中村 雅也 (ナカムラ マサヤ)

Nakamura, Masaya

写真a

所属(所属キャンパス)

医学部 整形外科学教室 (信濃町)

職名

教授

外部リンク

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  • 1987年 3月  慶應義塾大学医学部卒業 1998年 1月  米国ジョージタウン大学客員研究員 2000年 10月  慶應義塾大学医学部助手(整形外科学) 2004年 4月  慶應義塾大学医学部専任講師(整形外科学) 2007年 10月  京都大学再生医科学研究所非常勤講師兼務 2012年 6月  慶應義塾大学医学部准教授(整形外科学)  2015年 2月  慶應義塾大学医学部教授(整形外科学)               現在に至る [主な専門分野] 脊椎・脊髄外科, 脊髄再生, iPS細胞, 神経幹細胞, 神経栄養因子, Neuroimaging [主な学会活動歴] 日本整形外科学会(代議員・移植再生委員会委員長),日本再生医療学会(理事),日本脊髄障害医学会(理事・脊髄再生医療委員会委員長),日本脊椎脊髄病学会(理事),日本運動器疼痛学会(理事),東日本整形外科災害外科学会(評議員),日本運動器移植・再生医学研究会(幹事),日本腰痛学会(評議員), 運動器と痛みの国際シンポジウム(世話人),脊椎と神経を語る会(世話人)など [受賞歴] 平成 8年 慶應義塾大学医学部三四会奨励賞 平成16年 Cervical spine research society Basic science research award 平成17年 Cervical spine research society Basic science research award 平成18年 日本整形外科学会・学会奨励賞        慶應義塾大学医学部三四会・北島賞 平成19年 Cervical spine research society Basic science research award 平成20年 Cervical spine research society Basic science research award 平成26年 日本再生医療学会・学会賞(臨床)       Journal of Orthopaedic Science, Best paper award 2013    第51回 ベルツ賞(1等賞) 平成27年 Journal of Orthopaedic Science, Best paper award 2014

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  •  

    慶應義塾大学, 医学部

    大学

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  • 博士号(医学), 慶應義塾大学, 論文, 1995年11月

免許・資格 【 表示 / 非表示

  • 医師免許取得, 1987年

  • 日本整形外科学会専門医, 1994年

  • 日本脊椎脊髄病学会脊椎脊髄外科指導医, 2003年

  • 日本整形外科学会脊椎脊髄病医, 2004年

 

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  • Generation and characterization of a novel shoulder contracture mouse model

    Oki Satoshi, Shirasawa Hideyuki, Yoda Masaki, Matsumura Noboru, Tohmonda Takahide, Yuasa Kazuki, Nakamura Masaya, Matsumoto Morio, Horiuchi Keisuke

    Journal of Orthopaedic Research 33 ( 11 ) 1732 - 1738 2015年11月

    ISSN  0736-0266

     概要を見る

    <p>Frozen shoulder is a relatively common disorder that leads to severe pain and stiffness in the shoulder joint. Although this disorder is self-limiting in nature, the symptoms often persist for years, resulting in severe disability. Recent studies using human specimens and animal models have shown distinct changes in the gene expression patterns in frozen shoulder tissue, indicating that novel therapeutic intervention could be achieved by controlling the genes that are potentially involved in the development of frozen shoulder. To achieve this goal, it is imperative to develop a reliable animal joint contracture model in which gene expression can be manipulated by gene targeting and transgenic technologies. Here, we describe a novel shoulder contracture mouse model. We found that this model mimics the clinical presentation of human frozen shoulder and recapitulates the changes in the gene expression pattern and the histology of frozen shoulder and joint contracture in humans and other larger animal models. The model is highly reproducible, without any major complications. Therefore, the present model may serve as a useful tool for investigating frozen shoulder etiology and for identifying its potential target genes.</p>

  • A Novel Percutaneous Guide Wire (S-Wire) for Percutaneous Pedicle Screw Insertion

    Ishii Ken, Kaneko Yasuhito, Funao Haruki, Ishihara Shinichi, Shinohara Akira, Nakanishi Kazuo, Hikata Tomohiro, Fujita Nobuyuki, Iwanami Akio, Hosogane Naobumi, Watanabe Kota, Nagura Takeo, Nakamura Masaya, Toyama Yoshiaki, Matsumoto Morio

