| 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/32086 |
|---|---|
| FullText URL | fulltext.pdf |
| Author | Takata, Hidehiko| Tomizawa, Kazuhito| Matsushita, Masayuki| Matsui, Hideki| |
| Abstract | <p>Protein transduction therapy using poly-arginine peptide can deliver the biologically active proteins. A previous study showed that 11 poly-arginine fused p53 protein (11R-p53) effectively penetrated across the plasma membrane and inhibited the proliferation of oral cancer cells. However, the intracellular half-life of the delivered protein was less than 36 h. Previous studies also showed that 2-methoxyestradiol (2-ME), an endogenous non-toxic estrogenic metabolite, induces the stabilization of the wild-type p53 protein in human cancer cells posttranscriptionally. In the present study, we examined whether 2-ME induced the stabilization of 11R-p53 and had an inhibitory effect on the proliferation of oral cancer cells. The application of 2-ME significantly enhanced the inhibitory effect of 11R-p53 on the proliferation of oral cancer cells. However, 2-ME had no effect on the intracellular half-life of 11R-p53 in oral cancer cells. Of interest is the finding that 2-ME suppressed the transcriptional activity of NFkappaB, which has an important role in tumorigenesis, but did not affect p53 transcriptional activity. These results suggest that 2-ME synergistically enhances the 11R-p53-induced inhibition of the proliferation of oral cancer cells through the suppression of NFkB transcription.</p> |
| Keywords | tumor TAT poly arginine gene therapy protein therapy |
| Amo Type | Article |
| Published Date | 2004-08 |
| Publication Title | Acta Medica Okayama |
| Volume | volume58 |
| Issue | issue4 |
| Publisher | Okayama University Medical School |
| Start Page | 181 |
| End Page | 187 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| Content Type | Journal Article |
| language | 英語 |
| File Version | publisher |
| Refereed | True |
| PubMed ID | 15551755 |
| Web of Science KeyUT | 000223559700002 |
| 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 |
| 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 |
| 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 |
| 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/30810 |
|---|---|
| FullText URL | fulltext.pdf |
| Author | Ezawa, Kazuhiko| Yamamura, Masahiro| Matsui, Hideki| Ota, Zensuke| Makino, Hirofumi| |
| Abstract | <p> To determine whether the predominant infiltration with memory CD4<sup>+</sup>T cells in joints is specific to the local immune and inflammatory response in rheumatoid arthritis (RA), the proportions of CD45RA<sup>+</sup> or CD45RO<sup>+</sup> cells in the CD4<sup>+</sup>T cell populations in three different compartments (i.e., peripheral blood, synovial fluid, and synovial tissue) from patients with RA and osteoarthritis (OA) were compared by two-color flow-cytometric analysis. In the CD4<sup>+</sup>T cell population of peripheral blood, the number of CD45RO<sup>+</sup> cells was relatively higher than CD45RA<sup>+</sup> cells in both RA and OA patients, but their percentages did not differ from those found in healthy individuals. However, the great majority of CD4<sup>+</sup>T cells present in synovial fluid and synovial tissue were CD45RO-positive and CD45RA-negative in both patient groups; although CD4<sup>+</sup>T cells infiltrating both the disease compartments were markedly greater in RA joints, their mean percentages of CD45RO<sup>+</sup> cells were not significantly different from those in OA joints. These data indicate that an accumulation of CD45RO<sup>+</sup> memory CD4+T cells is a generalized phenomenon during local inflammatory responses in both RA and OA joints, and may be due mainly to the propensity of these cells to preferentially transmigrate into the inflamed joint via adhesion molecules as compared with CD45RA<sup>+</sup> naive CD4<sup>+</sup>T cells.</p> |
| Keywords | rheumatoid arthritis ostroarthritis CD45RO<sup>+</sup> CD4<sup>+</sup>T cells |
| Amo Type | Article |
| Published Date | 1997-02 |
| Publication Title | Acta Medica Okayama |
| Volume | volume51 |
| Issue | issue1 |
| Publisher | Okayama University Medical School |
| Start Page | 25 |
| End Page | 31 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| Content Type | Journal Article |
| language | 英語 |
| File Version | publisher |
| Refereed | True |
| PubMed ID | 9057932 |
| Web of Science KeyUT | A1997WL24600005 |
| 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 μM) prevented the induction of LTP, but not LTD. In contrast, a high concentration of APV(25 μM) 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 α-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 |
| 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 |
| JaLCDOI | 10.18926/AMO/31596 |
|---|---|
| FullText URL | fulltext.pdf |
| Author | Miyamoto, Osamu| Itano, Toshifumi| Fujisawa, Mutsuo| Tokuda, Masaaki| Matsui, Hideki| Nagao, Seigo| Hatase, Osamu| |
| Abstract | <p>Basic fibroblast growth factor (bFGF) and nerve growth factor (NGF) were administered into the rat brain following unilateral fimbria-fornix transection. Both bFGF and NGF stimulated the sprouting of acetylcholinesterase (AChE) positive fibers in the hippocampus on the lesioned side. Furthermore, a small number of AChE-positive fibers were regenerated even when only the vehicle was administered. Rats treated with NGF as well as control group had only thin fibers, whereas those treated with bFGF had not only thin fibers but also thick fibers. These results indicate that intrinsic NGF is released and acts on damaged neurons directly, while bFGF acts them on directly and/or indirectly after brain injury.</p> |
