九州大学 研究者情報
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基本情報 研究活動 教育活動 社会活動 病院臨床活動
辛島 裕士(からしま ゆうじ) データ更新日:2022.06.20

准教授 /  九州大学病院 手術部 麻酔・蘇生学分野


主な研究テーマ
GIRKチャネルによる痛み制御機構
キーワード:GIRKチャネル、痛み
2017.04~2020.12.
麻酔データウェアハウス(DWH)の構築と活用
キーワード:麻酔データウェアハウス
2017.04~2019.03.
TRPチャネルと痛みに関する基礎的研究
キーワード:TRPチャネル、痛み、麻酔薬
2009.04~2019.03.
従事しているプロジェクト研究
高密度スキャフォールドフリー脂肪由来幹細胞構造体を用いた骨軟骨組織再生の臨床研究
2010.12~2011.10, 代表者:松田 秀一 , 九州大学大学院医学研究院 整形外科 , 日本.
エスラックス静注 使用成績調査
2009.05~2012.03, 代表者:山浦 健, 九州大学病院 麻酔科蘇生科
エスラックス静注50mg/5.0mlの使用実態下での安全性および有効性に関する情報を収集する。.
6%HES130/0.4第3相臨床試験
2009.08~2010.07, 代表者:外 須美夫, 九州大学大学院医学研究院 麻酔・蘇生学
整形外科手術患者を対象とした6%ヒドロキシエチルデンプン130/0.4の6%ヒドロキシエチルデンプン70/0.5に対する有効性と安全性についての多施設共同並行群間2重盲検比較第3相試験.
研究業績
主要著書
主要原著論文
1. Masami Kimura, Hiroaki Shiokawa, Yuji Karashima, Makoto Sumie, Sumio Hoka, Ken Yamaura, Antinociceptive effect of selective G protein-gated inwardly rectifying K+ channel agonist ML297 in the rat spinal cord, PloS one, 10.1371/journal.pone.0239094, 15, 9, e0239094, 2020.09, [URL], The G protein-gated inwardly rectifying K+ (GIRK) channels play important signaling roles in the central and peripheral nervous systems. However, the role of GIRK channel activation in pain signaling remains unknown mainly due to the lack of potent and selective GIRK channel activators until recently. The present study was designed to determine the effects and mechanisms of ML297, a selective GIRK1/2 activator, on nociception in the spinal cord by using behavioral studies and whole-cell patch-clamp recordings from substantia gelatinosa (SG) neurons. Rats were prepared for chronic lumber catheterization and intrathecal administration of ML297. The nociceptive flexion reflex was tested using an analgesy-meter, and the influence on motor performance was assessed using an accelerating rotarod. We also investigated pre- and post-synaptic actions of ML297 in spinal cord preparations by whole-cell patch-clamp recordings. Intrathecal administration of ML297 increased the mechanical nociceptive threshold without impairing motor function. In voltage-clamp mode of patch-clamp recordings, bath application of ML297 induced outward currents in a dose-dependent manner. The ML297-induced currents demonstrated specific equilibrium potential like other families of potassium channels. At high concentration, ML297 depressed miniature excitatory postsynaptic currents (mEPSCs) but not their amplitude. The ML297-induced outward currents and suppression of mEPSCs were not inhibited by naloxone, a μ-opioid receptor antagonist. These results demonstrated that intrathecal ML297 showed the antinociceptive effect, which was mediated through direct activation of pre- and post-synaptic GIRK channels. Selective GIRK channel activation is a promising strategy for the development of new agents against chronic pain and opioid tolerance..
