start-ver=1.4 cd-journal=joma no-vol=330 cd-vols= no-issue= article-no= start-page=788 end-page=196 dt-received= dt-revised= dt-accepted= dt-pub-year=2020 dt-pub=20201111 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Self-assembling A6K peptide nanotubes as a mercaptoundecahydrododecaborate (BSH) delivery system for boron neutron capture t (BNCT) en-subtitle= kn-subtitle= en-abstract= kn-abstract=Boron neutron capture therapy (BNCT) is a tumor selective therapy, the effectiveness of which depends on sufficient 10B delivery to and accumulation in tumors. In this study, we used self-assembling A6K peptide nanotubes as boron carriers and prepared new boron agents by simple mixing of A6K and BSH. BSH has been used to treat malignant glioma patients in clinical trials and its drug safety and availability have been confirmed; however, its contribution to BNCT efficacy is low. A6K nanotube delivery improved two major limitations of BSH, including absence of intracellular transduction and non-specific drug delivery to tumor tissue. Varying the A6K peptide and BSH mixture ratio produced materials with different morphologies?determined by electron microscopy?and intracellular transduction efficiencies. We investigated the A6K/BSH 1:10 mixture ratio and found high intracellular boron uptake with no toxicity. Microscopy observation showed intracellular localization of A6K/BSH in the perinuclear region and endosome in human glioma cells. The intracellular boron concentration using A6K/BSH was almost 10 times higher than that of BSH. The systematic administration of A6K/BSH via mouse tail vein showed tumor specific accumulation in a mouse brain tumor model with immunohistochemistry and pharmacokinetic study. Neutron irradiation of glioma cells treated with A6K/BSH showed the inhibition of cell proliferation in a colony formation assay. Boron delivery using A6K peptide provides a unique and simple strategy for next generation BNCT drugs. en-copyright= kn-copyright= en-aut-name=MichiueHiroyuki en-aut-sei=Michiue en-aut-mei=Hiroyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=KitamatsuMizuki en-aut-sei=Kitamatsu en-aut-mei=Mizuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=FukunagaAsami en-aut-sei=Fukunaga en-aut-mei=Asami kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TsuboiNobushige en-aut-sei=Tsuboi en-aut-mei=Nobushige kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=FujimuraAtsushi en-aut-sei=Fujimura en-aut-mei=Atsushi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=MatsushitaHiroaki en-aut-sei=Matsushita en-aut-mei=Hiroaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=IgawaKazuyo en-aut-sei=Igawa en-aut-mei=Kazuyo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=KasaiTomonari en-aut-sei=Kasai en-aut-mei=Tomonari kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=KondoNatsuko en-aut-sei=Kondo en-aut-mei=Natsuko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=MatsuiHideki en-aut-sei=Matsui en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= en-aut-name=FuruyaShuichi en-aut-sei=Furuya en-aut-mei=Shuichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 ORCID= affil-num=1 en-affil=Neutron Therapy Research Center, Okayama University kn-affil= affil-num=2 en-affil=Department of Applied Chemistry, Kindai University kn-affil= affil-num=3 en-affil=Department of Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=4 en-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences kn-affil= affil-num=5 en-affil=Department of Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=6 en-affil=Department of Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences kn-affil= affil-num=7 en-affil=Neutron Therapy Research Center, Okayama University kn-affil= affil-num=8 en-affil=Neutron Therapy Research Center, Okayama University kn-affil= affil-num=9 en-affil=Institute for Integrated Radiation and Nuclear Science, Kyoto University kn-affil= affil-num=10 en-affil=Neutron Therapy Research Center, Okayama University kn-affil= affil-num=11 en-affil=Neutron Therapy Research Center, Okayama University kn-affil= en-keyword=Malignant brain tumor kn-keyword=Malignant brain tumor en-keyword=Boron neutron capture therapy (BNCT) kn-keyword=Boron neutron capture therapy (BNCT) en-keyword=Peptide nanotube kn-keyword=Peptide nanotube en-keyword=Boron drug kn-keyword=Boron drug en-keyword=Drug delivery system (DDS) kn-keyword=Drug delivery system (DDS) en-keyword=A6K peptide kn-keyword=A6K peptide END start-ver=1.4 cd-journal=joma no-vol=49 cd-vols= no-issue=3 article-no= start-page=521 end-page=526 dt-received= dt-revised= dt-accepted= dt-pub-year=2007 dt-pub=20071121 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Rasmussen encephalitis associated with SCN1A mutation en-subtitle= kn-subtitle= en-abstract= kn-abstract= Mutations in the SCN 1 A gene, encoding the neuronal voltage-gated sodium channel alpha1 subunit, cause SMEI, GEFS+, and related epileptic syndromes. We herein report the R1575C-SCN 1 A mutation identified in a patient with Rasmussen encephalitis. R1575C were constructed in a recombinant human SCN 1 A and then heterologously expressed in HEK293 cells along with the human beta1 and beta2 sodium channel accessory subunits. Whole-cell patch-clamp recording was used to define biophysical properties. The R1575C channels exhibited increased channel availability and an increased persistent sodium current in comparison to the wild-type. These defects of electrophysiological properties can result in neuronal hyperexitability. The seizure susceptibility allele may influence the pathogenesis of Rasmussen encephalitis in this case. en-copyright= kn-copyright= en-aut-name=OhmoriIori en-aut-sei=Ohmori en-aut-mei=Iori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=OuchidaMamoru en-aut-sei=Ouchida en-aut-mei=Mamoru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KobayashiKatsuhiro en-aut-sei=Kobayashi en-aut-mei=Katsuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=JitsumoriYoshimi en-aut-sei=Jitsumori en-aut-mei=Yoshimi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=InoueTakushi en-aut-sei=Inoue en-aut-mei=Takushi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=ShimizuKenji en-aut-sei=Shimizu en-aut-mei=Kenji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=MatsuiHideki en-aut-sei=Matsui en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=OhtsukaYoko en-aut-sei=Ohtsuka en-aut-mei=Yoko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=MaegakiYoshihiro en-aut-sei=Maegaki en-aut-mei=Yoshihiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= affil-num=1 en-affil=Departments of Cellular Physiology, Graduate School of Medicine,Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=2 en-affil=Departments of Molecular Genetics, Graduate School of Medicine,Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=3 en-affil=Departments of Child Neurology, Graduate School of Medicine,Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=4 en-affil= kn-affil= affil-num=5 en-affil=Departments of Child Neurology, Graduate School of Medicine,Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=6 en-affil=Departments of Molecular Genetics, Graduate School of Medicine,Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=7 en-affil=Departments of Cellular Physiology, Graduate School of Medicine,Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=8 en-affil=Departments of Child Neurology, Graduate School of Medicine,Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=9 en-affil=Division of Child Neurology, Institute of Neurological Sciences, Faculty of Medicine, Tottori University kn-affil= en-keyword=Rasmussen encephalitis kn-keyword=Rasmussen encephalitis en-keyword=SCN1A kn-keyword=SCN1A en-keyword=genetic-environmental interaction kn-keyword=genetic-environmental interaction END start-ver=1.4 cd-journal=joma no-vol=105 cd-vols= no-issue=1-2 article-no= start-page=220 end-page=224 dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=201307 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Inhalation of 10% carbon dioxide rapidly