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
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
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
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 Sience KeyUT 000287620500001
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 Sience KeyUT 000247574700005
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 Sience KeyUT 000247574700001
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 Sience KeyUT 000247574700003
JaLCDOI 10.18926/AMO/32414
FullText URL fulltext.pdf
Author Matsui, Hideki| Kurosaki, Tomohiro| Tokuda, Masaaki| Hatase, Osamu|
Abstract <p>2-Mercaptoethanol increases the optical density of assay solutions at wavelengths between 280 to 400 nm, and therefore interferes with the measurement of protein concentration by the microbiuret method. Protein concentration can be determined in the presence of 2-mercaptoethanol up to 6 mM by modification of the method as follows: after the precipitation of protein by trichloroacetic acid in the presence of deoxycholate, the precipitate is resolubilized with NaOH solution. Dithiothreitol interfered with the protein determinations could by made in the presence of 4 mM of dithiothreitol with the modified microbiuret method. This modified method is time-saving and more reliable than other methods for protein determination, such as Lowry's method, in the presence of sulfhydryl reagents.</p>
Keywords microbiuret method sulfhydryl reagent protein determination
Amo Type Article
Published Date 1983-04
Publication Title Acta Medica Okayama
Volume volume37
Issue issue2
Publisher Okayama University Medical School
Start Page 125
End Page 129
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 6869062
Web of Sience KeyUT A1983QN63900004
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 Sience KeyUT 000222273300005
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 Sience KeyUT 000223559700002
JaLCDOI 10.18926/AMO/32071
FullText URL fulltext.pdf
Author Takahashi, Fumio| Kuramitsu, Makoto| Tokuda, Masaaki| Matsui, Hideki| Itano, Toshifumi| Murakami, Tetsu-Hide| Hatase, Osamu| Nishida, Isamu|
Abstract <p>Cellular stimulating factors on cell proliferation in the supernatants of chick embryo carcases and adult muscles were studied. There were plural stimulating factors in embryonic and adult muscular supernatants that promoted cell proliferation without any supplement of sera and other materials. Salting-out methods with ammonium sulfate, ethanol fractionation, and isoelectric precipitation were used to isolate the stimulating factors, and these three methods proved the presence of plural stimulants on cell proliferation in the supernatants of chick embryo and adult muscles. The stimulants had altered physico-chemical properties and biological activities due to embryological development. The embryonic stimulants enhanced the synthesis of DNA and protein remarkably, and RNA synthesis in whole cell systems slightly. The muscular stimulants enhanced protein synthesis without any stimulation of DNA and RNA synthesis. Partial purification of the stimulants from the ethanol fractions was performed by DEAE-cellulose chromatography and Sephadex gel chromatography.</p>
Keywords chick growth factors cell proliferation growth regulation DNA and RNA synthesis protein synthesis
Amo Type Article
Published Date 1979-06
Publication Title Acta Medica Okayama
Volume volume33
Issue issue3
Publisher Okayama University Medical School
Start Page 167
End Page 176
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 158945
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 Sience KeyUT 000263730300001
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 Sience KeyUT 000273145900002
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 Sience KeyUT A1993LL12400001
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 Sience KeyUT 000253549500004
JaLCDOI 10.18926/AMO/30810
FullText URL fulltext.pdf
Author Ezawa, Kazuhiko| Yamamura, Masahiro| Matsui, Hideki| Ota, Zensuke| Makino, Hirofumi|
Abstract <p>&#8195;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 Sience KeyUT A1997WL24600005
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 Sience KeyUT 000237001900001
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 Sience KeyUT A1982NE20000001
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 Sience KeyUT A1990CT06800001
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