2. Yuji Karashima, Jean Prenen, Karel Talavera, Annelies Janssens, Thomas Voets, Bernd Nilius, Agonist-induced changes in Ca2+ permeation through the nociceptor cation channel TRPA1, Biophysical Journal, 10.1016/j.bpj.2009.11.007, 98, 5, 773-783, 2010.03, [URL], The Ca2+-permeable cation channel TRPA1 acts as an ionotropic receptor for various pungent compounds and as a noxious cold sensor in sensory neurons. It is unclear what proportion of the TRPA1-mediated current is carried by Ca2+ ions and how the permeation pathway changes during stimulation. Here, based on the relative permeability of the nonstimulated channel to cations of different size, we estimated a pore diameter of ∼11 Å. Combined patch-clamp and Fura-2 fluorescence recordings revealed that with 2 mM extracellular Ca2+, and at a membrane potential of -80 mV, ∼17% of the inward TRPA1 current is carried by Ca2+. Stimulation with mustard oil evoked an apparent dilatation of the pore of 3 Å and an increase in divalent cation selectivity and fractional Ca2+ current. Mutations in the putative pore that reduced the divalent permeability and fractional Ca2+ current also prevented mustard-oil-induced increases in Ca2+ permeation. It is interesting that fractional Ca2+ currents for wild-type and mutant TRPA1 were consistently higher than values predicted based on biionic reversal potentials using the Goldman-Hodgkin-Katz equation, suggesting that binding of Ca2+ in the pore hinders monovalent cation permeation. We conclude that the pore of TRPA1 is dynamic and supports a surprisingly large Ca2+ influx..
3. Karel Talavera, Maarten Gees, Yuji Karashima, Víctor M. Meseguer, Jeroen A.J. Vanoirbeek, Nils Damann, Wouter Everaerts, Melissa Benoit, Annelies Janssens, Rudi Vennekens, Félix Viana, Benoit Nemery, Bernd Nilius, Thomas Voets, Nicotine activates the chemosensory cation channel TRPA1, Nature Neuroscience, 10.1038/nn.2379, 12, 10, 1293-1299, 2009.10, [URL], Topical application of nicotine, as used in nicotine replacement therapies, causes irritation of the mucosa and skin. This reaction has been attributed to activation of nicotinic acetylcholine receptors (nAChRs) in chemosensory neurons. In contrast with this view, we found that the chemosensory cation channel transient receptor potential A1 (TRPA1) is crucially involved in nicotine-induced irritation. We found that micromolar concentrations of nicotine activated heterologously expressed mouse and human TRPA1. Nicotine acted in a membrane-delimited manner, stabilizing the open state(s) and destabilizing the closed state(s) of the channel. In the presence of the general nAChR blocker hexamethonium, nociceptive neurons showed nicotine-induced responses that were strongly reduced in TRPA1-deficient mice. Finally, TRPA1 mediated the mouse airway constriction reflex to nasal instillation of nicotine. The identification of TRPA1 as a nicotine target suggests that existing models of nicotine-induced irritation should be revised and may facilitate the development of smoking cessation therapies with less adverse effects..
4. Yuji Karashima, Karel Talavera, Wouter Everaerts, Annelies Janssens, Kelvin Y. Kwan, Rudi Vennekens, Bernd Nilius, Thomas Voets, TRPA1 acts as a cold sensor in vitro and in vivo, Proceedings of the National Academy of Sciences of the United States of America, 10.1073/pnas.0808487106, 106, 4, 1273-1278, 2009.01, [URL], TRPA1 functions as an excitatory ionotropic receptor in sensory neurons. It was originally described as a noxious cold-activated channel, but its cold sensitivity has been disputed in later studies, and the contribution of TRPA1 to thermosensing is currently a matter of strong debate. Here, we provide several lines of evidence to establish that TRPA1 acts as a cold sensor in vitro and in vivo. First, we demonstrate that heterologously expressed TRPA1 is activated by cold in a Ca2+-independent and Ca2+ store-independent manner; temperature-dependent gating of TRPA1 is mechanistically analogous to that of other temperature-sensitive TRP channels, and it is preserved after treatment with the TRPA1 agonist mustard oil. Second, we identify and characterize a specific subset of cold-sensitive trigeminal ganglion neurons that is absent in TRPA1-deficient mice. Finally, cold plate and tail-flick experiments reveal TRPA1-dependent, cold-induced nociceptive behavior in mice. We conclude that TRPA1 acts as a major sensor for noxious cold..