terminates Scn1a mutation-related hyperthermia-induced seizures en-subtitle= kn-subtitle= en-abstract= kn-abstract= The aim of this study was to assess the anticonvulsant effect of carbon dioxide (CO2) on Scn1a mutation-related febrile seizures. We examined physiological changes in the blood gas levels after the induction of hyperthermia-induced seizures (HISs), which were associated with the Scn1a missense mutation. We determined the efficacy of inhalation of 5% or 10% CO2 to treat HISs. HISs were evoked in Scn1a mutant and wild-type (WT) rats by hot water baths. To determine the anticonvulsant effect of CO2 inhalation, rats were placed in a chamber filled with air or mixed gas containing 5% CO2 or 10% CO2 for 3 min, immediately after the induction of HISs. We also analyzed the blood gas levels at the end of inhalation of CO2. Hot water bathing induced a significant reduction in the partial pressure of CO2 (pCO2) and respiratory alkalosis in the WT and Scn1a mutant rats. HISs were evoked in 100% of the Scn1a mutant rats within 5 min, but in none of the WT rats. The Scn1a mutant rats demonstrated a higher HISs susceptibility associated with respiratory alkalosis than the WT rats. Inhalation of 10% CO2 shortened the seizure duration from 62.6±12.1 s to 15.5±1.0 s. Blood gas analysis after the inhalation of 10% CO2 demonstrated an elevated pCO2 level and respiratory acidosis. Inhalation of 10% CO2 demonstrated a potent and fast-acting anticonvulsant effect against HISs. en-copyright= kn-copyright= en-aut-name=OhmoriIori en-aut-sei=Ohmori en-aut-mei=Iori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=HayashiKeiichiro en-aut-sei=Hayashi en-aut-mei=Keiichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=WangHaijiao en-aut-sei=Wang en-aut-mei=Haijiao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=OuchidaMamoru en-aut-sei=Ouchida en-aut-mei=Mamoru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=FujitaNaohiro en-aut-sei=Fujita en-aut-mei=Naohiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=InoueTakushi en-aut-sei=Inoue en-aut-mei=Takushi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=MichiueHiroyuki en-aut-sei=Michiue en-aut-mei=Hiroyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=NishikiTeiichi en-aut-sei=Nishiki en-aut-mei=Teiichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=MatsuiHideki en-aut-sei=Matsui en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= affil-num=1 en-affil=Department of Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=2 en-affil=Department of Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=3 en-affil=Department of Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=4 en-affil=Department of Molecular Genetics, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=5 en-affil=Department of Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=6 en-affil=Department of Child Neurology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=7 en-affil=Department of Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=8 en-affil=Department of Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=9 en-affil=Department of Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= END start-ver=1.4 cd-journal=joma no-vol=50 cd-vols= no-issue= article-no= start-page=209 end-page=217 dt-received= dt-revised= dt-accepted= dt-pub-year=2013 dt-pub=201302 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=CACNA1A variants may modify the epileptic phenotype of Dravet syndrome en-subtitle= kn-subtitle= en-abstract= kn-abstract= Dravet syndrome is an intractable epileptic syndrome beginning in the first year of life. De novo mutations of SCN1A, which encode the Na(v)1.1 neuronal voltage-gated sodium channel, are considered the major cause of Dravet syndrome. In this study, we investigated genetic modifiers of this syndrome. We performed a mutational analysis of all coding exons of CACNA1A in 48 subjects with Dravet syndrome. To assess the effects of CACNA1A variants on the epileptic phenotypes of Dravet syndrome, we compared clinical features in two genotype groups: 1) subjects harboring SCN1A mutations but no CACNA1A variants (n=20) and 2) subjects with SCN1A mutations plus CACNA1A variants (n=20). CACNA1A variants detected in patients were studied using heterologous expression of recombinant human Ca(v)2.1 in HEK 293 cells and whole-cell patch-clamp recording. Nine CACNA1A variants, including six novel ones, were detected in 21 of the 48 subjects (43.8%). Based on the incidence of variants in healthy controls, most of the variants seemed to be common polymorphisms. However, the subjects harboring SCN1A mutations and CACNA1A variants had absence seizures more frequently than the patients with only SCN1A mutations (8/20 vs. 0/20, p=0.002). Moreover, the former group of subjects exhibited earlier onset of seizures and more frequent prolonged seizures before one year of age, compared to the latter group of subjects. The electrophysiological properties of four of the five novel Ca(v)2.1 variants exhibited biophysical changes consistent with gain-of-function. We conclude that CACNA1A variants in some persons with Dravet syndrome may modify the epileptic phenotypes. en-copyright= kn-copyright= en-aut-name=OhmoriIori en-aut-sei=Ohmori en-aut-mei=Iori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=OuchidaMamoru en-aut-sei=Ouchida en-aut-mei=Mamoru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=KobayashiKatsuhiro en-aut-sei=Kobayashi en-aut-mei=Katsuhiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=JitsumoriYoshimi en-aut-sei=Jitsumori en-aut-mei=Yoshimi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=MoriAkiko en-aut-sei=Mori en-aut-mei=Akiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=MichiueHiroyuki en-aut-sei=Michiue en-aut-mei=Hiroyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=NishikiTeiichi en-aut-sei=Nishiki en-aut-mei=Teiichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=OhtsukaYoko en-aut-sei=Ohtsuka en-aut-mei=Yoko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=MatsuiHideki en-aut-sei=Matsui en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= affil-num=1 en-affil=Department of Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=2 en-affil=Department of Molecular Genetics, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=3 en-affil= kn-affil= affil-num=4 en-affil= kn-affil= affil-num=5 en-affil=Department of Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=6 en-affil=Department of Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=7 en-affil=Department of Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=8 en-affil= kn-affil= affil-num=9 en-affil=Department of Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= END start-ver=1.4 cd-journal=joma no-vol=52 cd-vols= no-issue=5 article-no= start-page=1010 end-page=1017 dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=201105 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Therapy for hyperthermia-induced seizures in Scn1a mutant rats en-subtitle= kn-subtitle= en-abstract= kn-abstract=Purpose: Mutations in the SCN1A gene, which encodes the alpha 1 subunit of voltage-gated sodium channels, cause generalized epilepsy with febrile seizures plus (GEFS+) and severe myoclonic epilepsy of infancy (SMEI). N1417H-Scn1a mutant rats are considered to be an animal model of human FS+ or GEFS+. To assess the pharmacologic validity of this model, we compared the efficacies of eight different antiepileptic drugs (AEDs) for the treatment of hyperthermia-induced seizures using N1417H-Scn1a mutant rats. Methods: AEDs used in this study included valproate, carbamazepine (CBZ), phenobarbital, gabapentin, acetazolamide, diazepam (DZP), topiramate, and potassium bromide (KBr). The effects of these AEDs were evaluated using the hot water model, which is a model of experimental FS. Five-week-old rats were pretreated with each AED and immersed in water at 45 degrees C to induce hyperthermia-induced seizures. The seizure manifestations and video-electroencephalographic recordings were evaluated. Furthermore, the effects of each AED on