Faculty Profiles - TAKEMOTO Mami

Papers - TAKEMOTO Mami

Division display 141 - 160 of about 253 ／ All the affair displays >>

パーキンソン病とレビー小体型認知症の検査所見やmicrobleeds出現頻度の違いについて

武本麻美, 佐藤恒太, 太田康之, 山下徹, 菱川望, 阿部康二

臨床神経学 59 ( Suppl. ) S266 - S266 2019.11

筋萎縮性側索硬化症患者の前頭葉機能の特徴

太田康之, 山下徹, 菱川望, 佐藤恒太, 武本麻美, 表芳夫, 阿部康二

Dementia Japan 33 ( 4 ) 529 - 529 2019.10

多発性の大脳・脳幹病変を認め、診断及び治療に苦慮した抗MOG抗体関連症候群の1例

松本菜見子, 佐藤恒太, 河原由子, 武本麻美, 菱川望, 表芳夫, 商敬偉, 太田康之, 山下徹, 藤井謙太郎, 黒住和彦, 伊達勲, 阿部康二

神経治療学 36 ( 6 ) S251 - S251 2019.10

アルツハイマー病の進行に関する臨床的予測因子(Clinical predictors of Alzheimer's disease progression)

菱川望, 表芳夫, 武本麻美, 太田康之, 山下徹, 阿部康二

Dementia Japan 33 ( 4 ) 523 - 523 2019.10

Sleep problems in subacute myelo-optico neuropathy (SMON)

Nozomi Hishikawa, Mami Takemoto, Kota Sato, Toru Yamashita, Yasuyuki Ohta, Kenichi Sakai, Koji Abe

JOURNAL OF CLINICAL NEUROSCIENCE 68 128 - 133 2019.10

Language：English Publishing type：Research paper (scientific journal) Publisher：ELSEVIER SCI LTD

Subacute myelo optico neuropathy (SMON) patients typically suffer from sequelae that cause sleep disturbances. We sought to examine the prevalence of sleep problems among SMON patients. We conducted a questionnaire-based survey concerning sleep problems among 106 SMON patients, and 110 age- and gender-matched control participants. The prevalence of subjective insomnia (6 <= Athens Insomnia Scale score) was 89.6% among SMON patients, which was significantly higher than among control participants 54.4%. Sleep quality measured with the Pittsburgh Sleep Quality Index (PSQI) revealed that the prevalence of poor sleepers (6 <= PSQI score) was higher among SMON patients than control participants (75.6% vs 39.6%, respectively). Subscale analyses of rapid eye movement sleep behavior disorder screening questionnaire revealed that scores on two items ("dreams match nocturnal behavior" and "limb movements") were significantly higher among SMON patients than control participants. In addition, daytime sleepiness scores were significantly higher among SMON patients than control participants (4 <= Epworth Sleepiness Scale scores: 54.0% vs 29.0%, respectively). The current study revealed that most SMON patients suffer from insomnia with dissatisfactory sleep quality, likely due to their long-term physical sequelae. Moreover, SMON patients showed higher rates of daytime sleepiness and sleep medication intake, which could be related to reduced activity during the day, as well as insomnia. (C) 2019 Elsevier Ltd. All rights reserved.

DOI： 10.1016/j.jocn.2019.07.013

Web of Science

researchmap

Sleep problems in subacute myelo-optico neuropathy (SMON)

Nozomi Hishikawa, Mami Takemoto, Kota Sato, Toru Yamashita, Yasuyuki Ohta, Kenichi Sakai, Koji Abe

Journal of Clinical Neuroscience 68 128 - 133 2019.10

Publishing type：Research paper (scientific journal)

