Title Alternative The 10th Congress on Neutron Capture Therapy
FullText URL 126_73.pdf
Author Matsui, Hideki|
Publication Title 岡山医学会雑誌
Published Date 2014-04-01
Volume volume126
Issue issue1
Start Page 73
End Page 74
ISSN 0030-1558
Related Url http://www.okayama-u.ac.jp/user/oma/
language 日本語
Copyright Holders Copyright (c) 2014 岡山医学会
File Version publisher
DOI 10.4044/joma.126.73
FullText URL EpilepsyRes105_1_220.pdf
Author Ohmori, Iori| Hayashi, Keiichiro| Wang, Haijiao| Ouchida, Mamoru| Fujita, Naohiro| Inoue, Takushi| Michiue, Hiroyuki| Nishiki, Teiichi| Matsui, Hideki|
Published Date 2013-07
Publication Title Epilepsy Research
Volume volume105
Issue issue1-2
Publisher Elsevier Science
Start Page 220
End Page 224
ISSN 09201211
NCID AA10726642
Content Type Journal Article
language 英語
OAI-PMH Set 岡山大学
File Version author
PubMed ID 23375560
DOI 10.1016/j.eplepsyres.2013.01.003
Web of Science KeyUT 000320737500027
Related Url isVersionOf https://doi.org/10.1016/j.eplepsyres.2013.01.003
FullText URL NeurobiolDis_50_209.pdf
Author Ohmori, Iori| Ouchida, Mamoru| Kobayashi, Katsuhiro| Jitsumori, Yoshimi| Mori, Akiko| Michiue, Hiroyuki| Nishiki, Teiichi| Ohtsuka, Yoko| Matsui, Hideki|
Note CACNA1A variants contribute to severity of seizures in Dravet syndrome|
Published Date 2013-02
Publication Title Neurobiology of disease
Volume volume50
Publisher Academic Press
Start Page 209
End Page 217
ISSN 09699961
NCID AA11645502
Content Type Journal Article
language 英語
OAI-PMH Set 岡山大学
File Version author
PubMed ID 23103419
DOI 10.1016/j.nbd.2012.10.016
Web of Science KeyUT 000313758100023
Related Url isVersionOf https://doi.org/10.1016/j.nbd.2012.10.016
Author Masumoto, Toshio| Suzuki, Koichiro| Ohmori, Iori| Michiue, Hiroyuki| Tomizawa, Kazuhito| Fujimura, Atsushi| Nishiki, Tei-ichi| Matsui, Hideki|
Published Date 2012-01
Publication Title Molecular and Cellular Neuroscience
Volume volume49
Issue issue1
Content Type Journal Article
Author Fujimura, Atsushi| Michiue, Hiroyuki| Nishiki, Tei-ichi| Ohmori, Iori| Wei, Fanyan| Matsui, Hideki| Tomizawa, Kazuhito|
Published Date 2011-05-14
Publication Title PLoS ONE
Volume volume6
Issue issue3
Content Type Journal Article
Author Hayashi, Keiichiro| Ueshima, Satoshi| Ouchida, Mamoru| Mashimo, Tomoji| Nishiki, Teiichi| Sendo, Toshiaki| Serikawa, Tadao| Matsui, Hideki| Ohmori, Iori|
Published Date 2011-05
Publication Title Epilepsia
Volume volume52
Issue issue5
Content Type Journal Article
JaLCDOI 10.18926/AMO/43824
FullText URL 65_1_1.pdf
Author Han, Xiao-Jian| Tomizawa, Kazuhito| Fujimura, Atsushi| Ohmori, Iori| Nishiki, Tei-ichi| Matsushita, Masayuki| Matsui, Hideki|
Abstract Mitochondria are important cellular organelles in most metabolic processes and have a highly dynamic nature, undergoing frequent fission and fusion. The dynamic balance between fission and fusion plays critical roles in mitochondrial functions. In recent studies, several large GTPases have been identified as key molecular factors in mitochondrial fission and fusion. Moreover, the posttranslational modifications of these large GTPases, including phosphorylation, ubiquitination and SUMOylation, have been shown to be involved in the regulation of mitochondrial dynamics. Neurons are particularly sensitive and vulnerable to any abnormalities in mitochondrial dynamics, due to their large energy demand and long extended processes. Emerging evidences have thus indicated a strong linkage between mitochondria and neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease and Huntington's disease. In this review, we will describe the regulation of mitochondrial dynamics and its role in neurodegenerative diseases.