motor coordination and balance were assessed using the balance-beam test. Key Findings: KBr significantly reduced seizure durations, and its anticonvulsant effects were comparable to those of DZP. On the other hand, CBZ decreased the seizure threshold. In addition, DZP and not KBr showed significant impairment in motor coordination and balance. Significance: DZP and KBr showed potent inhibitory effects against hyperthermia-induced seizures in the Scn1a mutant rats, whereas CBZ exhibited adverse effects. These responses to hyperthermia-induced seizures were similar to those in patients with GEFS+ and SMEI. N1417H-Scn1a mutant rats may, therefore, be useful for testing the efficacy of new AEDs against FS in GEFS+ and SMEI patients. en-copyright= kn-copyright= en-aut-name=HayashiKeiichiro en-aut-sei=Hayashi en-aut-mei=Keiichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=UeshimaSatoshi en-aut-sei=Ueshima en-aut-mei=Satoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=OuchidaMamoru en-aut-sei=Ouchida en-aut-mei=Mamoru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=MashimoTomoji en-aut-sei=Mashimo en-aut-mei=Tomoji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=NishikiTeiichi en-aut-sei=Nishiki en-aut-mei=Teiichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=SendoToshiaki en-aut-sei=Sendo en-aut-mei=Toshiaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=SerikawaTadao en-aut-sei=Serikawa en-aut-mei=Tadao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=MatsuiHideki en-aut-sei=Matsui en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=OhmoriIori en-aut-sei=Ohmori en-aut-mei=Iori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Physiol affil-num=2 en-affil= kn-affil=Okayama Univ Hosp, Dept Pharm affil-num=3 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Mol Genet affil-num=4 en-affil= kn-affil=Kyoto Univ, Grad Sch Med, Inst Lab Anim affil-num=5 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Physiol affil-num=6 en-affil= kn-affil=Okayama Univ Hosp, Dept Pharm affil-num=7 en-affil= kn-affil=Kyoto Univ, Grad Sch Med, Inst Lab Anim affil-num=8 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Physiol affil-num=9 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Physiol en-keyword=Febrile seizure kn-keyword=Febrile seizure en-keyword=Animal models kn-keyword=Animal models en-keyword=Scn1a gene kn-keyword=Scn1a gene en-keyword=Generalized epilepsy with febrile seizures plus kn-keyword=Generalized epilepsy with febrile seizures plus en-keyword=Severe myoclonic epilepsy of infancy kn-keyword=Severe myoclonic epilepsy of infancy END start-ver=1.4 cd-journal=joma no-vol=49 cd-vols= no-issue=1 article-no= start-page=1 end-page=8 dt-received= dt-revised= dt-accepted= dt-pub-year=2012 dt-pub=201201 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Ca2+-independent syntaxin binding to the C2B effector region of synaptotagmin en-subtitle= kn-subtitle= en-abstract= kn-abstract=Although synaptotagmin I, which is a calcium (Ca2+)-binding synaptic vesicle protein, may trigger soluble N-ethylmaleimide-sensitive factor attachment protein receptor (SNARE)-mediated synaptic vesicle exocytosis, the mechanisms underlying the interaction between these proteins remain controversial, especially with respect to the identity of the protein(s) in the SNARE complex that bind(s) to synaptotagmin and whether Ca2+ is required for their highly effective binding. To address these questions, native proteins were solubilized, immunoprecipitated from rat brain extracts, and analyzed by immunoblotting. SNARE complexes comprising syntaxin 1, 25-kDa synaptosomal-associated protein (SNAP-25), and synaptobrevin 2 were coprecipitzted with synaptotagmin I in the presence of ethylene glycol tetraacetic acid. The amount of cop recipitated proteins was significantly unaltered by the addition of Ca2+ to the brain extract. To identify the component of the SNARE complex that bound to synaptotagmin, SNARE was coexpressed with synaptotagmin in HEK293 cells and immunoprecipitated. Syntaxin, but not SNAP-25 and synaptobrevin, bound to synaptotagmin in a Ca2+-independent manner, and the binding was abolished in the presence of 1 M NaCl. Synaptotagmin contains 2 Ca2+-binding domains (C(2)A, C2B). Mutating the positively charged lysine residues in the putative effector-binding region of the C2B domain, which are critical for transmitter release, markedly inhibited synaptotagmin-syntaxin binding, while similar mutations in the C(2)A domain had no effect on binding. Synaptotagmin-syntaxin binding was reduced by mutating multiple negatively charged glutamate residues in the amino-terminal half of the syntaxin SNARE motif. These results indicate that synaptotagmin I binds to syntaxin 1 electrostatically through its C2B domain effector region in a Ca2+-independent fashion, providing biochemical evidence that synaptotagmin I binds SNARE complexes before Ca2+ influx into presynaptic nerve terminals. en-copyright= kn-copyright= en-aut-name=MasumotoToshio en-aut-sei=Masumoto en-aut-mei=Toshio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=SuzukiKoichiro en-aut-sei=Suzuki en-aut-mei=Koichiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=OhmoriIori en-aut-sei=Ohmori en-aut-mei=Iori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=MichiueHiroyuki en-aut-sei=Michiue en-aut-mei=Hiroyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TomizawaKazuhito en-aut-sei=Tomizawa en-aut-mei=Kazuhito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=FujimuraAtsushi en-aut-sei=Fujimura en-aut-mei=Atsushi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=NishikiTei-ichi en-aut-sei=Nishiki en-aut-mei=Tei-ichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=MatsuiHideki en-aut-sei=Matsui en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Physiol affil-num=2 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Physiol affil-num=3 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Physiol affil-num=4 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Physiol affil-num=5 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Physiol affil-num=6 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Physiol affil-num=7 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Physiol affil-num=8 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Physiol en-keyword=Neurotransmitter release kn-keyword=Neurotransmitter release en-keyword=Synaptic vesicle kn-keyword=Synaptic vesicle en-keyword=Exocytosis kn-keyword=Exocytosis en-keyword=SNAP-25 kn-keyword=SNAP-25 en-keyword=Synaptobrevin kn-keyword=Synaptobrevin END start-ver=1.4 cd-journal=joma no-vol=126 cd-vols= no-issue=1 article-no= start-page=73 end-page=74 dt-received= dt-revised= dt-accepted= dt-pub-year=2014 dt-pub=20140401 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=The 10th Congress on Neutron Capture Therapy kn-title=第10回日本中性子捕捉療法学会学術大会報告 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=MatsuiHideki en-aut-sei=Matsui en-aut-mei=Hideki kn-aut-name=松井秀樹 kn-aut-sei=松井 kn-aut-mei=秀樹 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　細胞生理学 END start-ver=1.4 cd-journal=joma no-vol=6 cd-vols= no-issue=3 article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=20110514 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Expression of a Constitutively Active Calcineurin Encoded by an Intron-Retaining mRNA in Follicular Keratinocytes en-subtitle= kn-subtitle= en-abstract= kn-abstract=Hair growth is a highly regulated cyclical process. Immunosuppressive immunophilin ligands such as cyclosporin A (CsA) and FK506 are known as potent hair growth modulatory agents in rodents and humans that induce active hair growth and inhibit hair follicle regression. The immunosuppressive effectiveness of these drugs has been generally attributed to inhibition of T cell activation through well-characterized pathways. Specifically, CsA and FK506 bind to intracellular proteins, principally cyclophilin A and FKBP12, respectively, and thereby inhibit the phosphatase calcineurin (Cn). The calcineurin (Cn)/NFAT pathway has an important, but poorly