© 2019 Elsevier Ltd Subacute myelo-optico neuropathy (SMON) patients typically suffer from sequelae that cause sleep disturbances. We sought to examine the prevalence of sleep problems among SMON patients. We conducted a questionnaire-based survey concerning sleep problems among 106 SMON patients, and 110 age- and gender-matched control participants. The prevalence of subjective insomnia (6 ≤ Athens Insomnia Scale score) was 89.6% among SMON patients, which was significantly higher than among control participants 54.4%. Sleep quality measured with the Pittsburgh Sleep Quality Index (PSQI) revealed that the prevalence of poor sleepers (6 ≤ PSQI score) was higher among SMON patients than control participants (75.6% vs 39.6%, respectively). Subscale analyses of rapid eye movement sleep behavior disorder screening questionnaire revealed that scores on two items (“dreams match nocturnal behavior” and “limb movements”) were significantly higher among SMON patients than control participants. In addition, daytime sleepiness scores were significantly higher among SMON patients than control participants (4 ≤ Epworth Sleepiness Scale scores: 54.0% vs 29.0%, respectively). The current study revealed that most SMON patients suffer from insomnia with dissatisfactory sleep quality, likely due to their long-term physical sequelae. Moreover, SMON patients showed higher rates of daytime sleepiness and sleep medication intake, which could be related to reduced activity during the day, as well as insomnia.

DOI： 10.1016/j.jocn.2019.07.013

Scopus

PubMed

researchmap

Twendee X Ameliorates Phosphorylated Tau, alpha-Synuclein and Neurovascular Dysfunction in Alzheimer's Disease Transgenic Mice With Chronic Cerebral Hypoperfusion

Xia Liu, Toru Yamashita, Jingwei Shang, Xiaowen Shi, Ryuta Morihara, Yong Huang, Kota Sato, Mami Takemoto, Nozomi Hishikawa, Yasuyuki Ohta, Koji Abe

JOURNAL OF STROKE & CEREBROVASCULAR DISEASES 28 ( 10 ) 104310 - 104310 2019.10

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

Background: The pathological impact of chronic cerebral hypoperfusion (CCH) on Alzheimer's disease (AD) is still poorly understood. In the present study, we investigated the role of CCH on an AD mouse model in phosphorylated tau and alpha-synudein pathology, neurovascular unit, cerebrovascular remodeling, and neurovascular trophic coupling. Moreover, examined protective effect of a new antioxidant Twendee X (TwX). Methods: APP23 mice were implanted to bilateral common carotid arteries stenosis with ameroid constrictors to gradually decrease the cerebral blood flow. The effects of the administration of TwX were evaluated by immunohistochemical analysis and Immunofluorescent histochemistry. Results: The present study revealed that the expressions of phospho-tau and phospho-alpha-synudein were significantly increased in the APP23 + CCH mice group as compared with wild type and APP23 mice groups (*P < .05 and **P < .01 versus WT; P-# < .05 and (##) P < .01 versus APP23). In addition, CCH significantly exacerbated MMP-9 activation relating to blood-brain barrier destruction (*P < .01 versus WT; (#) P < .05, and (##) P < .01 versus APP23), enhanced neurovascular remodeling, and impaired a neurovascular trophic coupling in the vascular endothelial BDNF expression of the APP23 + CCH group. TwX treatment (20 mg/kg/ day, from 4.5 to 12 months) significantly reduced tau and oc-synudein pathologies, ameliorated neurovascular dysfunction compared with APP23 + CCH group. Conclusions: Our findings indicate that administration of a new antioxidative mixture TwX substantially reduced the above neuropathologic abnormalities, suggesting a potential therapeutic benefit of TwX for AD with CCH.

DOI： 10.1016/j.jstrokecerebrovasdis.2019.104310

Web of Science

researchmap

胃瘻造設後に高浸透圧高血糖症候群を発症した進行性核上性麻痺の1例

田所功, 佐藤恒太, 森原隆太, 商敬偉, 武本麻美, 表芳夫, 太田康之, 山下徹, 菱川望, 阿部康二

神経治療学 36 ( 6 ) S269 - S269 2019.10

Chronic Cerebral Hypoperfusion Activates the Coagulation and Complement Cascades in Alzheimer's Disease Mice

Xiaowen Shi, Yasuyuki Ohta, Xia Liu, Jingwei Shang, Ryuta Morihara, Yumiko Nakano, Tian Feng, Yong Huang, Kota Sato, Mami Takemoto, Nozomi Hishikawa, Toru Yamashita, Koji Abe

NEUROSCIENCE 416 126 - 136 2019.9

Language：English Publishing type：Research paper (scientific journal) Publisher：PERGAMON-ELSEVIER SCIENCE LTD