Keywords mitochondria phosphorylation ubiquitination SUMOylation neurodegeneration
Amo Type Review
Published Date 2011-02
Publication Title Acta Medica Okayama
Volume volume65
Issue issue1
Publisher Okayama University Medical School
Start Page 1
End Page 10
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
Copyright Holders CopyrightⒸ 2011 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 21339790
Web of Science KeyUT 000287620500001
Title Alternative A CACNB4 mutation showing altered Ca(v)2.1 function in a patient with Dravet syndrome
FullText URL 121_149.pdf
Author Ohmori, Iori| Ouchida, Mamoru| Mimaki, Nobuyoshi| Nishiki, Teiichi| Tomizawa, Kazuhito| Matsui, Hideki|
Keywords てんかん Dravet 症候群 CACNB4遺伝子 SCN1A 遺伝子
Publication Title 岡山医学会雑誌
Published Date 2009-12-01
Volume volume121
Issue issue3
Start Page 149
End Page 156
ISSN 0030-1558
language 日本語
Copyright Holders 岡山医学会
File Version publisher
DOI 10.4044/joma.121.149
NAID 120002308814
Author Matsui, Hideki|
Published Date 2009-12-01
Publication Title 岡山医学会雑誌
Volume volume121
Issue issue3
Content Type Journal Article
JaLCDOI 10.18926/AMO/31822
FullText URL fulltext.pdf
Author Wu, Yumei| Matsui, Hideki| Tomizawa, Kazuhito|
Abstract <p>Amphiphysin I, known as a major dynamin-binding partner localized on the collars of nascent vesicles, plays a key role in clathrin-mediated endocytosis (CME) of synaptic vesicles. Amphiphysin I mediates the invagination and fission steps of synaptic vesicles by sensing or facilitating membrane curvature and stimulating the GTPase activity of dynamin. Amphiphysin I may form a homodimer by itself or a heterodimer with amphiphysin II in vivo. Both amphiphysin I and II function as multilinker proteins in the clathrin-coated complex. Under normal physiological conditions, the functions of amphiphysin I and some other endocytic proteins are known to be regulated by phosphorylation and dephosphorylation. During hyperexcited conditions, the most recent data showed that amphiphysin I is truncated by the ca2-dependent protease calpain. Overexpression of the truncated form of amphi-physin I inhibited transferrin uptake and synaptic vesicle endocytosis (SVE). This suggests that amphi-physin I may be an important regulator for SVE when massive amounts of Ca2 flow into presynaptic terminals, a phenomenon observed in neurodegenerative disorders such as ischemia/anoxia, epilepsy, stroke, trauma and Alzheimer's disease. This review describes current knowledge regarding the general properties and functions of amphiphysin I as well as the functional regulations such as phosphorylation and proteolysis in nerve terminals.</p>
Keywords amphiphysin I calpain SVE hyperexcitation seizure
Amo Type Review
Published Date 2009-12
Publication Title Acta Medica Okayama
Volume volume63
Issue issue6
Publisher Okayama University Medical School
Start Page 305
End Page 323
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 20035287
Web of Science KeyUT 000273145900002
JaLCDOI 10.18926/AMO/31858
FullText URL fulltext.pdf
Author Ogawa, Tomoyuki| Ono, Shigeki| Ichikawa, Tomotsugu| Arimitsu, Seiji| Onoda, Keisuke| Tokunaga, Koji| Sugiu, Kenji| Tomizawa, Kazuhito| Matsui, Hideki| Date, Isao|
Abstract <p>Many studies have shown that a motif of 11 consecutive arginines (11R) is one of the most effective protein transduction domains (PTD) for introducing proteins into the cell membrane. By conjugating this &#34;11R&#34;, all sorts of proteins can effectively and harmlessly be transferred into any kind of cell. We therefore examined the transduction efficiency of 11R in cerebral arteries and obtained results showing that 11R fused enhanced green fluorescent protein (11R-EGFP) immediately and effectively penetrated all layers of the rat basilar artery (BA), especially the tunica media. This method provides a revolutionary approach to cerebral arteries and ours is the first study to demonstrate the successful transductionof a PTD fused protein into the cerebral arteries. In this review, we present an outline of our studies and other key studies related to cerebral vasospasm and 11R, problems to be overcome, and predictions regarding future use of the 11R protein transduction method for cerebral vasospasm (CV).</p>