understood, role in the regulation of hair follicle development. Here we show that a novel-splicing variant of calcineurin A beta CnA beta-FK, which is encoded by an intron-retaining mRNA and is deficient in the autoinhibitory domain, is predominantly expressed in mature follicular keratinocytes but not in the proliferating keratinocytes of rodents. CnA beta-FK was weakly sensitive to Ca(2+) and dephosphorylated NFATc2 under low Ca(2+) levels in keratinocytes. Inhibition of Cn/NFAT induced hair growth in nude mice. Cyclin G2 was identified as a novel target of the Cn/NFATc2 pathway and its expression in follicular keratinocytes was reduced by inhibition of Cn/NFAT. Overexpression of cyclin G2 arrested the cell cycle in follicular keratinocytes in vitro and the Cn inhibitor, cyclosporin A, inhibited nuclear localization of NFATc2, resulting in decreased cyclin G2 expression in follicular keratinocytes of rats in vivo. We therefore suggest that the calcineurin/NFAT pathway has a unique regulatory role in hair follicle development. en-copyright= kn-copyright= en-aut-name=FujimuraAtsushi en-aut-sei=Fujimura en-aut-mei=Atsushi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MichiueHiroyuki en-aut-sei=Michiue en-aut-mei=Hiroyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=NishikiTei-ichi en-aut-sei=Nishiki en-aut-mei=Tei-ichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=OhmoriIori en-aut-sei=Ohmori en-aut-mei=Iori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=WeiFanyan en-aut-sei=Wei en-aut-mei=Fanyan kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=MatsuiHideki en-aut-sei=Matsui en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=TomizawaKazuhito en-aut-sei=Tomizawa en-aut-mei=Kazuhito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=Okayama Univ, Dept Physiol, Grad Sch Med Dent & Pharmaceut Sci affil-num=2 en-affil= kn-affil=Okayama Univ, Dept Physiol, Grad Sch Med Dent & Pharmaceut Sci affil-num=3 en-affil= kn-affil=Okayama Univ, Dept Physiol, Grad Sch Med Dent & Pharmaceut Sci affil-num=4 en-affil= kn-affil=Okayama Univ, Dept Physiol, Grad Sch Med Dent & Pharmaceut Sci affil-num=5 en-affil= kn-affil=Kumamoto Univ, Dept Mol Physiol, Fac Life Sci affil-num=6 en-affil= kn-affil=Okayama Univ, Dept Physiol, Grad Sch Med Dent & Pharmaceut Sci affil-num=7 en-affil= kn-affil=Kumamoto Univ, Dept Mol Physiol, Fac Life Sci END start-ver=1.4 cd-journal=joma no-vol=65 cd-vols= no-issue=1 article-no= start-page=1 end-page=10 dt-received= dt-revised= dt-accepted= dt-pub-year=2011 dt-pub=201102 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Regulation of Mitochondrial Dynamics and Neurodegenerative Diseases en-subtitle= kn-subtitle= en-abstract= kn-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. en-copyright= kn-copyright= en-aut-name=HanXiao-Jian en-aut-sei=Han en-aut-mei=Xiao-Jian kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TomizawaKazuhito en-aut-sei=Tomizawa en-aut-mei=Kazuhito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=FujimuraAtsushi en-aut-sei=Fujimura en-aut-mei=Atsushi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=OhmoriIori en-aut-sei=Ohmori en-aut-mei=Iori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=NishikiTei-ichi en-aut-sei=Nishiki en-aut-mei=Tei-ichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=MatsushitaMasayuki en-aut-sei=Matsushita en-aut-mei=Masayuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=MatsuiHideki en-aut-sei=Matsui en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=Department of Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Department of Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=6 en-affil= kn-affil=Department of Molecular and Cellular Physiology, School of Medicine, University of the Ryukyus affil-num=7 en-affil= kn-affil=Department of Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=mitochondria kn-keyword=mitochondria en-keyword=phosphorylation kn-keyword=phosphorylation en-keyword=ubiquitination kn-keyword=ubiquitination en-keyword=SUMOylation kn-keyword=SUMOylation en-keyword=neurodegeneration kn-keyword=neurodegeneration END start-ver=1.4 cd-journal=joma no-vol=61 cd-vols= no-issue=3 article-no= start-page=161 end-page=166 dt-received= dt-revised= dt-accepted= dt-pub-year=2007 dt-pub=200706 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Colocalization of oxytocin and phosphorylated form of elongation factor 2 in the rat hypothalamus en-subtitle= kn-subtitle= en-abstract= kn-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. en-copyright= kn-copyright= en-aut-name=FujisawaToru en-aut-sei=Fujisawa en-aut-mei=Toru kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MoriwakiAkiyoshi en-aut-sei=Moriwaki en-aut-mei=Akiyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=MatsushitaMasayuki en-aut-sei=Matsushita en-aut-mei=Masayuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TomizawaKazuhito en-aut-sei=Tomizawa en-aut-mei=Kazuhito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=MatsuiHideki en-aut-sei=Matsui en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University affil-num=5 en-affil= kn-affil=Okayama University en-keyword=oxytocin kn-keyword=oxytocin en-keyword=PVN kn-keyword=PVN en-keyword=SON kn-keyword=SON en-keyword=elongation factor 2 kn-keyword=elongation factor 2 en-keyword=local translation kn-keyword=local translation END start-ver=1.4 cd-journal=joma no-vol=61 cd-vols= no-issue=3 article-no= start-page=123 end-page=137 dt-received= dt-revised= dt-accepted= dt-pub-year=2007 dt-pub=200706 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Calpain-calcineurin signaling in the pathogenesis of calcium-dependent disorder. en-subtitle= kn-subtitle= en-abstract= kn-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. en-copyright= kn-copyright= en-aut-name=WuHai-Yan en-aut-sei=Wu en-aut-mei=Hai-Yan kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TomizawaKazuhito en-aut-sei=Tomizawa en-aut-mei=Kazuhito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=MatsuiHideki en-aut-sei=Matsui en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University en-keyword=calpain kn-keyword=calpain en-keyword=calcineurin kn-keyword=calcineurin en-keyword=calcium kn-keyword=calcium en-keyword=proteolysis kn-keyword=proteolysis en-keyword=neurodegeneration kn-keyword=neurodegeneration END start-ver=1.4 cd-journal=joma no-vol=61 cd-vols= no-issue=3 article-no= start-page=147 end-page=152 dt-received= dt-revised= dt-accepted= dt-pub-year=2007 dt-pub=200706 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Inhibitory effect of polyunsaturated fatty acids on apoptosis induced by etoposide, okadaic acid and AraC in Neuro2a cells en-subtitle= kn-subtitle= en-abstract= kn-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. en-copyright= kn-copyright= en-aut-name=WuYumei en-aut-sei=Wu en-aut-mei=Yumei kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TadaMikiro en-aut-sei=Tada en-aut-mei=Mikiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TakahataKyoya en-aut-sei=Takahata en-aut-mei=Kyoya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TomizawaKazuhito en-aut-sei=Tomizawa en-aut-mei=Kazuhito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=MatsuiHideki en-aut-sei=Matsui en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University affil-num=5 en-affil= kn-affil=Okayama University en-keyword=polyunsaturated fatty acid (PUFA) kn-keyword=polyunsaturated fatty acid (PUFA) en-keyword=neurodegenerative disease kn-keyword=neurodegenerative disease en-keyword=caspase kn-keyword=caspase en-keyword=neuronal apoptosis kn-keyword=neuronal apoptosis en-keyword=DHA kn-keyword=DHA END start-ver=1.4 cd-journal=joma no-vol=37 cd-vols= no-issue=2 article-no= start-page=125 end-page=129 dt-received= dt-revised= dt-accepted= dt-pub-year=1983 dt-pub=198304 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Modulation of optical density by sulfhydryl reagents in microbiuret method: a modified method for protein determination in the presence of sulfhydryl reagents. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