Alzheimer's disease (AD) in the elderly is frequently accompanied by chronic cerebral hypoperfusion (CCH), which impairs the clearance of amyloid beta (A beta) due to the dysfunction of the blood-brain barrier (BBB) and accelerates the AD pathology. Since the coagulation and complement cascades are associated with BBB dysfunction and AD pathology, we investigated the expression changes of coagulation (fibrinogen alpha chain-FGA, coagulation factor XIII A chain-Factor XIII alpha) and complement (plasma protease C1 inhibitor-C1-INH, Complement component 3-C3) factors in the brain of novel AD model (APP23) mice with CCH at 12 months of age. Immunohistochemical and immunofluorescent analysis showed that the expressions of FGA, Factor XIII alpha, C1-INH and C3 were significantly increased in cerebral neocortex, hippocampus, and thalamus of APP23 + CCH group (n = 12) as compared with wild type (WT, n = 10) and APP23 (n = 10) groups (*P < . 05 and ** P < .01 vs WT; P-# < .05 and P-## < .01 vs APP23), especially near and inside of neurovascular unit. The present study suggests that CCH activated both the coagulation and complement cascades in a novel AD model mice brain accompanied by the acceleration of AD pathology. (C) 2019 IBRO. Published by Elsevier Ltd. All rights reserved.

DOI： 10.1016/j.neuroscience.2019.07.050

Web of Science

researchmap

Late presented congenital myasthenic syndrome with novel compound heterozygous CHRNE mutations mimicking seronegative myasthenia gravis

Yumiko Nakano, Keiichiro Tsunoda, Toru Yamashita, Jun Mitsui, Kota Sato, Mami Takemoto, Nozomi Hishikawa, Yasuyuki Ohta, Tatsushi Toda, Shoji Tsuji, Koji Abe

NEUROLOGY AND CLINICAL NEUROSCIENCE 7 ( 5 ) 288 - 290 2019.9

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

We found a late presented congenital myasthenic syndrome (CMS) patient with novel CHRNE gene mutations. Although our patient has shown blepharoptosis since youth, fatigable muscle weakness began at age 71. Genetic analysis revealed novel compound heterozygous CHRNE mutations (c.1032+2T>G, c.1306_1307 delGA). His myasthenic symptoms were well managed by oral anti-cholinesterase drug until he died at 82-year-old. The present case showed mild myasthenic symptoms with very late presentation and slow progression. Late presented CMS is often underdiagnosed; therefore, genetic testing is important to distinguish it from other myasthenic disease.

DOI： 10.1111/ncn3.12317

Web of Science

researchmap

Imaging Hypoxic Stress and the Treatment of Amyotrophic Lateral Sclerosis with Dimethyloxalylglycine in a Mice Model

Emi Nomura, Yasuyuki Ohta, Koh Tadokoro, Jingwei Shang, Tian Feng, Xia Liu, Xiaowen Shi, Namiko Matsumoto, Ryo Sasaki, Keiichiro Tsunoda, Kota Sato, Mami Takemoto, Nozomi Hishikawa, Toru Yamashita, Takahiro Kuchimaru, Shinae Kizaka-Kondoh, Koji Abe

NEUROSCIENCE 415 31 - 43 2019.9

Language：English Publishing type：Research paper (scientific journal) Publisher：PERGAMON-ELSEVIER SCIENCE LTD

Hypoxia inducible factor-1 alpha (HIF-1 alpha) is a key transcription factor that maintains oxygen homeostasis. Hypoxic stress is related to the pathogenesis of amyotrophic lateral sclerosis (ALS), and impaired HIF-1 alpha induces motor neuron degeneration in ALS. Dimethyloxalylglycine (DMOG) upregulates the stability of HIF-1 alpha expression and shows neuroprotective effects, but has not been used in ALS as an anti-hypoxic stress treatment. In the present study, we investigated hypoxic stress in ALS model mice bearing G93A-human Cu/Zn superoxide dismutase by in vivo HIF-1 alpha imaging, and treated the ALS mice with DMOG. In vivo HIF-1 alpha imaging analysis showed enhanced hypoxic stress in both the spinal cord and muscles of lower limbs of ALS mice, even at the pre-symptomatic stage. HIF-1 alpha expression decreased as the disease progressed until 126 days of age. DMOG treatment significantly ameliorated the decrease in HIF-1 alpha expression, the degeneration of both spinal motor neurons and myofibers in lower limbs, gliosis and apoptosis in the spinal cord. This was accompanied by prolonged survival. The present study suggests that in vivo bioluminescence resonance energy transfer (BRET) HIF-1 alpha imaging is useful for evaluating hypoxic stress in ALS, and that the enhancement of HIF-1 alpha is a therapeutic target for ALS patients. (C) 2019 IBRO. Published by Elsevier Ltd. All rights reserved.