Keywords cerebral vasospasm 11 consecutive arginines (11R) enhanced green fluorescent protein (EGFP)
Amo Type Review
Published Date 2009-02
Publication Title Acta Medica Okayama
Volume volume63
Issue issue1
Publisher Okayama University Medical School
Start Page 1
End Page 7
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 19247417
Web of Science KeyUT 000263730300001
Title Alternative Novel protein transduction method for cerebral arteries using 11R
FullText URL 120_129.pdf
Author Ogawa, Tomoyuki| Ono, Shigeki| Ichikawa, Tomotsugu| Arimitsu, Seiji| Onoda, Keisuke| Tokunaga, Koji| Sugiu, Kenji| Tomizawa, Kazuhito| Matsui, Hideki| Date, Isao|
Keywords cerebral vasospasm 11R protein transduction method
Publication Title 岡山医学会雑誌
Published Date 2008-08-01
Volume volume120
Issue issue2
Start Page 129
End Page 133
ISSN 00301558
language 日本語
Copyright Holders 岡山医学会
File Version publisher
DOI 10.4044/joma.120.129
NAID 120002310545
JaLCDOI 10.18926/AMO/30989
FullText URL fulltext.pdf
Author Taniike, Naoki| Lu, Yun-Fei| Tomizawa, Kazuhito| Matsui, Hideki|
Abstract <p>The induction of both long-term potentiation (LTP) and long-term depression (LTD) in the hippocampal CA1 region is triggered by the activation of N-methyl-D-aspartate (NMDA) receptors and the subsequent postsynaptic intracellular Ca2+ increase. However, how NMDA receptor activation differs between LTP and LTD induction is unclear. In the present study, we examined the eff ects of the magnitude and duration of NMDA receptor activation on the induction of LTP and LTD. Partial blockage of NMDA receptors by a low concentration of aminophosphonovaleric acid (APV)(2 &#956;M) prevented the induction of LTP, but not LTD. In contrast, a high concentration of APV(25 &#956;M) blocked both LTP and LTD. Tetanus stimulation-induced LTP was impaired when hippocampal slices were given the tetanus stimulation for more than 5 min. Under partial blockage of NMDA receptors, the prolonged-tetanus stimulation induced LTD but not LTP. This phenomenon was mimicked by the application of glutamate to the slices. Finally, LTD induced by prolonged activation of NMDA receptors was not aff ected by inhibition of the desensitization of &#945;-amino-3-hydroxy-5 methylisoxazole-4-propionic acid (AMPA) receptors. These results suggest that critical diff erences exist between the induction of LTP and that of LTD in terms of both the magnitude and the duration of NMDA receptor activation. The duration of the increase in intracellular Ca2+ concentration may be critical for determining whether LTP or LTD induction occurs.</p>
Keywords LTP LTD NMDA receptor learning and memory hippocampus
Amo Type Original Article
Published Date 2008-02
Publication Title Acta Medica Okayama
Volume volume62
Issue issue1
Publisher Okayama University Medical School
Start Page 21
End Page 28
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 18323868
Web of Science KeyUT 000253549500004
FullText URL Epilepsia_49_3_521.pdf
Author Ohmori, Iori| Ouchida, Mamoru| Kobayashi, Katsuhiro| Jitsumori, Yoshimi| Inoue, Takushi| Shimizu, Kenji| Matsui, Hideki| Ohtsuka, Yoko| Maegaki, Yoshihiro|
Keywords Rasmussen encephalitis SCN1A genetic-environmental interaction
Published Date 2007-11-21
Publication Title Epilepsia
Volume volume49
Issue issue3
Publisher Blackwell
Start Page 521
End Page 526
ISSN 0013-9580
NCID AA00180597
Content Type Journal Article