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.

en-copyright= kn-copyright= en-aut-name=MatsuiHideki en-aut-sei=Matsui en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=KurosakiTomohiro en-aut-sei=Kurosaki en-aut-mei=Tomohiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TokudaMasaaki en-aut-sei=Tokuda en-aut-mei=Masaaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=HataseOsamu en-aut-sei=Hatase en-aut-mei=Osamu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= affil-num=1 en-affil= kn-affil=Kagawa Medical School affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Kagawa Medical School en-keyword=microbiuret method kn-keyword=microbiuret method en-keyword=sulfhydryl reagent kn-keyword=sulfhydryl reagent en-keyword=protein determination kn-keyword=protein determination END start-ver=1.4 cd-journal=joma no-vol=58 cd-vols= no-issue=3 article-no= start-page=143 end-page=149 dt-received= dt-revised= dt-accepted= dt-pub-year=2004 dt-pub=200406 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Exposure of mouse to high gravitation forces induces long-term potentiation in the hippocampus. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

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.

en-copyright= kn-copyright= en-aut-name=IshiiMasamitsu en-aut-sei=Ishii en-aut-mei=Masamitsu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TomizawaKazuhito en-aut-sei=Tomizawa en-aut-mei=Kazuhito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=MatsushitaMasayuki en-aut-sei=Matsushita en-aut-mei=Masayuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=MatsuiHideki en-aut-sei=Matsui en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University en-keyword=long-term potentiation (LTP) kn-keyword=long-term potentiation (LTP) en-keyword=AMPA receptor kn-keyword=AMPA receptor en-keyword= cyclic AMP-responsive element binding protein (CREB) kn-keyword= cyclic AMP-responsive element binding protein (CREB) en-keyword=plasticity kn-keyword=plasticity en-keyword=synapse kn-keyword=synapse END start-ver=1.4 cd-journal=joma no-vol=58 cd-vols= no-issue=4 article-no= start-page=181 end-page=187 dt-received= dt-revised= dt-accepted= dt-pub-year=2004 dt-pub=200408 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=2-methoxyestradiol enhances p53 protein transduction therapy-associated inhibition of the proliferation of oral cancer cells through the suppression of NFkappaB activity. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

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.

en-copyright= kn-copyright= en-aut-name=TakataHidehiko en-aut-sei=Takata en-aut-mei=Hidehiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=TomizawaKazuhito en-aut-sei=Tomizawa en-aut-mei=Kazuhito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=MatsushitaMasayuki en-aut-sei=Matsushita en-aut-mei=Masayuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=MatsuiHideki en-aut-sei=Matsui en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University en-keyword=tumor kn-keyword=tumor en-keyword=TAT kn-keyword=TAT en-keyword=poly arginine kn-keyword=poly arginine en-keyword=gene therapy kn-keyword=gene therapy en-keyword=protein therapy kn-keyword=protein therapy END start-ver=1.4 cd-journal=joma no-vol=33 cd-vols= no-issue=3 article-no= start-page=167 end-page=176 dt-received= dt-revised= dt-accepted= dt-pub-year=1979 dt-pub=197906 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Partial purification and biological activities and properties of chick growth factors. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

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.

en-copyright= kn-copyright= en-aut-name=TakahashiFumio en-aut-sei=Takahashi en-aut-mei=Fumio kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=KuramitsuMakoto en-aut-sei=Kuramitsu en-aut-mei=Makoto kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TokudaMasaaki en-aut-sei=Tokuda en-aut-mei=Masaaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=MatsuiHideki en-aut-sei=Matsui en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=ItanoToshifumi en-aut-sei=Itano en-aut-mei=Toshifumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=MurakamiTetsu-Hide en-aut-sei=Murakami en-aut-mei=Tetsu-Hide kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=HataseOsamu en-aut-sei=Hatase en-aut-mei=Osamu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=NishidaIsamu en-aut-sei=Nishida en-aut-mei=Isamu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University affil-num=5 en-affil= kn-affil=Okayama University affil-num=6 en-affil= kn-affil=Okayama University affil-num=7 en-affil= kn-affil=Okayama University affil-num=8 en-affil= kn-affil=Okayama University en-keyword=chick growth factors kn-keyword=chick growth factors en-keyword=cell proliferation kn-keyword=cell proliferation en-keyword=growth regulation kn-keyword=growth regulation en-keyword=DNA and RNA synthesis kn-keyword=DNA and RNA synthesis en-keyword=protein synthesis kn-keyword=protein synthesis END start-ver=1.4 cd-journal=joma no-vol=63 cd-vols= no-issue=1 article-no= start-page=1 end-page=7 dt-received= dt-revised= dt-accepted= dt-pub-year=2009 dt-pub=200902 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Protein Transduction Method for Cerebrovascular Disorders en-subtitle= kn-subtitle= en-abstract= kn-abstract=

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 "11R", 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).

en-copyright= kn-copyright= en-aut-name=OgawaTomoyuki en-aut-sei=Ogawa en-aut-mei=Tomoyuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=OnoShigeki en-aut-sei=Ono en-aut-mei=Shigeki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=IchikawaTomotsugu en-aut-sei=Ichikawa en-aut-mei=Tomotsugu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=ArimitsuSeiji en-aut-sei=Arimitsu en-aut-mei=Seiji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=OnodaKeisuke en-aut-sei=Onoda en-aut-mei=Keisuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=TokunagaKoji en-aut-sei=Tokunaga en-aut-mei=Koji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=SugiuKenji en-aut-sei=Sugiu en-aut-mei=Kenji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=TomizawaKazuhito en-aut-sei=Tomizawa en-aut-mei=Kazuhito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=MatsuiHideki en-aut-sei=Matsui en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=DateIsao en-aut-sei=Date en-aut-mei=Isao kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= affil-num=1 en-affil= kn-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=4 en-affil= kn-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=5 en-affil= kn-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=6 en-affil= kn-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=7 en-affil= kn-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=8 en-affil= kn-affil=Department of Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=9 en-affil= kn-affil=Department of Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=10 en-affil= kn-affil=Department of Neurological Surgery, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences en-keyword=cerebral vasospasm kn-keyword=cerebral vasospasm en-keyword=11 consecutive arginines (11R) kn-keyword=11 consecutive arginines (11R) en-keyword=enhanced green fluorescent protein (EGFP) kn-keyword=enhanced green fluorescent protein (EGFP) END start-ver=1.4 cd-journal=joma no-vol=63 cd-vols= no-issue=6 article-no= start-page=305 end-page=323 dt-received= dt-revised= dt-accepted= dt-pub-year=2009 dt-pub=200912 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Amphiphysin I and regulation of synaptic vesicle endocytosis en-subtitle= kn-subtitle= en-abstract= kn-abstract=

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.

en-copyright= kn-copyright= en-aut-name=WuYumei en-aut-sei=Wu en-aut-mei=Yumei kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MatsuiHideki en-aut-sei=Matsui en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TomizawaKazuhito en-aut-sei=Tomizawa en-aut-mei=Kazuhito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= affil-num=1 en-affil= kn-affil=Department of Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=2 en-affil= kn-affil=Department of Physiology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences affil-num=3 en-affil= kn-affil=Department of Molecular Physiology, Faculty of Medical and Pharmaceutical Sciences, Kumamoto University en-keyword=amphiphysin I kn-keyword=amphiphysin I en-keyword=calpain kn-keyword=calpain en-keyword=SVE kn-keyword=SVE en-keyword=hyperexcitation kn-keyword=hyperexcitation en-keyword=seizure kn-keyword=seizure END start-ver=1.4 cd-journal=joma no-vol=47 cd-vols= no-issue=3 article-no= start-page=139 end-page=144 dt-received= dt-revised= dt-accepted= dt-pub-year=1993 dt-pub=199306 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Exogenous Basic Fibroblast Growth Factor and Nerve Growth Factor Enhance Sprouting of Acetylcholinesterase Positive Fibers in Denervated Rat Hippocampus en-subtitle= kn-subtitle= en-abstract= kn-abstract=

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.