5. Yuji Karashima, Jean Prenen, Victor Meseguer, Grzegorz Owsianik, Thomas Voets, Bernd Nilius, Modulation of the transient receptor potential channel TRPA1 by phosphatidylinositol 4,5-biphosphate manipulators, Pflugers Archiv European Journal of Physiology, 10.1007/s00424-008-0493-6, 457, 1, 77-89, 2008.10, [URL], The transient receptor potential channel of the ankyrin-binding repeat subfamily, TRPA1, is a Ca2+-permeable non-selective cation channel that depolarizes the plasma membrane and causes Ca2+ influx. A typical feature of TRPA1 is its rapid desensitization following activation by agonists such as mustard oil (MO), cinnamaldehyde, and a high intracellular Ca2+ concentration. In whole-cell recordings on Chinese hamster ovary (CHO) cells expressing TRPA1, desensitization was delayed when phosphatidylinositol 4,5-biphosphate (PIP2) was supplemented via the patch pipette, whereas the PIP2 scavenger neomycin accelerated desensitization. Preincubation with the PI-4 kinase inhibitor wortmannin reduced both constitutive TRPA1 channels activity and the response to MO. Run down was also accelerated by high intracellular Mg2+ concentrations, whereas chelating intracellular Mg2+ with 10 mM ethylenedinitrilotetraacetic acid (EDTA) increased the basal channel activity. In inside-out patches, we observed a rapid run down of TRPA1 activity, which could be prevented by application of diC8-PIP2 or 2 mM Mg-ATP but not Na2-ATP to the cytosolic side of the excised patches. In isolated trigeminal ganglion neurons, preincubation with wortmannin resulted in inhibition of endogenous TRPA1 activation by MO. Taken together, our data indicate that PIP2 modulates TRPA1, albeit to a lesser extent than other known PIP 2-dependent TRP channels, and that tools modifying the plasma membrane PIP2 content often have direct effects on this channel..
6. Victor Meseguer, Yuji Karashima, Karel Talavera, Dieter D'Hoedt, Tansy Donovan-Rodríguez, Felix Viana, Bernd Nilius, Thomas Voets, Transient receptor potential channels in sensory neurons are targets of the antimycotic agent clotrimazole, Journal of Neuroscience, 10.1523/JNEUROSCI.4772-07.2008, 28, 3, 576-586, 2008.01, [URL], Clotrimazole (CLT) is a widely used drug for the topical treatment of yeast infections of skin, vagina, and mouth. Common side effects of topical CLT application include irritation and burning pain of the skin and mucous membranes. Here, we provide evidence that transient receptor potential (TRP) channels in primary sensory neurons underlie these unwanted effects of CLT. We found that clinically relevant CLT concentrations activate heterologously expressed TRPV1 and TRPA1, two TRP channels that act as receptors of irritant chemical and/or thermal stimuli in nociceptive neurons. In line herewith, CLT stimulated a subset of capsaicin-sensitive and mustard oil-sensitive trigeminal neurons, and evoked nocifensive behavior and thermal hypersensitivity with intraplantar injection in mice. Notably, CLT-induced pain behavior was suppressed by the TRPV1-antagonist BCTC [(N-(-4-tertiarybutylphenyl)-4-(3- cholorpyridin-2-yl)tetrahydropyrazine-1(2H)-carboxamide)] and absent in TRPV1-deficient mice. In addition, CLT inhibited the cold and menthol receptor TRPM8, and blocked menthol-induced responses in capsaicin- and mustard oil-insensitive trigeminal neurons. The concentration for 50% inhibition (IC50) of inward TRPM8 current was ∼200 nM, making CLT the most potent known TRPM8 antagonist and a useful tool to discriminate between TRPM8- and TRPA1-mediated responses. Together, our results identify TRP channels in sensory neurons as molecular targets of CLT, and offer means to develop novel CLT preparations with fewer unwanted sensory side effects..
7. Yuji Karashima, Nils Damann, Jean Prenen, Karel Talavera, Andrei Segal, Thomas Voets, Bernd Nilius, Bimodal action of menthol on the transient receptor potential channel TRPA1, Journal of Neuroscience, 10.1523/JNEUROSCI.2221-07.2007, 27, 37, 9874-9884, 2007.09, [URL], TRPA1 is a calcium-permeable nonselective cation transient receptor potential (TRP) channel that functions as an excitatory ionotropic receptor in nociceptive neurons. TRPA1 is robustly activated by pungent substances in mustard oil, cinnamon, and garlic and mediates the inflammatory actions of environmental irritants and proalgesic agents. Here, we demonstrate a bimodal sensitivity of TRPA1 to menthol, a widely used cooling agent and known activator of the related cold receptor TRPM8. In whole-cell and single-channel recordings of heterologously expressed TRPA1, submicromolar to low-micromolar concentrations of menthol cause channel activation, whereas higher concentrations lead to a reversible channel block. In addition, we provide evidence for TRPA1-mediated menthol responses in mustard oil-sensitive trigeminal ganglion neurons. Our data indicate that TRPA1 is a highly sensitive menthol receptor that very likely contributes to the diverse psychophysical sensations after topical application of menthol to the skin or mucous membranes of the oral and nasal cavities..
