研究者詳細 - 清水　忍

論文 - 清水　忍

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医師主導治験における標準業務手順書の適切な作成と効率的な運用に向けた検討．査読有り

林宏至，岩崎幸司，熊谷いづみ，横式沙紀，菊池佳代子，清水忍，寺町真由美，加賀山祐樹，松山琴音，笠井宏委，内山麻希子，山本学

薬理と治療 47 巻頁： s134 - s147 2019年

腹圧性尿失禁に対する治療括約筋再生

山本徳則，清水忍，後藤百万

臨床泌尿器科 73 巻 ( 2 ) 頁： 130 - 135 2019年

Phase I study of combined therapy with vorinostat and gefitinib to treat BIM deletion polymorphism-associated resistance in EGFR-mutant lung cancer (VICTROY-J)

Hase, T; Takeuchi, S; Ando, M; Hata, A; Kenmotsu, H; Fujiwara, T; Shimizu, S; Nagase, K; Yoshimura, K; Katakami, N; Takahashi, T; Hasegawa, Y; Yano, S

ANNALS OF ONCOLOGY 28 巻 2017年11月

Design of a single-arm clinical trial of regenerative therapy by periurethral injection of adipose-derived regenerative cells for male stress urinary incontinence in Japan: the ADRESU study protocol 査読有り

Shimizu, S; Yamamoto, T; Nakayama, S; Hirakawa, A; Kuwatsuka, Y; Funahashi, Y; Matsukawa, Y; Takanari, K; Toriyama, K; Kamei, Y; Narimoto, K; Yamanishi, T; Ishizuka, O; Mizuno, M; Gotoh, M

BMC UROLOGY 17 巻 ( 1 ) 頁： 89 2017年9月

Human Muse Cells, Nontumorigenic Pluripotent-Like Stem Cells, Have Liver Regeneration Capacity Through Specific Homing and Cell Replacement in a Mouse Model of Liver Fibrosis 査読有り

Iseki, M; Kushida, Y; Wakao, S; Akimoto, T; Mizuma, M; Motoi, F; Asada, R; Shimizu, S; Unno, M; Chazenbalk, G; Dezawa, M

CELL TRANSPLANTATION 26 巻 ( 5 ) 頁： 821 - 840 2017年

Phase I study of combined therapy with vorinostat and gefitinib to treat BIM deletion polymorphism-associated resistance in EGFR-mutant lung cancer (VICTROY-J): a study protocol. 査読有り

Takeuchi S, Yoshimura K, Fujiwara T, Ando M, Shimizu S, Nagase K, Hasegawa Y, Takahashi T, Katakami N, Inoue A, Yano S

The journal of medical investigation : JMI 64 巻 ( 3.4 ) 頁： 321 - 325 2017年

尿失禁に対する脂肪幹細胞が作り出す微小環境を活用した治療の開発

山本徳則，舟橋康人，松川宜久，中山忍，清水忍，後藤百万

泌尿器外科 29 巻 ( 4 ) 頁： 335-338 2016年

実用化に向けた非臨床開発の基本的考え方招待有り

清水忍

神経治療 33 巻 ( 3 ) 頁： 453-458 2016年

抗悪性腫瘍薬の臨床データパッケージ分析からみる今後の課題査読有り

平川晃弘，木下文恵，森由美子，清水忍

医薬品医療機器レギュラトリーサイエンス 46 巻 ( 10 ) 頁： 714-720 2015年

What Factors Lead to prolonged Regulatory Review Times for New Drugs in Japan? 査読有り

Yoneda S, Asada R, Shimizu S, Ono S, Yamaguchi T

J Clin Trials 5 巻 ( 6 ) 頁： 247 2015年

名古屋大学における生命倫理審査委員会の事前審査に関する状況調査査読有り

清水忍，中山忍，飯島祥彦，加藤勝義，安藤昌彦，水野正明，直江知樹

臨床薬理 44 巻 ( 6 ) 頁： 443-450 2013年11月

Analysis of new drugs whose clinical development and regulatory approval were hampered during their introduction in Japan. 査読有り

Asada R, Shimizu S, Ono S, Ito T, Shimizu A, Yamaguchi T.