en-copyright= kn-copyright= en-aut-name=MiyamotoOsamu en-aut-sei=Miyamoto en-aut-mei=Osamu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=ItanoToshifumi en-aut-sei=Itano en-aut-mei=Toshifumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=FujisawaMutsuo en-aut-sei=Fujisawa en-aut-mei=Mutsuo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=TokudaMasaaki en-aut-sei=Tokuda en-aut-mei=Masaaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=MatsuiHideki en-aut-sei=Matsui en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=NagaoSeigo en-aut-sei=Nagao en-aut-mei=Seigo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=HataseOsamu en-aut-sei=Hatase en-aut-mei=Osamu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=Kagawa Medical School affil-num=2 en-affil= kn-affil=Kagawa Medical School affil-num=3 en-affil= kn-affil=Kagawa Medical School affil-num=4 en-affil= kn-affil=Kagawa Medical School affil-num=5 en-affil= kn-affil=Kagawa Medical School affil-num=6 en-affil= kn-affil=Kagawa Medical School affil-num=7 en-affil= kn-affil=Kagawa Medical School en-keyword=bFGF kn-keyword=bFGF en-keyword=NGF kn-keyword=NGF en-keyword=regeneration kn-keyword=regeneration en-keyword=acetylcholinesterase positive fibers kn-keyword=acetylcholinesterase positive fibers en-keyword=sprouting kn-keyword=sprouting END start-ver=1.4 cd-journal=joma no-vol=62 cd-vols= no-issue=1 article-no= start-page=21 end-page=28 dt-received= dt-revised= dt-accepted= dt-pub-year=2008 dt-pub=200802 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Critical Differences in Magnitude and Duration of N-methyl-D-aspartate (NMDA) Receptor Activation between Long-term Potentiation (LTP) and Long-term Depression (LTD) Induction en-subtitle= kn-subtitle= en-abstract= kn-abstract=

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.

en-copyright= kn-copyright= en-aut-name=TaniikeNaoki en-aut-sei=Taniike en-aut-mei=Naoki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=LuYun-Fei en-aut-sei=Lu en-aut-mei=Yun-Fei kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TomizawaKazuhito en-aut-sei=Tomizawa en-aut-mei=Kazuhito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=MatsuiHideki en-aut-sei=Matsui en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University en-keyword=LTP kn-keyword=LTP en-keyword=LTD kn-keyword=LTD en-keyword=NMDA receptor kn-keyword=NMDA receptor en-keyword=learning and memory kn-keyword=learning and memory en-keyword=hippocampus kn-keyword=hippocampus END start-ver=1.4 cd-journal=joma no-vol=51 cd-vols= no-issue=1 article-no= start-page=25 end-page=31 dt-received= dt-revised= dt-accepted= dt-pub-year=1997 dt-pub=199702 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Comparative analysis of CD45RA- and CD45RO-positive CD4+T cells in peripheral blood, synovial fluid, and synovial tissue in patients with rheumatoid arthritis and osteoarthritis en-subtitle= kn-subtitle= en-abstract= kn-abstract=

 To determine whether the predominant infiltration with memory CD4+T cells in joints is specific to the local immune and inflammatory response in rheumatoid arthritis (RA), the proportions of CD45RA+ or CD45RO+ cells in the CD4+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+T cell population of peripheral blood, the number of CD45RO+ cells was relatively higher than CD45RA+ 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+T cells present in synovial fluid and synovial tissue were CD45RO-positive and CD45RA-negative in both patient groups; although CD4+T cells infiltrating both the disease compartments were markedly greater in RA joints, their mean percentages of CD45RO+ cells were not significantly different from those in OA joints. These data indicate that an accumulation of CD45RO+ 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+ naive CD4+T cells.

en-copyright= kn-copyright= en-aut-name=EzawaKazuhiko en-aut-sei=Ezawa en-aut-mei=Kazuhiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=YamamuraMasahiro en-aut-sei=Yamamura en-aut-mei=Masahiro kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=MatsuiHideki en-aut-sei=Matsui en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=OtaZensuke en-aut-sei=Ota en-aut-mei=Zensuke kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=MakinoHirofumi en-aut-sei=Makino en-aut-mei=Hirofumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University affil-num=5 en-affil= kn-affil=Okayama University en-keyword=rheumatoid arthritis kn-keyword=rheumatoid arthritis en-keyword=ostroarthritis kn-keyword=ostroarthritis en-keyword=CD45RO+ kn-keyword=CD45RO+ en-keyword=CD4+T cells kn-keyword=CD4+T cells END start-ver=1.4 cd-journal=joma no-vol=60 cd-vols= no-issue=2 article-no= start-page=71 end-page=76 dt-received= dt-revised= dt-accepted= dt-pub-year=2006 dt-pub=200604 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Immunosuppression for islet transplantation. en-subtitle= kn-subtitle= en-abstract= kn-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. en-copyright= kn-copyright= en-aut-name=NoguchiHirofumi en-aut-sei=Noguchi en-aut-mei=Hirofumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MatsumotoShinichi en-aut-sei=Matsumoto en-aut-mei=Shinichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=MatsushitaMasayuki en-aut-sei=Matsushita en-aut-mei=Masayuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=KobayashiNaoya en-aut-sei=Kobayashi en-aut-mei=Naoya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TanakaKoichi en-aut-sei=Tanaka en-aut-mei=Koichi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=MatsuiHideki en-aut-sei=Matsui en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=TanakaNoriaki en-aut-sei=Tanaka en-aut-mei=Noriaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= affil-num=1 en-affil= kn-affil=Okayama University affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Okayama University affil-num=5 en-affil= kn-affil=Okayama University affil-num=6 en-affil= kn-affil=Okayama University affil-num=7 en-affil= kn-affil=Okayama University en-keyword=islet transplantation kn-keyword=islet transplantation en-keyword=steroid-free kn-keyword=steroid-free en-keyword=Edmonton protocol kn-keyword=Edmonton protocol en-keyword=protein transduction syst kn-keyword=protein transduction syst END start-ver=1.4 cd-journal=joma no-vol=36 cd-vols= no-issue=1 article-no= start-page=1 end-page=10 dt-received= dt-revised= dt-accepted= dt-pub-year=1982 dt-pub=198202 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Factors inhibiting cell proliferation in rat liver cytoplasm. en-subtitle= kn-subtitle= en-abstract= kn-abstract=

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.

en-copyright= kn-copyright= en-aut-name=KuramitsuMakoto en-aut-sei=Kuramitsu en-aut-mei=Makoto kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=MatsuiHideki en-aut-sei=Matsui en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=TokudaMasaaki en-aut-sei=Tokuda en-aut-mei=Masaaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=HataseOsamu en-aut-sei=Hatase en-aut-mei=Osamu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= affil-num=1 en-affil= kn-affil=Kochi Medical College affil-num=2 en-affil= kn-affil=Okayama University affil-num=3 en-affil= kn-affil=Okayama University affil-num=4 en-affil= kn-affil=Kagawa Medical School en-keyword=cell proliferation kn-keyword=cell proliferation en-keyword=growth factor kn-keyword=growth factor en-keyword=inhibiting factor kn-keyword=inhibiting factor en-keyword=rat liver cytosol kn-keyword=rat liver cytosol en-keyword=L-cells kn-keyword=L-cells END start-ver=1.4 cd-journal=joma no-vol=44 cd-vols= no-issue=1 article-no= start-page=1 end-page=8 dt-received= dt-revised= dt-accepted= dt-pub-year=1990 dt-pub=199002 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=In Vivo Analysis of Extracellular Proteins in Rat Brains with a Newly Developed Intracerebral Microdialysis Probe en-subtitle= kn-subtitle= en-abstract= kn-abstract=

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.