DOI： 10.1016/j.neuroscience.2019.06.025

Web of Science

researchmap

A Japanese patient with a VCP mutation c.290G > A (p.G97E) presenting a rapid progressive respiratory failure.

Nomura E, Ohta Y, Sato K, Kawahara Y, Takemoto M, Takahashi Y, Matsumoto N, Yunoki T, Yamashita T, Hishikawa N, Nishino I, Abe K

Neuro Clin Neurosci 7 ( 6 ) 361 - 364 2019.8

A Unique Recurrent Stroke Case due to Bilateral Vertebral Artery Dissection with Familial Hirschsprung Disease

Kota Sato, Ryo Sasaki, Yasuyuki Ohta, Mami Takemoto, Nozomi Hishikawa, Toru Yamashita, Koji Abe

Journal of Stroke and Cerebrovascular Diseases 28 ( 8 ) e113 - e115 2019.8

Publishing type：Research paper (scientific journal)

© 2019 Elsevier Inc. Vertebral artery (VA) dissection is one major cause of brain infarction in young and middle-aged adults. Risk factors for VA dissection are hypertension, diabetes mellitus, hyperlipidemia, trauma, and genetic factors. A 32-year-old man with familial Hirschsprung disease at the age of 2 presented cerebellar ischemic stroke due to bilateral VA dissections. A stroke recurred within 17 days despite oral dual antiplatelet therapy. Bilateral VA dissections and recurrent dissections are related to genetic mutations associated with connective tissue diseases. A part of familial Hirschsprung disease has genetic factors in common with cerebrovascular disease. There may be a common genetic background between his VA dissection and Hirschsprung disease.

DOI： 10.1016/j.jstrokecerebrovasdis.2019.04.035

Scopus

PubMed

researchmap

Clinical and Pathological Benefit of Twendee X in Alzheimer's Disease Transgenic Mice with Chronic Cerebral Hypoperfusion

Xia Liu, Toru Yamashita, Jingwei Shang, Xiaowen Shi, Ryuta Morihara, Yong Huang, Kota Sato, Mami Takemoto, Nozomi Hishikawa, Yasuyuki Ohta, Koji Abe

JOURNAL OF STROKE & CEREBROVASCULAR DISEASES 28 ( 7 ) 1993 - 2002 2019.7

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

Background: Multiple pathogeneses are involved in Alzheimer's disease (AD), such as amyloid-beta accumulation, neuroinflammation, and oxidative stress. The pathological impact of chronic cerebral hypoperfusion on Alzheimer's disease is still poorly understood. Methods: APP23 mice were implanted to bilateral common carotid arteries stenosis with ameroid constrictors for slowly progressive chronic cerebral hypoperfusion (CCH). The effects of the administration of Twendee X (TwX) were evaluated by behavioral analysis, immunohistochemical analysis, and immunofluorescent histochemistry. Results: In the present study, chronic cerebral hypoperfusion, which is commonly found in aged Alzheimer's disease, significantly exacerbated motor dysfunction of APP23 mice from 5 months and cognitive deficit from 8 months of age, as well as neuronal loss, extracellular amyloid-beta plaque and intracellular oligomer formations, and amyloid angiopathy at 12 months. Severe upregulations of oxidative markers and inflammatory markers were found in the cerebral cortex, hippocampus, and thalamus at 12 months. Twendee X treatment (20 mg/kg/d, from 4.5 to 12 months) substantially rescued the cognitive deficit and reduced the above amyloid-b pathology and neuronal loss, alleviated neuroinflammation and oxidative stress. Conclusions: The present findings suggested a potential therapeutic benefit of Twendee X for Alzheimer's disease with chronic cerebral hypoperfusion.

