gt;+&lt;/sup&gt;輸送とK&lt;sup&gt;+&lt;/sup&gt;濃度バランスに寄与すること,そしてNKCCはほとんど機能していないことを明らかにした.これらに基づいて,NHKモデルを改訂した.今後シミュレーションを行うことにより,輸送体阻害薬の経動脈投与の実験結果を正確に再現することが期待される.

    DOI: 10.1254/fpj.147.80

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Awards

  • Best research award

    2023.9   Measuring the permittivity of liposome and yeast using a 3D printed electrode-replaceable measuring cell

    Yuuji Kageyama, Haruna Sueoka, Akira Kimura, Masaki Sato, Akira Ito, Tetsuro Horie, Genki Ogata, Yasuaki Einaga, Hiroaki Suzuki, Shingo Murakami

  • 日本生体医工学会関東支部若手研究者発表会2022優秀論文発表賞

    2022.12   日本生体医工学会   誘電スペクトロスコピーにおける微生物の誘電率計測

    影山湧二, 木村暁, 伊東章, 堀江哲郎, 緒方元気, 栄長泰明, 鈴木宏明, 村上慎吾

  • Best research award

    2021.9   Quantitative Evaluation of VR Immersion in 2D and 3D Images Using Event-Related Potentials

    Ryo Ogawa, Kaito Kageyama, Yasushi Nakatani, Yumie Ono, Shingo Murakami

Research Projects

  • 光音響効果による心臓深部のカルシウムイメージング手法

    Grant number:23K11834  2023.4 - 2026.3

    日本学術振興会  科学研究費助成事業  基盤研究(C)  中央大学

    村上 慎吾

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    Grant amount: \4680000 ( Direct Cost: \3600000 、 Indirect Cost: \1080000 )

    本研究の初年度である令和5年度においては、光音響イメージング装置の改良と、ランゲンドルフ灌流下におけるウシガエルの心臓からの光音響イメージングによる電気活動の計測を行った。ノイズの影響を受けやすい光音響イメージングでのノイズ軽減を行うために、光学系を改良して光音響信号を検出する断面のみを励起させる薄いシート状のレーザ光を発生させる装置を構築し、ファントムとウシガエルの心臓で装置改良の効果を確認した。その結果、計測対象である断面以外からのノイズの発生が抑えられただけでなく、計測可能な深度も改善された。この改善により、心臓壁の表面だけでなく内部まで一度に計測できるようになった。次に、改良された光音響イメージング装置を用いて、カルシウム濃度依存的な吸光試薬や電位依存的蛍光試薬をランゲンドルフ灌流下におけるウシガエルの心臓に適用し、心電図を計測しながら心臓の電気活動の光音響イメージングを行った。その結果、心電図から判断するに心臓の電気活動と同期した心臓のカルシウム動態や電気活動と推測される光音響イメージングの予備的な計測結果を得られることができた。本結果は、我々が知る限り心臓の電気活動を光音響イメージングで計測した初めての結果であり、光音響イメージングが心臓壁内部や内膜まで同時に計測できることから、心臓をはじめとする電気的に興奮することができる組織の計測において、非常に大きな意義があると考えている。

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  • Predicting risk by assessing substrate and trigger for drug-induced arrhythmia

    Grant number:19K07106  2019.4 - 2022.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)  Chuo University

    Murakami Shingo

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    Grant amount: \4290000 ( Direct Cost: \3300000 、 Indirect Cost: \990000 )

    In the present study, to predict the different risks of drug-induced arrhythmia under various IKr blockers, we investigated the mechanism of pharmacological effects on the repolarization reserve and early afterdepolarization (EAD) by using the O'Hara-Rudy human ventricular myocyte model, three drug models (amiodarone, bepridil, terfenadine), and hypothetical drug models. We rigorously redefined repolarization reserve and constructed a new quantitative risk assessment method based on this redefinition. In addition, it was shown that the difference of the drug effect on L-type calcium current (ICaL) affected the generation frequency of EAD. Based on the mechanisms identified above, we proposed a protocol for risk prediction and confirmed its validity.