    Surgical Innovation 22 ( 5 ) 469 - 473 2015年10月

    ISSN  1553-3506

     概要を見る

    <p>Purpose. Minimally invasive spine stabilization (MISt) procedures, including MIS-transforaminal lumbar interbody fusion (MIS-TLIF), rely on precise placement of percutaneous pedicle screws (PPS). Serious intraoperative complications associated with PPS placement include great vessel and bowel injuries due to the guide-wire's anterior migration and penetration through the anterior aspect of the vertebral body. To address this issue, we developed a novel percutaneous guide wire (S-wire) and compared the biomechanical characteristics of S-wire and conventional wire in cadaveric spines, and to evaluate the S-wire's efficacy and safety in a clinical trial. Methods. The S-wire is hollow, with braided wires extending at one tip. We compared the push-out and penetration forces of the S-wire and conventional wire in fresh cadaveric lumbar spines, from L1 to L5. Results. Push-out forces caused the braided tip of the S-wire to bend or spread, and thus to resist anterior migration. The mean push-out forces for the S-wire and conventional wire were 15.5 ± 1.9 and 5.7 ± 0.8 N, respectively (P &lt;.0001); the mean penetration forces were 69.1 ± 4.2 and 37.1± 4.8 N, respectively (P &lt;.0005). There was no wire breakage or anterior-wall penetration in a clinical trial of 922 S-wires; interestingly, the pull-out force increased in 780 (84.6%) S-wires after placement. Conclusions. The mean push-out and penetration forces for the S-wire were approximately 3 and 2 times greater than those of conventional wire, respectively. The S-wire effectively prevented guide-wire anterior migration and penetration of the anterior vertebral-body wall. The S-wire device should effectively improve the safety of MISt procedures, including MIS-TLIF and percutaneous kyphoplasty in selected patient with osteoporosis.</p>

  • Histological and electrophysiological analysis of the corticospinal pathway to forelimb motoneurons in common marmosets

    Kondo Takahiro, Yoshihara Yamato, Yoshino-Saito Kimika, Sekiguchi Tomofumi, Kosugi Akito, Miyazaki Yuta, Nishimura Yukio, Okano Hirotaka J., Nakamura Masaya, Okano Hideyuki, Isa Tadashi, Ushiba Junichi

    Neuroscience Research 98   35 - 44 2015年09月

    ISSN  0168-0102

     概要を見る

    <p>Using histological and electrophysiological methods, we identified the neuroanatomical properties of the common marmoset corticospinal tract (CST), which underlies hand/arm motor control. Biotinylated dextran amine (BDA) was injected into the primary motor cortex to anterogradely label CST axons in the cervical segments, revealing that most CST axons descend in the contralateral dorsolateral funiculus (DLF; 85.0%), and some in the ipsilateral DLF (10.7%). Terminal buttons were mainly found in the contralateral lamina VII of the gray matter, but projection to lamina IX, where forelimb motoneurons are located, was rare. Bilateral projections were more abundant than found in the rat CST, resembling the CST organization of other primates. Intracellular recordings were made from 57 forelimb motoneurons on the contralateral side to stimulation, which revealed no monosynaptic excitatory postsynaptic potentials (EPSPs), but di- or polysynaptic EPSPs and inhibitory synaptic potentials were commonly found. Local field potentials showed monosynaptic excitation mainly in laminae VII, where abundant BDA-labeled CST terminals were observed. These results suggest that direct corticomotoneuronal projection is absent in common marmosets but di- or oligosynaptic effects would be mediated by spinal interneurons.</p>

  • BDNF Induced by Treadmill Training Contributes to the Suppression of Spasticity and Allodynia After Spinal Cord Injury via Upregulation of KCC2

    Tashiro Syoichi, Shinozaki Munehisa, Mukaino Masahiko, Renault-Mihara François, Toyama Yoshiaki, Liu Meigen, Nakamura Masaya, Okano Hideyuki

    Neurorehabilitation and Neural Repair 29 ( 7 ) 677 - 689 2015年08月

    ISSN  1545-9683

     概要を見る

    <p>Background. Spasticity and allodynia are major sequelae that affect the quality of life and daily activities of spinal cord injury (SCI) patients. Although rehabilitation ameliorates spasticity and allodynia, the molecular mechanisms involved in these processes remain elusive. Objective. To investigate the molecular mechanisms by which rehabilitation ameliorates spasticity and allodynia after SCI in rats. Methods. The expression levels of brain-derived neurotrophic factor (BDNF) and potassium-chloride cotransporter-2 (KCC2), as well as the localization of KCC2, were examined in the lumbar enlargements of untrained and treadmill-trained thoracic SCI model rats. Spasticity and allodynia were determined via behavioral and electrophysiological analyses. The effects of BDNF on spasticity, allodynia, and KCC2 activation were determined by inhibition of BDNF signaling via intrathecal administration of TrkB-IgG. The effects of SCI and training on the expression levels of functional phospholipase C-γ in the lumbar enlargement were also examined. Results. Treadmill training after SCI upregulated endogenous BDNF expression and posttranslational modification of KCC2 in the lumbar enlargement significantly. There were also significant correlations between increased KCC2 expression and ameliorated spasticity and allodynia. Administration of TrkB-IgG abrogated the training-induced upregulation of KCC2 and beneficial effects on spasticity and allodynia. The expression level of functional phospholipase C-γ was reduced significantly after SCI, which may have contributed to the change in the function of BDNF, whereby it did not trigger short-term downregulation or induce long-term upregulation of KCC2 expression secondary to training. Conclusions. BDNF-mediated restoration of KCC2 expression underlies the suppression of spasticity and allodynia caused by rehabilitation.</p>