DOI： 10.1016/j.jstrokecerebrovasdis.2019.03.029

Web of Science

researchmap

In vivo direct reprogramming of glial linage to mature neurons after cerebral ischemia

Toru Yamashita, Jingwei Shang, Yumiko Nakano, Ryuta Morihara, Kota Sato, Mami Takemoto, Nozomi Hishikawa, Yasuyuki Ohta, Koji Abe

SCIENTIFIC REPORTS 9 ( 1 ) 10956 - 10956 2019.7

Language：English Publishing type：Research paper (scientific journal) Publisher：NATURE PUBLISHING GROUP

The therapeutic effect of in vivo direct reprogramming on ischemic stroke has not been evaluated. In the present study, a retroviral solution (1.5-2.0 x 10(7) /ul) of mock pMX-GFP (n = 13) or pMX-Ascl1/Sox2/NeuroD1 (ASN) (n = 14) was directly injected into the ipsilateral striatum and cortex 3 days after 30 min of transient cerebral ischemia. The reprogrammed cells first expressed neuronal progenitor marker Dcx 7 and 21 days after viral injection, then expressed mature neuronal marker NeuN. This was accompanied by morphological changes, including long processes and synapse-like structures, 49 days after viral injection. Meanwhile, therapeutic improvement was not detected both in clinical scores or infarct volume. The present study provides a future novel self-repair strategy for ischemic stroke with beneficial modifications of the inducer-suppressor balance.

DOI： 10.1038/s41598-019-47482-0

Web of Science

researchmap

A pneumococcal meningoencephalitis with a small spleen

Keiichiro Tsunoda, Kota Sato, Yoshiaki Takahashi, Koh Tadokoro, Ryo Sasaki, Emi Nomura, Mami Takemoto, Nozomi Hishikawa, Yasuyuki Ohta, Toru Yamashita, Koji Abe

NEUROLOGY AND CLINICAL NEUROSCIENCE 7 ( 4 ) 215 - 217 2019.7

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

Streptococcus pneumoniae is a major cause of bacterial meningitis usually in children or elder adults. We report a case of a 38-year-old man having pneumococcal meningoencephalitis with a small spleen (35 cm(3)), compared to seven previous patients with pneumococcal meningitis in our department. Among the eight patients, four cases were due to sinusitis, but the origin could not be identified in the other four cases, including the present case who was the youngest patient with the smallest splenic size. Of interest in the present analysis was the negative or positive correlation between splenic size and age, with or without sinusitis. This is the first report on pneumococcal meningoencephalitis that takes into consideration age, splenic size, and the origin of infection.

DOI： 10.1111/ncn3.12290

Web of Science

researchmap

Acceleration of NLRP3 inflammasome by chronic cerebral hypoperfusion in Alzheimer's disease model mouse

Jingwei Shang, Toru Yamashita, Yun Zhai, Yumiko Nakano, Ryuta Morihara, Xianghong Li, Feng Tian, Xia Liu, Yong Huang, Xiaowen Shi, Kota Sato, Mami Takemoto, Nozomi Hishikawa, Yasuyuki Ohta, Koji Abe

NEUROSCIENCE RESEARCH 143 61 - 70 2019.6

Language：English Publishing type：Research paper (scientific journal) Publisher：ELSEVIER IRELAND LTD

Cerebral neuroinflammation defines a novel pathway for progressing Alzheimer's disease (AD) pathology. We investigated immunohistological changes of neuroinflammation with nucleotide-binding domain and leucine-rich repeat (NLR)-protein 3 (NLRP3), activated caspase-1 and interleukin-1 beta (IL-1 beta) in a novel AD (APP23) mice with chronic cerebral hypoperfusion (CCH) model from 4 months (M) of age, moreover, examined protective effect of galantamine. CCH strongly enhanced NLRP3, activated caspase-1 and IL-1 beta expressions in hippocampus and thalamus at age 12 M of AD mice. CCH also exaggerated amyloid-beta (A beta) 40 depositions in cerebral cortex. Furthermore, CCH exacerbated a marked dissociation of neurovascular unit (NVU). These pathological changes were ameliorated by galantamine treatment. The present study demonstrated that CCH strongly enhanced primary AD pathology including neuroinflammation, A beta accumulations and NVU dissociation in AD mice, which was greatly protected by an allosterically potentiating ligand galantamine. (C) 2018 Elsevier B.V. and Japan Neuroscience Society. All rights reserved.