language 英語
OAI-PMH Set 岡山大学
File Version author
PubMed ID 18031552
DOI 10.1111/j.1528-1167.2007.01411.x
Web of Science KeyUT 000253477800020
Related Url isVersionOf https://doi.org/10.1111/j.1528-1167.2007.01411.x
JaLCDOI 10.18926/AMO/32907
FullText URL fulltext.pdf
Author Fujisawa, Toru| Moriwaki, Akiyoshi| Matsushita, Masayuki| Tomizawa, Kazuhito| Matsui, Hideki|
Abstract Oxytocin (OT) is one of the neuropituitary hormones and is synthesized in the neurons of the paraventricular nucleus (PVN) and supraoptic nucleus (SON). Previous studies have shown that the mRNAs encoding OT are delivered from the soma to both dendrites and axons of the neurons in the PVN and SON. However, it has not been elucidated whether a translational regulation mechanism to enable local synthesis of the hormone exists in the axons of the neurons of PVN and SON. Elongation factor 2 (EF2) is essential for polypeptide synthesis during protein translation. Moreover, phosphorylation of EF2 by EF2 kinase enhances the translation of certain mRNA species. In the present study, in order to shed light on the mechanisms involved in the translational regulation of OT synthesis, we investigated the localization of phosphorylated EF2. Phospho-EF2 was localized in the soma of the neurons in PVN and SON, and in the swellings of the median eminence where axonal tracts of the neurons in the PVN and SON exist. The phosphorylated form was also observed in the rat hypophysis. Moreover, phospho-EF2 and OT were colocalized in a part of the neurons in the PVN and SON. These results suggest that OT may be partially translated in the axons of neurons in the PVN and SON, and then secreted from the pituitary.
Keywords oxytocin PVN SON elongation factor 2 local translation
Amo Type Original Article
Published Date 2007-06
Publication Title Acta Medica Okayama
Volume volume61
Issue issue3
Publisher Okayama University Medical School
Start Page 161
End Page 166
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 17593952
Web of Science KeyUT 000247574700005
JaLCDOI 10.18926/AMO/32903
FullText URL fulltext.pdf
Author Wu, Yumei| Tada, Mikiro| Takahata, Kyoya| Tomizawa, Kazuhito| Matsui, Hideki|
Abstract Neuronal apoptosis is involved in neurodegenerative diseases such as Alzheimer's disease and Parkinson.s disease. An efficient means of preventing it remains to be found. Some n-3 polyunsaturated fatty acids (PUFAs) such as docosahexaenoic acid (DHA, 22 : 6n-3) and eicosapentaenoic acid (EPA, 20 : 5n-3) have been reported to be protective against the neuronal apoptosis and neuronal degeneration seen after spinal cord injury (SCI) [1]. However, it is unclear which kinds of PUFAs have the most potent ability to inhibit neuronal apoptosis and whether the simultaneous treatment of PUFAs inhibits the apoptosis. In the present study, we compared the abilities of various n-3- and n-6- PUFAs to inhibit the apoptosis induced after the administration of different apoptotic inducers, etoposide, okadaic acid, and AraC, in mouse neuroblastoma cells (Neuro2a). Preincubation with DHA (22 : 6n-3), eicosapentaenoic acid (EPA, 20 : 5n-3), alpha-linolenic acid (alpha-LNA, 18 : 3n-3), linoleic acid (LA, 18 : 2n-6), arachidonic acid (AA, 20 : 4n-3), and gamma-linolenic acid (gamma-LNA, 18 : 3n-6) significantly inhibited caspase-3 activity and LDH leakage but simultaneous treatment with the PUFAs had no effect on the apoptosis of Neuro2a cells. There were no significant differences of the anti-apoptotic eff ect among the PUFAs. These results suggest that PUFAs may not be effective for inhibiting neuronal cell death after acute and chronic neurodegenerative disorders. However, dietary supplementation with PUFAs may be beneficial as a potential means to delay the onset of the diseases and/or their rate of progression.