J Clin Pharm Ther. 38 巻 ( 4 ) 頁： 309-313 2013年8月

記述言語：英語掲載種別：研究論文（学術雑誌）

What is known and Objective: Many drugs fail during development. However, detailed reasons for failure during drug development are almost never disclosed. We focused on the drugs whose clinical development and registration were initially hampered, but which were finally approved to identify reasons that delayed their marketing approval in Japan.
Methods: We analysed 727 new drug applications (NDAs) approved in Japan between 2001 and 2011.
Results and Discussion: Fifty-three NDAs had serious and identifiable problems during drug development. Of these, 43 NDAs had `problem related to clinical data'. We found that the problems for withdrawal of these NDAs could be ascribed largely to inappropriate clinical data package and study design for supporting the intended indications and usage and to unclear clinical results for defining dosage regimen or efficacy of the drugs.
What is new and Conclusion: Our results indicate the importance of careful determination of the optimal dosage regimen and the choice of objective endpoints in clinical trials. Further, it is important to establish a clear strategy for generating the clinical data package, to include careful design of clinical trials on the basis of the nature of the target disease and target population. For drugs marketed in Japan, there is a need to include sufficient numbers of Japanese patients in the trials.

DOI： 10.1111/jcpt.

Functional alteration of inhibitory influences on spinal motor output in painful diabetic neuropathy in rats. 査読有り

Tanabe M, Shimizu S, Takabayashi K, Honda M, Ono H.

Neurosci Lett. 389 巻 ( 3 ) 頁： 152-156 2005年12月

記述言語：英語掲載種別：研究論文（学術雑誌）

Diabetes is frequently accompanied by painful polyneuropathies that are mediated by enhanced neuronal excitability in the spinal cord, partly because of decrease in spinal intrinsic inhibitory influences. Changes in spinal excitatory-inhibitory balance may alter spinal segmental motor output. In the study presented here, the mono- and disynaptic (the fastest polysynaptic) reflexes (MSR and DSR, respectively) were recorded from L5 ventral roots in response to stimulation of the ipsilateral L5 dorsal root in spinalized streptozotocin (STZ)-induced diabetic rats with a reduced withdrawal threshold to mechanical stimuli. The diabetic rats generally exhibited larger spinal reflex amplitudes, the DSR being influenced in particular. We addressed whether recurrent and presynaptic inhibition of the spinal reflexes were altered in STZ-treated animals. The recurrent inhibition of the MSR and DSR elicited by preceding antidromic conditioning stimulation delivered to the recorded L5 ventral root was markedly suppressed in diabetic rats. By contrast, the presynaptic inhibition of the MSR and DSR elicited by preceding conditioning stimulation to the ipsilateral L4 dorsal root was not impaired. Thus, in diabetic painful neuropathy, reduced spinal intrinsic inhibition in the ventral horn contributes to an enhanced spinal segmental motor output.

Role of descending noradrenergic system and spinal α₂-adrenergic receptors in the effects of gabapentin on thermal and mechanical nociception after partial nerve injury in the mouse. 査読有り

Tanabe M, Takasu K, Kasuya N, Shimizu S, Honda M, Ono H.