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  • Simulation analysis on astrocytic K+ buffering

    Grant number:25460331  2013.4 - 2016.3

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (C)  Osaka University

    Murakami Shingo

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    Grant amount: \5200000 ( Direct Cost: \4000000 、 Indirect Cost: \1200000 )

    In response to elevation of extracellular K+ concentration ([K+]out), astrocytes clear excessive extracellular K+ to maintain proper environment for neural activity. Here we conducted simulation analysis on the mechanisms of the astrocytic K+ clearance and swelling. Astrocyte models were constructed by incorporating into a compartment model various mechanisms. Simulated response of astrocyte models to high [K+]out revealed significant contributions of NKCC and Na,K-ATPase to the increases of the intracellular K+ and Cl- concentrations, and swelling. Moreover, we show that the KIR channel localized at synaptic cleft absorbs the excessive K+, while the K+ release through KIR channel localized at perivascular is enhanced. Further analysis of simulated drug effects shows that K+ uptake, K+ release and swelling can be modulated differently by blocking each of the ion channels and transporters.

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  • Search for new antiarrhythmic drugs based on inhibition of trigger in atrial fibrillation

    Grant number:22790251  2010 - 2011

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Young Scientists (B)  Osaka University

    MURAKAMI Shingo

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    Grant amount: \3900000 ( Direct Cost: \3000000 、 Indirect Cost: \900000 )

    In this study, in order to facilitate the development of new antiarrhythmic drugs specific for atrial fibrillation, we studied the potential of TRPM4 channel inhibitors antiarrhythmic drugs. TRPM4 channel can be activated by elavated intracellular Ca^<2+> con(as) cen(new) tration and therefore can be triggers for atrial fibrillation, Since TRPM4 channels are not functional in the human ventricular, selective inhibitors of TRPM4 channels are expected to cause limited side effect in the ventricular. By using the human atrial model and TRPM4 channel model, we showed that inhibitors of TRPM4 channel may suppress atrial fibrillation and may be a good candidate for new antiarrhythmic drugs.

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  • Studies on the structure-activity relationship on pharmacological modulations of potassium channels

    Grant number:20249012  2008 - 2010

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research (A)  Osaka University

    KURACHI Yoshihisa, INANOBE Atsushi, HIBINO Hiroshi, MURAKAMI Shingo, FURUTANI Kazuharu

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    Grant amount: \50700000 ( Direct Cost: \39000000 、 Indirect Cost: \11700000 )

    Ion channel functions are modulated by the drugs. However, the mechanisms underling drug actions are often not well understood. In this study, we examined the mechanisms of drug actions in inward-rectifier potassium channels and voltage-dependent potassium channel. Our studies reveal structural bases of drug-channel interactions and their functional alterations in potassium channel. Moreover, our results provide better understandings of their clinical efficacy or undesirable side effects, and shed light on the rational development of pharmacological agents.

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  • Development of mathematical model of a Human atrial myocyte to evaluate new antiarrhythmic drugs for atrial fibrillation

    Grant number:20790206  2008 - 2009

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Young Scientists (B)  Osaka University

    MURAKAMI Shingo

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    Grant amount: \4290000 ( Direct Cost: \3300000 、 Indirect Cost: \990000 )

    In this study, I have developed a mathematical model of a Human atrial myocyte. Since characteristics of atrial myocyte differ among animals, the developed model allows us to evaluate effects of antiarrhythmic drug specifically for human. Although human atrial myocytes are difficult to obtain for experiments, by using the developed model, we can examine effects of virtual drug profiles in human atrial myocytes. The developed model may improve efficiency of drug development.

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  • Physiological regulation of G protein signaling by RGS proteins

    Grant number:17079005  2005 - 2009

    Japan Society for the Promotion of Science  Grants-in-Aid for Scientific Research  Grant-in-Aid for Scientific Research on Priority Areas  Osaka University

    KURACHI Yoshihisa, INANOBE Atsushi, MURAKAMI Shingo, FURUTANI Kazuharu, ISHII Masaru

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    Grant amount: \72900000 ( Direct Cost: \72900000 )

    Trimeric G proteins transmit extracellular signals to regulate the intracellular effectors. The spatiotemporal regulation of this signal closely links to the cellular responses. In this study, we addressed the regulation of G protein signaling by RGS proteins, the mathematical models of G protein signaling and the structure-function relationship of K^+ channel to analyze the physiological regulation of G protein signaling.

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