| Keywords | bFGF NGF regeneration acetylcholinesterase positive fibers sprouting |
| Amo Type | Article |
| Published Date | 1993-06 |
| Publication Title | Acta Medica Okayama |
| Volume | volume47 |
| Issue | issue3 |
| Publisher | Okayama University Medical School |
| Start Page | 139 |
| End Page | 144 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| Content Type | Journal Article |
| language | 英語 |
| File Version | publisher |
| Refereed | True |
| PubMed ID | 8379341 |
| Web of Science KeyUT | A1993LL12400001 |
| JaLCDOI | 10.18926/AMO/32113 |
|---|---|
| FullText URL | fulltext.pdf |
| Author | Ishii, Masamitsu| Tomizawa, Kazuhito| Matsushita, Masayuki| Matsui, Hideki| |
| Abstract | <p>The central nervous system is highly plastic and has been shown to undergo both transient and chronic adaptive changes in response to environmental influences. The purpose of this study was to investigate the effect of hypergravic field on long-term potentiation (LTP) in the mouse hippocampus. Exposure of mice to 4G fields for 48 h had no effect on input-output coupling during extracellular stimulation of Schaffer collaterals and paired pulse facilitation, suggesting that the hypergravic exposure had no detrimental effect on basal neurotransmission in the hippocampus. However, the exposure to 4G fields for 48 h significantly induced LTP compared with the control mouse hippocampus. In contrast, no significant changes of late-phase LTP (L-LTP) were found in the hippocampi of mice exposed to the hypergravic field. Exposure of mice to 4G fields for 48 h enhanced AMPA receptor phosphorylation but not cyclic AMP-responsive element binding protein (CREB) phosphorylation. These results suggest that exposure to hyperdynamic fields influences the synaptic plasticity in the hippocampus.</p> |
| Keywords | long-term potentiation (LTP) AMPA receptor cyclic AMP-responsive element binding protein (CREB) plasticity synapse |
| Amo Type | Article |
| Published Date | 2004-06 |
| Publication Title | Acta Medica Okayama |
| Volume | volume58 |
| Issue | issue3 |
| Publisher | Okayama University Medical School |
| Start Page | 143 |
| End Page | 149 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| Content Type | Journal Article |
| language | 英語 |
| File Version | publisher |
| Refereed | True |
| PubMed ID | 15471436 |
| Web of Science KeyUT | 000222273300005 |
| 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 |
| JaLCDOI | 10.18926/AMO/30708 |
|---|---|
| FullText URL | fulltext.pdf |
| Author | Kuramitsu, Makoto| Matsui, Hideki| Tokuda, Masaaki| Hatase, Osamu| |
| Abstract | <p>Two factors from normal rat liver cytoplasm inhibited the proliferation of cultured L-929 fibroblasts. One was arginase, the other was a small molecular weight inhibitor stable to trypsin and heat treatment. The small molecular weight inhibitor inhibited the protein and DNA synthesis of L-cells. Inhibition of DNA synthesis was thought to be secondary to the inhibition of protein synthesis.</p> |
| Keywords | cell proliferation growth factor inhibiting factor rat liver cytosol L-cells |
| Amo Type | Article |
| Published Date | 1982-02 |
| Publication Title | Acta Medica Okayama |
| Volume | volume36 |
| 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 |
| File Version | publisher |
| Refereed | True |
| PubMed ID | 7064729 |
| Web of Science KeyUT | A1982NE20000001 |
| Author | Kuramitsu, Makoto| Itano, Toshifumi| Matsui, Hideki| Tokuda, Masaaki| Hatase, Osamu| Murakami, Tetsuhide| Nisida, Isamu| Hayashi, Hideo| |
|---|---|
| Published Date | 1979-04-30 |
| Publication Title | 岡山医学会雑誌 |
| Volume | volume91 |
| Issue | issue3-4 |
| Content Type | Journal Article |
| 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 |
| JaLCDOI | 10.18926/AMO/30465 |
|---|---|
| FullText URL | fulltext.pdf |
| Author | Nakamura, Mitsuo| Itano, Toshifumi| Yamaguchi, Fuminori| Mizobuchi, Masayuki| Tokuda, Masaaki| Matsui, Hideki| Etoh, Siji| Hosokawa, Kiyoshi| Ohmoto, Takashi| Hatase, Osamu| |
| Abstract | <p>Peptides and proteins in the extracellular space in the central nervous system were investigated in vivo using an intracerebral microdialysis probe. The molecular cut-off of the hollow fiber which was used for the probe was approximately 100 kDa. We examined recovery rates of several compounds in vitro. The recovery rates of proteins and peptides were between 7-28%, with the exceptions of substance P and insulin-like growth factor I. The recovery rates of monoamines and their metabolites were 22-40%. In in vivo studies, two major proteins with apparent molecular weights of 62 kDa and 12 kDa, and several minor proteins (28 kDa, 43 kDa, 52 kDa and 70 kDa) were detected by SDS-polyacrylamide gel electrophoresis in the dialysate from a probe implanted in the striatum of anesthetized rats. These results suggest that the newly developed, intracerebral microdialysis probe might be useful for investigating the dynamic changes of peptides and proteins in the central nervous system.</p> |
| Keywords | protein peptide microdialysis extracellular space probe |
| Amo Type | Article |
| Published Date | 1990-02 |
| Publication Title | Acta Medica Okayama |
| Volume | volume44 |
| Issue | issue1 |
| Publisher | Okayama University Medical School |
| Start Page | 1 |
| End Page | 8 |
| ISSN | 0386-300X |
| NCID | AA00508441 |
| Content Type | Journal Article |
| language | 英語 |
| File Version | publisher |
| Refereed | True |
| PubMed ID | 2330841 |
| Web of Science KeyUT | A1990CT06800001 |
| 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 |