Br J Pharmacol. 144 巻頁： 703-714 2005年3月

記述言語：英語掲載種別：研究論文（学術雑誌）

1. To gain further insight into the mechanisms underlying the antihyperalgesic and antiallodynic actions of gabapentin, a chronic pain model was prepared by partially ligating the sciatic nerve in mice. The mice then received systemic or local injections of gabapentin combined with either central noradrenaline (NA) depletion by 6-hydroxydopamine (6-OHDA) or α-adrenergic receptor blockade. 2. Intraperitoneally (i.p.) administered gabapentin produced antihyperalgesic and antiallodynic effects that were manifested by elevation of the withdrawal threshold to a thermal (plantar test) or mechanical (von Frey test) stimulus, respectively. 3. Similar effects were obtained in both the plantar and von Frey tests when gabapentin was injected intracerebroventricularly (i.c.v.) or intrathecally (i.t.), suggesting that it acts at both supraspinal and spinal loci. This novel supraspinal analgesic action of gabapentin was only obtained in ligated neuropathic mice, and gabapentin (i.p. and i.c.v.) did not affect acute thermal and mechanical nociception. 4. In mice in which central NA levels were depleted by 6-OHDA, the antihyperalgesic and antiallodynic effects of i.p. and i.c.v. gabapentin were strongly suppressed. 5. The antihyperalgesic and antiallodynic effects of systemic gabapentin were reduced by both systemic and i.t. administration of yohimbine, an α₂-adrenergic receptor antagonist. By contrast, prazosin (i.p. or i.t.), an α₁-adrenergic receptor antagonist, did not alter the effects of gabapentin. 6. It was concluded that the antihyperalgesic and antiallodynic effects of gabapentin are mediated substantially by the descending noradrenergic system, resulting in the activation of spinal α₂-adrenergic receptors.

DOI： 10.1038/sj.bjp.0706109

GABA_B receptors do not mediate the inhibitory actions of gabapentin on the spinal reflex in rats. 査読有り

Shimizu S, Honda M, Tanabe M, Ono H.

J Pharmacol Sci. 96 巻 ( 4 ) 頁： 444-449 2004年12月

担当区分：筆頭著者記述言語：英語掲載種別：研究論文（学術雑誌）

responsible for those actions, however, are still not clearly understood. We have recently demonstrated that gabapentin reduces the spinal reflex in rats via mechanisms that do not involve gamma-aminobutyric acid (GABA)_A receptors. In the study, we attempted to explore the involvement of GABA_B receptors in gabapentin-induced inhibition of the spinal reflexes in spinalized rats. Stimulation of the dorsal root at L5 elicited the segmental mono-(MSR) and polysynaptic reflex (PSR) in the ipsilateral ventral root. The microinjection of gabapentin (1.5 and 5 nmol) into the ventral horn reduced both MSR and PSR, whereas the injection into the dorsal horn only inhibited the PSR, indicating that systemic gabapentin inhibits the MSR at the ventral horn and it inhibits the PSR at both the ventral and dorsal horns. The GABA_B-receptor antagonist CGP35348 (0.5 nmol) injected into the ventral horn antagonized the inhibition of the spinal reflexes by the GABA_B-receptor agonist baclofen (i.v.) but not by gabapentin (i.v.). Thus, GABA_B receptors do not appear to contribute to the gabapentin-induced inhibition of the spinal reflex.

Endogenous GABA does not mediate the inhibitory effects of gabapentin on spinal reflexes in rats. 査読有り

Shimizu S, Honda M, Tanabe M, Oka J, Ono H.

J Pharmacol Sci. 94 巻 ( 2 ) 頁： 137-143 2004年2月

担当区分：筆頭著者記述言語：英語掲載種別：研究論文（学術雑誌）

The novel antiepileptic drug gabapentin was designed as a structural analog of gamma-aminobutyric acid (GABA). However, its mechanism of action remains unclear. In the present study, we investigated the effect of gabapentin on spinal reflexes in anesthetized rats. The mono- and polysynaptic reflex potentials were recorded from the ipsilateral L5 ventral root after stimulation of the L5 dorsal root. The dorsal root reflex potential, an index of presynaptic inhibition, was recorded from the ipsilateral L4 dorsal root. In non-spinalized (intact) and spinalized rats, intravenously administered gabapentin reduced the mono- and polysynaptic reflex potentials in a dose-dependent manner. These inhibitory effects of gabapentin were not suppressed by the GABA_A antagonist picrotoxin. Moreover, gabapentin also decreased spinal reflexes in spinalized rats depleted of spinal GABA with semicarbazide, an inhibitor of the GABA-synthesizing enzyme. The dorsal root reflex potentials were not affected by gabapentin. These results suggest that endogenous GABA does not mediate the inhibitory effects of gabapentin on spinal reflexes.

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