  • Migration and differentiation of transplanted enteric neural crest-derived cells in murine model of Hirschsprung’s disease

    Nishikawa Ryuhei, Hotta Ryo, Shimojima Naoki, Shibata Shinsuke, Nagoshi Narihito, Nakamura Masaya, Matsuzaki Yumi, Okano Hirotaka J., Kuroda Tatsuo, Okano Hideyuki, Morikawa Yasuhide

    Cytotechnology 67 ( 4 ) 661 - 670 2015年08月

    ISSN  0920-9069

     概要を見る

    <p>Stem cell therapy offers the potential of rebuilding the enteric nervous system (ENS) in the aganglionic bowel of patients with Hirschsprung’s disease. P0-Cre/Floxed-EGFP mice in which neural crest-derived cells express EGFP were used to obtain ENS stem/progenitor cells. ENS stem/progenitor cells were transplanted into the bowel of Ret&lt;sup&gt;−/−&lt;/sup&gt; mouse, an animal model of Hirschsprung’s disease. Immunohistochemical analysis was performed to determine whether grafted cells gave rise to neurons in the recipient bowel. EGFP expressing neural crest-derived cells accounted for 7.01 ± 2.52 % of total cells of gastrointestinal tract. ENS stem/progenitor cells were isolated using flow cytometry and expanded as neurosphere-like bodies (NLBs) in a serum-free culture condition. Some cells in NLBs expressed neural crest markers, p75 and Sox10 and neural stem/progenitor cells markers, Nestin and Musashi1. Multipotency of isolated ENS stem/progenitor cells was determined as they differentiated into neurons, glial cells, and myofibloblasts in culture. When co-cultured with explants of hindgut of Ret&lt;sup&gt;−/−&lt;/sup&gt; mice, ENS stem/progenitor cells migrated into the aganglionic bowel and gave rise to neurons. ENS stem/progenitor cells used in this study appear to be clinically relevant donor cells in cell therapy to treat Hirschsprung’s disease capable of colonizing the affected bowel and giving rise to neurons.</p>

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研究発表 【 表示 / 非表示

  • 脊髄損傷に対する神経幹細胞移植療法の確立を目指して

    中村 雅也

    第2回日本再生医療学会総会 (神戸) , 

    2003年03月

    口頭発表(一般)

  • 頚椎脊索腫摘出・プレート併用前方再建再建術後3年で食道穿孔を来たした1例

    岡田英次郎,松本守雄,西澤隆,中村雅也,丸岩博文,千葉一裕,戸山芳昭,塩谷彰浩

    第43回関東整形災害外科学会, 

    2003年03月

    口頭発表(一般)

  • ラット胎児脊髄由来神経幹細胞の3次元培養法の確立

    岡田誠司,中村雅也,大杉義征,戸山芳昭,岡野栄之

    第2回日本再生医療学会, 

    2003年03月

    口頭発表(一般)

  • 損傷部脊髄内セマフォリン3A阻害剤による損傷脊髄の再生

    金子慎二郎,岩波明生,中村雅也,宮尾幸代,岸野晶祥,木村徹,熊谷和夫,戸山芳昭,岡野栄之

    第2回日本再生医療学会, 

    2003年03月

    口頭発表(一般)

  • 脊髄損傷に対する神経幹細胞移植法の確立を目指して

    中村雅也,岩波明生,金子慎二郎,三上裕嗣,小川裕人,千葉一裕,岡野栄之,戸山芳昭

    第2回日本再生医療学会, 

    2003年03月

    口頭発表(一般)

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受賞 【 表示 / 非表示

  • 第51回ベルツ賞(1等賞)

    2014年, 幹細胞を用いた脊髄損傷の再生医療

  • 日本再生医療学会賞

    2014年, iPS細胞を用いた脊髄再生医療の実現

  • 日本整形外科学会・学会奨励賞

    2006年, 脊髄損傷に対する神経幹細胞移植

  • 慶應義塾大学医学部三四会・北島賞

    2006年, 脊髄損傷に対する神経幹細胞移植療法の確立に向けて

  • Cervical spine research society, Basic science research award

    2004年, Transplantation of human neural stem cells promotes functional recovery after spinal cord injury in primates.

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担当授業科目 【 表示 / 非表示

  • 整形外科学

    2024年度

  • 整形外科学演習

    2024年度

  • 整形外科学実習

    2024年度

  • 整形外科学講義

    2024年度

  • 整形外科学特論

    2024年度

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担当経験のある授業科目 【 表示 / 非表示

  • 大学院特別講義

    慶應義塾

    2015年04月
    -
    2016年03月

    講義, 専任, 1時間, 60人

  • 系統講義 整形外科各論

    慶應義塾

    2015年04月
    -
    2016年03月

    秋学期, 講義, 専任, 1時間, 80人