8. Yuji Karashima, Masahiro Oike, Shosuke Takahashi, Yushi Ito, Propofol prevents endothelial dysfunction induced by glucose overload, British Journal of Pharmacology, 10.1038/sj.bjp.0704912, 137, 5, 683-691, 2002.11, [URL], 1. Surgical operations often induce acute hyperglycemia, which is known to affect endothelial functions. In this study, we examined the effects of propofol, a commonly used general anaesthetic, on bovine aortic endothelial cell (BAEC) dysfunction induced by glucose overload. 2. D-glucose overload (23 mM) induced an accumulation of superoxide anion (O2-), assessed by MCLA chemiluminescence, to a similar extent as that generated by 233 μU ml-1 xanthine oxidase (XO) and 100 μM xanthine. Propofol inhibited this accumulation with an IC50 of 0.21 μM, whereas much higher concentrations of propofol were required to scavenge O2- generated by 250 μU ml-1 XO and 100 μM xanthine (IC50: 13.5 μM). 3. D-glucose overload attenuated ATP-induced NO production which was detected using diaminofluorescence-2 (DAF-2). The inhibition was reversed by propofol with an EC50 of 0.60 μM. In contrast, inhibitions caused by xanthine/XO were not altered by propofol (1 μM). 4. D-glucose overload suppressed ATP-induced Ca2+ oscillations and capacitative Ca2+ entry (CCE), which were both restored by superoxide dismutase, indicating that O2- was responsible. Propofol restored these attenuated Ca2+ oscillations and CCE with EC50 of 0.31 and 1.0 μM, respectively. 5. D-glucose overload (23 mM) increased the intracellular glucose concentration 4 fold, compared with cells exposed to 5.75 mM glucose, and 1 μM propofol reduced this increase to 2.8 fold. 6. We conclude from these results that anaesthetic concentrations of propofol prevent the impairment of Ca2+-dependent NO production in BAEC induced by glucose overload. This effect is mainly due to the reduction of O2- accumulation, and involves, at least in part, the inhibition of cellular glucose uptake..
主要総説, 論評, 解説, 書評, 報告書等
1. 辛島 裕士, 炎症性疼痛とTRPA1, Journal of Japan Society of Pain Clinicians, 2017.10, TRP(Transient Receptor Potential)チャネルは、様々な部位に発現し、多岐にわたる生体機能に関与する。そのうち、一次求心性侵害受容線維終末に発現が多くみられるTRPA1は、痛みに関係するチャネルとして研究が進んでいる。TRPA1は、多様な外因性の刺激物質によって活性化されて急性痛をおこすだけでなく、炎症に関与する内因性物質によっても活性化される。さらに炎症時には発現量の増加や、細胞表面への移動が見られることより、TRPA1は炎症性疼痛にも大きく関与する可能性が考えられている。TRPA1チャネル活性化による炎症性疼痛の増強は、臨床でよく用いられている麻酔薬でも認められることが報告されており留意する必要がある。最近、TRPA1の発現は、一次求心性線維の末梢側だけでなく中枢側にもみられ、中枢側でのTRPA1チャネル活性化は発痛ではなく、逆に鎮痛となる可能性が示された。このことも考慮に入れた上で、TRPA1をターゲットにした鎮痛薬創薬に期待したい。.
2. 辛島 裕士, 外 須美夫, 術後鎮痛, 臨床と研究, 2017.04.
3. Yuji Karashima, TRP channel and pain, Japanese Journal of Anesthesiology, 2016.01.
4. 辛島 裕士, 外 須美夫, 痛みの臨床「術後疼痛コントロール」, Modern Physician, 2014.06.
5. 辛島 裕士, 外 須美夫, 術後疼痛コントロール, 臨床と研究, 2012.02.
6. 辛島 裕士、外 須美夫, 感覚とTRPチャネル, 福岡医学雑誌, 2011.03.
主要学会発表等
1. 辛島 裕士, 炎症性疼痛とTRPチャネル, 日本ペインクリニック学会第50回大会, 2016.07.
2. 辛島 裕士, TRPチャネルと痛み, 日本麻酔科学会 第63回学術集会, 2016.05.