DOI： 10.1016/j.neures.2018.06.002

Web of Science

researchmap

Enhanced oxidative stress and the treatment by edaravone in mice model of amyotrophic lateral sclerosis

Yasuyuki Ohta, Emi Nomura, Jingwei Shang, Tian Feng, Yong Huang, Xia Liu, Xiaowen Shi, Yumiko Nakano, Nozomi Hishikawa, Kota Sato, Mami Takemoto, Toru Yamashita, Koji Abe

JOURNAL OF NEUROSCIENCE RESEARCH 97 ( 5 ) 607 - 619 2019.5

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

Oxidative stress is associated with the degeneration of both motor neurons and skeletal muscles in amyotrophic lateral sclerosis (ALS). A free radical scavenger edaravone has been proven as a therapeutic drug for ALS patients, but the neuroprotective mechanism for the oxidative stress of ALS has not been fully investigated. In this study, we investigated oxidative stress in ALS model mice bearing both oxidative stress sensor nuclear erythroid 2-related factor 2 (Nrf2) and G93A-human Cu/Zn superoxide dismutase (Nrf2/G93A) treated by edaravone. In vivo Nrf2 imaging analysis showed the accelerated oxidative stress both in spinal motor neurons and lower limb muscles of Nrf2/G93A mice according to disease progression in addition to the enhancement of serum oxidative stress marker dROMS. These were significantly alleviated by edaravone treatment accompanied by clinical improvements (rotarod test). The present study suggests that in vivo optical imaging of Nrf2 is useful for detecting oxidative stress in ALS, and edaravone alleviates the degeneration of both motor neurons and muscles related to oxidative stress in ALS patients.

DOI： 10.1002/jnr.24368

Web of Science

researchmap

Very rare solitary primary peripheral nerve onset cytotoxic molecule-positive peripheral T-cell lymphoma (PTCL)

Namiko Matsumoto, Kota Sato, Yoshiaki Takahashi, Yuko Kawahara, Taijun Yunoki, Jingwei Shang, Mami Takemoto, Nozomi Hishikawa, Yasuyuki Ohta, Toru Yamashita, Maiko Sakamoto, Eisei Kondou, Rei Shibata, Tadashi Yoshino, Toshifumi Ozaki, Koji Abe

NEUROLOGY AND CLINICAL NEUROSCIENCE 7 ( 3 ) 146 - 149 2019.5

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

Here we present the first report of solitary primary peripheral nerve onset cytotoxic molecule (CM)-positive peripheral T-cell lymphoma (PTCL) diagnosed after nerve biopsy. An 84-year-old female with rheumatoid arthritis (RA) complained of asymmetric severe tenderness in her upper limbs. The biopsy pathology revealed a direct invasion of CM-positive PTCL. When RA patients complain of numbness, tenderness, or weakness, lymphomatic peripheral nerve invasion should be considered.

DOI： 10.1111/ncn3.12280

Web of Science

researchmap

Multi-modal combination therapy rescued a frequent ischemic stroke patient due to giant cell arteritis Reviewed

Yoshiaki Takahashi, Kota Sato, Namiko Matsumoto, Yuko Kawahara, Taijun Yunoki, Jingwei Shang, Mami Takemoto, Nozomi Hishikawa, Yasuyuki Ohta, Toru Yamashita, Koji Abe

NEUROLOGY AND CLINICAL NEUROSCIENCE 7 ( 3 ) 132 - 135 2019.5

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

Ischemic stroke (IS) due to giant cell arteritis (GCA) is rare, but highly mortal. Here, we report a 72-year-old man who showed frequent IS with GCA. Initial therapy with prednisolone increased the frequency of IS, which disappeared after continuous multi-modal combination therapy with corticosteroids, immunosuppressive agents, antiplatelets, and statin. The present case was discharged with independent walk, suggesting that a multi-modal combination therapy rescued the GCA patient from frequent IS.

DOI： 10.1111/ncn3.12266

Web of Science

researchmap

　 PREV - NEXT 　

< TAKEMOTO Mami >

Papers - TAKEMOTO Mami