en-copyright= kn-copyright= en-aut-name=NakamuraMitsuo en-aut-sei=Nakamura en-aut-mei=Mitsuo kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=ItanoToshifumi en-aut-sei=Itano en-aut-mei=Toshifumi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=YamaguchiFuminori en-aut-sei=Yamaguchi en-aut-mei=Fuminori kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=MizobuchiMasayuki en-aut-sei=Mizobuchi en-aut-mei=Masayuki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=TokudaMasaaki en-aut-sei=Tokuda en-aut-mei=Masaaki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 ORCID= en-aut-name=MatsuiHideki en-aut-sei=Matsui en-aut-mei=Hideki kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 ORCID= en-aut-name=EtohSiji en-aut-sei=Etoh en-aut-mei=Siji kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=7 ORCID= en-aut-name=HosokawaKiyoshi en-aut-sei=Hosokawa en-aut-mei=Kiyoshi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=8 ORCID= en-aut-name=OhmotoTakashi en-aut-sei=Ohmoto en-aut-mei=Takashi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=9 ORCID= en-aut-name=HataseOsamu en-aut-sei=Hatase en-aut-mei=Osamu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=10 ORCID= affil-num=1 en-affil= kn-affil=Kagawa Medical School affil-num=2 en-affil= kn-affil=Kagawa Medical School affil-num=3 en-affil= kn-affil=Kagawa Medical School affil-num=4 en-affil= kn-affil=Kagawa Medical School affil-num=5 en-affil= kn-affil=Kagawa Medical School affil-num=6 en-affil= kn-affil=Kagawa Medical School affil-num=7 en-affil= kn-affil=Kagawa Medical School affil-num=8 en-affil= kn-affil=Kagawa Medical School affil-num=9 en-affil= kn-affil=Kagawa Medical School affil-num=10 en-affil= kn-affil=Kagawa Medical School en-keyword=protein kn-keyword=protein en-keyword=peptide kn-keyword=peptide en-keyword=microdialysis kn-keyword=microdialysis en-keyword=extracellular space kn-keyword=extracellular space en-keyword=probe kn-keyword=probe END start-ver=1.4 cd-journal=joma no-vol=121 cd-vols= no-issue=3 article-no= start-page=189 end-page=193 dt-received= dt-revised= dt-accepted= dt-pub-year=2009 dt-pub=20091201 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=ART (Advanced Research Training) is a new graduate school program for training physician scientists kn-title=ARTプログラム（先進医学修練）による医学研究者育成―学部・卒後臨床研修をシームレスにつなぐ早期大学院教育― en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=MatsuiHideki en-aut-sei=Matsui en-aut-mei=Hideki kn-aut-name=松井秀樹 kn-aut-sei=松井 kn-aut-mei=秀樹 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　細胞生理学 en-keyword=ART kn-keyword=ART en-keyword=医学研究者育成 kn-keyword=医学研究者育成 en-keyword=大学院改革推進GP kn-keyword=大学院改革推進GP en-keyword=卒後臨床研修 kn-keyword=卒後臨床研修 en-keyword=女性医師支援 kn-keyword=女性医師支援 END start-ver=1.4 cd-journal=joma no-vol=121 cd-vols= no-issue=3 article-no= start-page=149 end-page=156 dt-received= dt-revised= dt-accepted= dt-pub-year=2009 dt-pub=20091201 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=A CACNB4 mutation showing altered Ca(v)2.1 function in a patient with Dravet syndrome kn-title=Dravet 症候群患者に認められたカルシウムチャネル　機能異常を引き起こす CACNB4 遺伝子変異 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=OhmoriIori en-aut-sei=Ohmori en-aut-mei=Iori kn-aut-name=大守伊織 kn-aut-sei=大守 kn-aut-mei=伊織 aut-affil-num=1 ORCID= en-aut-name=OuchidaMamoru en-aut-sei=Ouchida en-aut-mei=Mamoru kn-aut-name=大内田守 kn-aut-sei=大内田 kn-aut-mei=守 aut-affil-num=2 ORCID= en-aut-name=MimakiNobuyoshi en-aut-sei=Mimaki en-aut-mei=Nobuyoshi kn-aut-name=御牧信義 kn-aut-sei=御牧 kn-aut-mei=信義 aut-affil-num=3 ORCID= en-aut-name=NishikiTeiichi en-aut-sei=Nishiki en-aut-mei=Teiichi kn-aut-name=西木禎一 kn-aut-sei=西木 kn-aut-mei=禎一 aut-affil-num=4 ORCID= en-aut-name=TomizawaKazuhito en-aut-sei=Tomizawa en-aut-mei=Kazuhito kn-aut-name=富澤一仁 kn-aut-sei=富澤 kn-aut-mei=一仁 aut-affil-num=5 ORCID= en-aut-name=MatsuiHideki en-aut-sei=Matsui en-aut-mei=Hideki kn-aut-name=松井秀樹 kn-aut-sei=松井 kn-aut-mei=秀樹 aut-affil-num=6 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　細胞生理学 affil-num=2 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　分子遺伝学 affil-num=3 en-affil= kn-affil=倉敷成人病センター　小児科 affil-num=4 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　細胞生理学 affil-num=5 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　細胞生理学 affil-num=6 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　細胞生理学 en-keyword=てんかん kn-keyword=てんかん en-keyword=Dravet 症候群 kn-keyword=Dravet 症候群 en-keyword=CACNB4遺伝子 kn-keyword=CACNB4遺伝子 en-keyword=SCN1A 遺伝子 kn-keyword=SCN1A 遺伝子 END start-ver=1.4 cd-journal=joma no-vol=91 cd-vols= no-issue=3-4 article-no= start-page=461 end-page=467 dt-received= dt-revised= dt-accepted= dt-pub-year=1979 dt-pub=19790430 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Analysis of the action of Illudin S: Effects of Illudin S on surface structures of L(929) fibroblasts kn-title=Illudin Sの作用機作の解折:Illudin SのL(929)線維芽細胞の表面形態に及ぼす影響について en-subtitle= kn-subtitle= en-abstract= kn-abstract=The effects of Illudin S (a toadstool poison) on surface structures of L(929) mouse fibroblasts were studied by scanning electron microscopy. Illudin S in a concentration of 1 ng/ml strongly inhibited cell proliferation, but had no effect on surface structures of L cells through all the cell phases. These results indicate that the biological effects of Illudin S were not manifested by changes in the cytoskeletal system, the cell ability to attach to the substrate, of the surface structures of the cell. It is suggested that the cellular sensitive sites to Illudin S are inside the cell. en-copyright= kn-copyright= en-aut-name=KuramitsuMakoto en-aut-sei=Kuramitsu en-aut-mei=Makoto kn-aut-name=倉光誠 kn-aut-sei=倉光 kn-aut-mei=誠 aut-affil-num=1 ORCID= en-aut-name=ItanoToshifumi en-aut-sei=Itano en-aut-mei=Toshifumi kn-aut-name=板野俊文 kn-aut-sei=板野 kn-aut-mei=俊文 aut-affil-num=2 ORCID= en-aut-name=MatsuiHideki en-aut-sei=Matsui en-aut-mei=Hideki kn-aut-name=松井秀樹 kn-aut-sei=松井 kn-aut-mei=秀樹 aut-affil-num=3 ORCID= en-aut-name=TokudaMasaaki en-aut-sei=Tokuda en-aut-mei=Masaaki kn-aut-name=徳田雅明 kn-aut-sei=徳田 kn-aut-mei=雅明 aut-affil-num=4 ORCID= en-aut-name=HataseOsamu en-aut-sei=Hatase en-aut-mei=Osamu kn-aut-name=畠瀬修 kn-aut-sei=畠瀬 kn-aut-mei=修 aut-affil-num=5 ORCID= en-aut-name=MurakamiTetsuhide