Keywords polyunsaturated fatty acid (PUFA) neurodegenerative disease caspase neuronal apoptosis DHA
Amo Type Original Article
Published Date 2007-06
Publication Title Acta Medica Okayama
Volume volume61
Issue issue3
Publisher Okayama University Medical School
Start Page 147
End Page 152
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 17593950
Web of Science KeyUT 000247574700003
JaLCDOI 10.18926/AMO/32905
FullText URL fulltext.pdf
Author Wu, Hai-Yan| Tomizawa, Kazuhito| Matsui, Hideki|
Abstract Intracellular calcium is a powerful secondary messenger that affects a number of calcium sensors, including calpain, a Ca2+-dependent cysteine protease, and calcineurin, a Ca2+/calmodulin-dependent protein phosphatase. Maintenance of low basal levels of intracellular calcium allows for the tightly regulated physiological activation of these proteins, which is crucial to a wide variety of cellular processes, such as fertilization, proliferation, development, learning, and memory. Deregulation of calpain and calcineurin has been implicated in the pathogenesis of several disorders, including hypertension, heart disease, diabetes, cerebral ischemia, and Alzheimer's disease. Recent studies have demonstrated an interplay between calpain and calcineurin, in which calpain can directly regulate calcineurin activity through proteolysis in glutamate-stimulated neurons in culture and in vivo. The calpain-mediated proteolytic cleavage of calcineurin increases phosphatase activity, which promotes caspase-mediated neuronal cell death. Thus, the activation of the calpain-calcineurin pathway could contribute to calcium-dependent disorders, especially those associated with Alzheimer's disease and myocardial hypertrophy. Here, we focus briefly on recent advances in revealing the structural and functional properties of these 2 calcium-activated proteins, as well as on the interplay between the 2, in an effort to understand how calpain-calcineurin signaling may relate to the pathogenesis of calcium- dependent disorders.
Keywords calpain calcineurin calcium proteolysis neurodegeneration
Amo Type Review
Published Date 2007-06
Publication Title Acta Medica Okayama
Volume volume61
Issue issue3
Publisher Okayama University Medical School
Start Page 123
End Page 137
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 17593948
Web of Science KeyUT 000247574700001
Author 魏 范研| 長嶋 一昭| 大島 登志男| 佐伯 恭範| 陸 雲飛| 松下 正之| 山田 祐一郎| 御子柴 克彦| 清野 裕| 松井 秀樹| 富澤 一仁|
Published Date 2007-05-01
Publication Title 岡山医学会雑誌
Volume volume119
Issue issue1
Content Type Journal Article
FullText URL 118_205.pdf
Author 道上 宏之| 富澤 一仁| 魏 范研| 松下 正之| 陸 雲飛| 市川 智継| 田宮 隆| 松井 秀樹| 伊達 勲|
Keywords プロテインセラピー 悪性脳腫瘍 p 53 エンドソーム 蛋白導入ドメイン
Publication Title 岡山医学会雑誌
Published Date 2007-01-04
Volume volume118
Issue issue3
Start Page 205
End Page 208
ISSN 00301558
language 日本語
Copyright Holders Copyright© 岡山医学会
File Version publisher
DOI 10.4044/joma1947.118.3_205
NAID 10018454083
JaLCDOI 10.18926/AMO/30733
FullText URL fulltext.pdf
Author Noguchi, Hirofumi| Matsumoto, Shinichi| Matsushita, Masayuki| Kobayashi, Naoya| Tanaka, Koichi| Matsui, Hideki| Tanaka, Noriaki|
Abstract The development by the Edmonton group of a sirolimus-based, steroid-free, low-tacrolimus regimen is a significant breakthrough that allows the rate of insulin independence after islet transplantation to increase from 13% to 80% at 1 year ; however, the rate is reduced to 50% at 3 years, attributed to prolonged tacrolimus exposure. Recently, immunosuppression agents such as cyclosporine, mycophenolate mofetil, and the novel agent FTY 720 have been used instead of tacrolimus. Lymphocytedepleting antibodies such as anti-thymocyte globulin, alemtuzumab, and hOKT3gamma 1 (ala, ala) have been launched, and a costimulatory blockade of anti-CD40 monoclonal antibodies and CTLA4-Ig will be attempted in the near future. Moreover, the potential of a novel immunosuppressing peptide could now be realized using new technology called the protein transduction system. In this review, we show some of the most recent contributions to the advancement of knowledge in this field.
Keywords islet transplantation steroid-free Edmonton protocol protein transduction syst
Amo Type Review
Published Date 2006-04
Publication Title Acta Medica Okayama
Volume volume60
Issue issue2
Publisher Okayama University Medical School
Start Page 71
End Page 76
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 16680182
Web of Science KeyUT 000237001900001