学会活動
所属学会名
日本麻酔科学会
日本心臓血管麻酔学会
European Society of Anaesthesiology
American Society of Anesthesiologists
日本臨床麻酔学会
日本循環制御医学会
日本ペインクリニック学会
日本集中治療医学会
日本小児麻酔学会
体液・代謝管理研究会
日本輸血・細胞治療学会
学協会役員等への就任
2020.09~2022.09, 日本麻酔科学会, 九州支部運営委員会 広報担当委員.
2020.05~2023.06, 日本麻酔科学会, 代議員.
2019.04~2022.03, 日本循環制御医学会, 評議員.
2018.10~2020.06, 日本麻酔科学会, 第67回学術集会実行委員会 第1・循環WG メンバー.
2019.07~2021.07, 日本ペインクリニック学会, 日本ペイクリニック学会誌編集委員会 査読委員.
2019.08~2022.06, 日本麻酔科学会, 学術集会実行委員会 第1・循環WG メンバー.
2019.11~2020.11, 日本臨床麻酔学会, 評議員.
2019.06~2021.05, 日本麻酔科学会, 国際交流委員会 委員.
2019.06~2021.05, 日本麻酔科学会, 代議員.
2018.05~2019.06, 日本麻酔科学会, 第66回学術集会 実行委員会 第1・循環ワーキンググループ サテライトメンバー.
2017.06~2018.06, 日本麻酔科学会, 第65回学術集会 実行委員会 第1・循環ワーキンググループ サテライトメンバー.
2016.09~2020.09, 日本心臓血管麻酔学会, 専門医問題作成委員会.
2015.10~2022.10, 日本臨床麻酔学会, 評議員.
2014.09~2020.09, 日本心臓血管麻酔学会, 学術委員会 経食道心エコー部会 委員.
2016.05~2022.09, 日本心臓血管麻酔学会, 評議員.
2016.05~2017.06, 日本麻酔科学会, 第64回学術集会 実行委員会 第1・循環ワーキンググループ サテライトメンバー.
2015.04~2016.03, 日本麻酔科学会, 第63回学術集会 実行委員会 第1・循環ワーキンググループ サテライトメンバー.
2014.06~2016.06, 日本麻酔科学会, 運営委員.
2015.06~2017.06, 日本麻酔科学会, 代議員.
2015.06~2018.06, 日本循環制御医学会, 評議員.
学会大会・会議・シンポジウム等における役割
2022.06.16~2022.06.18, 日本麻酔科学会 第69回学術集会, ポスターディスカッション座長.
2022.06.16~2022.06.18, 日本麻酔科学会 第69回学術集会, シンポジウム座長.
2021.02~2021.02.26, 第41回日本循環制御医学会総会, 座長.
2020.09~2020.10, 日本心臓血管麻酔学会第25回学術大会, シンポジスト.
2019.11.07~2019.11.09, 日本臨床麻酔学会第38回大会, シンポジスト.
2019.09.20~2019.09.22, 日本心臓血管麻酔学会第24回学術大会, 座長.
2019.09.14~2019.09.14, 九州麻酔科学会第57回大会, 座長.
2019.06.07~2019.06.08, 第40回日本循環制御医学会総会, 座長.
2019.05.30~2019.06.01, 日本麻酔科学会第66回学術集会, 座長.
2018.11.01~2018.11.03, 日本臨床麻酔学会 第38回大会, シンポジスト.
2018.11.01~2018.11.03, 日本臨床麻酔学会 第38回大会, 座長.
2018.09.08~2018.09.08, 九州麻酔科学会第56回大会, 座長.
2018.07.11~2018.07.11, 第73回日本消化器外科学会総会, シンポジスト.
2018.07.05~2018.07.05, 第55回外科代謝栄養学会, シンポジスト.
2018.06.01~2018.06.02, 第39回 日本循環制御医学会総会, 座長.
2018.05.17~2018.05.19, 日本麻酔科学会 第65回学術集会, コメンテーター.
2017.11.03~2017.11.05, 日本臨床麻酔学会 第37回大会, 座長(Chairmanship).
2017.09.16~2017.09.18, 日本心臓血管麻酔学会 第22回学術大会, 座長(Chairmanship).
2017.09.09~2017.09.09, 九州麻酔科学会第55回大会, 座長(Chairmanship).