en-aut-sei=Murakami en-aut-mei=Tetsuhide kn-aut-name=村上哲英 kn-aut-sei=村上 kn-aut-mei=哲英 aut-affil-num=6 ORCID= en-aut-name=NisidaIsamu en-aut-sei=Nisida en-aut-mei=Isamu kn-aut-name=西田勇 kn-aut-sei=西田 kn-aut-mei=勇 aut-affil-num=7 ORCID= en-aut-name=HayashiHideo en-aut-sei=Hayashi en-aut-mei=Hideo kn-aut-name=林英生 kn-aut-sei=林 kn-aut-mei=英生 aut-affil-num=8 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部第一生理学教室 affil-num=2 en-affil= kn-affil=岡山大学医学部第一生理学教室 affil-num=3 en-affil= kn-affil=岡山大学医学部第一生理学教室 affil-num=4 en-affil= kn-affil=岡山大学医学部第一生理学教室 affil-num=5 en-affil= kn-affil=岡山大学医学部第一生理学教室 affil-num=6 en-affil= kn-affil=岡山大学医学部第一生理学教室 affil-num=7 en-affil= kn-affil=岡山大学医学部第一生理学教室 affil-num=8 en-affil= kn-affil=岡山大学医学部細菌学教室 en-keyword=Illudin S kn-keyword=Illudin S en-keyword=細胞表面形態 kn-keyword=細胞表面形態 en-keyword=L細胞 kn-keyword=L細胞 END start-ver=1.4 cd-journal=joma no-vol=94 cd-vols= no-issue=3-4 article-no= start-page=341 end-page=348 dt-received= dt-revised= dt-accepted= dt-pub-year=1982 dt-pub=19820430 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=On the proliferation regulatory mechanism of spontaneously transformed L cell(L-N) kn-title=自然形質転換したL細胞(L-N)の増殖制御機構について en-subtitle= kn-subtitle= en-abstract= kn-abstract=1) The L-0 cell absolutely required serum for proliferation, but L-N cell grew rapidly in serum free medium. 2) L-N cell cultured in MEM medium with TPB reached high saturation density as in serum containing medium. 3) The growth rate of L-N cell in serum free medium was dependent on initial density of cell population just before logarithmic growing phase. 4) L-N cell rounded cell cycle from G-1 phase to S phase 4 hours faster than L-0 cell. en-copyright= kn-copyright= en-aut-name=MatsuiHideki en-aut-sei=Matsui en-aut-mei=Hideki kn-aut-name=松井秀樹 kn-aut-sei=松井 kn-aut-mei=秀樹 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学医学部第一生理学教室 en-keyword=無血清 kn-keyword=無血清 en-keyword=細胞増殖制御 kn-keyword=細胞増殖制御 en-keyword=L細胞 kn-keyword=L細胞 en-keyword=形質転換 kn-keyword=形質転換 en-keyword=DNA合成 kn-keyword=DNA合成 END start-ver=1.4 cd-journal=joma no-vol=117 cd-vols= no-issue=2 article-no= start-page=105 end-page=108 dt-received= dt-revised= dt-accepted= dt-pub-year=2005 dt-pub=20050901 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=蛋白導入システムによる薬剤開発と膵島移植への応用 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=野口洋文 kn-aut-sei=野口 kn-aut-mei=洋文 aut-affil-num=1 ORCID= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=松下正之 kn-aut-sei=松下 kn-aut-mei=正之 aut-affil-num=2 ORCID= en-aut-name=KobayashiNaoya en-aut-sei=Kobayashi en-aut-mei=Naoya kn-aut-name=小林直哉 kn-aut-sei=小林 kn-aut-mei=直哉 aut-affil-num=3 ORCID= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=SusanBonner-Weir kn-aut-sei=Susan kn-aut-mei=Bonner-Weir aut-affil-num=4 ORCID= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=松井秀樹 kn-aut-sei=松井 kn-aut-mei=秀樹 aut-affil-num=5 ORCID= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=田中紀章 kn-aut-sei=田中 kn-aut-mei=紀章 aut-affil-num=6 ORCID= en-aut-name= en-aut-sei= en-aut-mei= 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aut-affil-num=8 ORCID= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=伊達勲 kn-aut-sei=伊達 kn-aut-mei=勲 aut-affil-num=9 ORCID= affil-num=1 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　神経病態外科学 affil-num=2 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　細胞生理学 affil-num=3 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　細胞生理学 affil-num=4 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　細胞生理学 affil-num=5 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　細胞生理学 affil-num=6 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　神経病態外科学 affil-num=7 en-affil= kn-affil=香川大学医学部　脳神経外科 affil-num=8 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　細胞生理学 affil-num=9 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　神経病態外科学 en-keyword=プロテインセラピー kn-keyword=プロテインセラピー en-keyword=悪性脳腫瘍 kn-keyword=悪性脳腫瘍 en-keyword=p 53 kn-keyword=p 53 en-keyword=エンドソーム kn-keyword=エンドソーム en-keyword=蛋白導入ドメイン kn-keyword=蛋白導入ドメイン END start-ver=1.4 cd-journal=joma no-vol=120 cd-vols= no-issue=2 article-no= start-page=129 end-page=133 dt-received= dt-revised= dt-accepted= dt-pub-year=2008 dt-pub=20080801 dt-online= en-article= 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kn-affil=岡山大学大学院医歯薬学総合研究科　細胞生理学 affil-num=10 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　脳神経外科 en-keyword=cerebral vasospasm kn-keyword=cerebral vasospasm en-keyword=11R kn-keyword=11R en-keyword=protein transduction method kn-keyword=protein transduction method END start-ver=1.4 cd-journal=joma no-vol=119 cd-vols= no-issue=1 article-no= start-page=17 end-page=20 dt-received= dt-revised= dt-accepted= dt-pub-year=2007 dt-pub=20070501 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Molecular mechanism on Cdk5-dependent insulin secretion kn-title=Cdk5によるインスリン分泌の制御機構 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=魏范研 kn-aut-sei=魏 kn-aut-mei=范研 aut-affil-num=1 ORCID= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=長嶋一昭 kn-aut-sei=長嶋 kn-aut-mei=一昭 aut-affil-num=2 ORCID= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=大島登志男 kn-aut-sei=大島 kn-aut-mei=登志男 aut-affil-num=3 ORCID= en-aut-name= 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en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　細胞生理学 affil-num=5 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　細胞生理学 affil-num=6 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　細胞生理学 affil-num=7 en-affil= kn-affil=京都大学大学院医学研究科　糖尿病栄養内科 affil-num=8 en-affil= kn-affil=理化学研究所　発生神経生物研究チーム affil-num=9 en-affil= kn-affil=京都大学大学院医学研究科　糖尿病栄養内科 affil-num=10 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　細胞生理学 affil-num=11 en-affil= kn-affil=岡山大学大学院医歯薬学総合研究科　細胞生理学 en-keyword=Insulin kn-keyword=Insulin en-keyword=Cdk5 kn-keyword=Cdk5 en-keyword=Calcium kn-keyword=Calcium END start-ver=1.4 cd-journal=joma no-vol= cd-vols= no-issue= article-no= start-page= end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=1982 dt-pub=19820331 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=自然形質転換したL細胞(L-N)の増殖制御機構について en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=松井秀樹 kn-aut-sei=松井 kn-aut-mei=秀樹 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学 END