2017.06.29~2017.07.01, 第14回麻酔科学サマーセミナー, 座長(Chairmanship).
2018.06.23~2018.06.23, 第65回日本輸血細胞治療学会, シンポジスト.
2017.06.08~2017.06.10, 日本麻酔科学会 第64回学術集会, 優秀演題審査員.
2016.11.03~2016.11.05, 日本臨床麻酔学会第36回大会, 座長(Chairmanship).
2016.09.03~2016.09.03, 九州麻酔科学会第54回大会, 座長(Chairmanship).
2015.12.05~2015.12.05, 第4回周術期の体液栄養管理セミナーin福岡, 座長(Chairmanship).
2015.10.21~2015.10.23, 日本臨床麻酔学会 第35回大会, 座長(Chairmanship).
2014.09.06~2014.09.06, 九州麻酔科学会第52回大会, 座長(Chairmanship).
2014.07.04~2014.07.05, 第35回日本循環制御医学会総会, ラウンドモデレーター.
2013.05.23~2013.05.25, 日本麻酔科学会第60回学術集会, 座長(Chairmanship).
2010.12.04~2010.12.04, 第5回九州周術期超音波研究会, 座長(Chairmanship).
2010.06.19~2010.06.19, 第4回九州周術期超音波研究会, 座長(Chairmanship).
2009.12.05~2009.12.05, 第3回九州周術期超音波研究会, 座長(Chairmanship).
2009.06.20~2009.06.20, 第2回九州周術期超音波研究会, 座長(Chairmanship).
2017.06.22~2017.06.24, 第65回日本輸血・細胞治療学会総会, シンポジスト.
2016.05.26~2016.05.28, 日本麻酔科学会第63回学術集会, 学術集会実行委員会 委員.
学会誌・雑誌・著書の編集への参加状況
2019.07~2021.07, 日本ペインクリニック学会, 国内, 査読委員.
2016.08~2018.08, Cardiovascular Anesthesia, 国際, 査読委員.
学術論文等の審査
年度 外国語雑誌査読論文数 日本語雑誌査読論文数 国際会議録査読論文数 国内会議録査読論文数 合計
2022年度      
2021年度   14  17 
2020年度     16  18 
2019年度   16  23 
2018年度   15  18 
2017年度     15  24 
2016年度     15  20 
2015年度       14  14 
2014年度       15  15 
2013年度       14  14 
2008年度      
その他の研究活動
海外渡航状況, 海外での教育研究歴
Department of Molecular Cell Biology, Laboratory of Ion Channel Research, KU Leuven, Belgium, 2005.09~2009.03.
外国人研究者等の受入れ状況
2017.09~2018.02, Department of Anesthesiology and Pain Medicine Seoul National University College of Medicine, Korea, Korea.
2015.10~2015.11, 1ヶ月以上, B.P. KOIRALA INSTITUTE OF HEALTH SCIENCE, Nepal, 日本麻酔科学会.
研究資金
科学研究費補助金の採択状況(文部科学省、日本学術振興会)
2021年度~2023年度, 基盤研究(C), 代表, TRPチャネル拮抗薬とGIRKチャネル作動薬の相互作用が鎮痛に及ぼす影響の解明.
2017年度~2019年度, 基盤研究(C), 分担, パッチクランプ法を用いたGIRKチャネル作動薬の鎮痛作用の検討.
2016年度~2018年度, 基盤研究(C), 代表, 術後痛に対する全身麻酔薬およびTRPチャネルの関与の検討.
2013年度~2015年度, 基盤研究(C), 分担, ケタミンの急性痛、慢性痛に対する異なる鎮痛作用機序の解明.
2011年度~2013年度, 若手研究(A), 代表, 鎮痛補助薬のTRPチャネルに対する作用の検討.
2010年度~2012年度, 基盤研究(C), 分担, インビボパッチクランプによる麻酔薬の脊髄膠様質抑制性、興奮性神経細胞に対する作用.
共同研究、受託研究(競争的資金を除く)の受入状況
2013.04~2019.03, 分担, 麻酔データウェアハウス(DWH)の構築と活用.

九大関連コンテンツ

pure2017年10月2日から、「九州大学研究者情報」を補完するデータベースとして、Elsevier社の「Pure」による研究業績の公開を開始しました。
 
 
九州大学知的財産本部「九州大学Seeds集」