start-ver=1.4 cd-journal=joma no-vol=63 cd-vols= no-issue=7 article-no= start-page=e80 end-page=e85 dt-received= dt-revised= dt-accepted= dt-pub-year=2022 dt-pub=20220528 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Novel animal model of combined generalized and focal epilepsy en-subtitle= kn-subtitle= en-abstract= kn-abstract=Thioredoxin, encoded by Txn1, is a critical antioxidant that protects against oxidative damage by regulating the dithiol/disulfide balance of interacting proteins. We recently discovered the Adem rat, an epileptic rat harboring the Txn1-F54L mutation, characterized by wild running and vacuolar degeneration in the midbrain. This study aimed to characterize the classification of epilepsy in Adem rats. We performed simultaneous video-electroencephalographic recordings, magnetic resonance imaging, neurotransmitter measurements using gas chromatography?mass spectrometry (GC-MS), and immunohistochemistry. Adem rats exhibited absence, tonic, and focal seizures. The type of epilepsy was classified as combined generalized and focal epilepsy. Neurotransmitters in the midbrain and cortex were measured at 3 weeks of age, when neuronal cell death occurs in the midbrain. The results of GC-MS ruled out the dominance of the excitatory system in the midbrain and cortex of Adem rats. Activation of astrocytes and microglia was more pronounced at 5 weeks of age, at which time epileptic seizures occurred frequently. The underlying pathology in Adem rats remains unknown. However, glial cell activation and inflammation may play a significant role in the occurrence of epilepsy. 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=ShinoharaMasakazu en-aut-sei=Shinohara en-aut-mei=Masakazu kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=KobayashiKiyoka en-aut-sei=Kobayashi en-aut-mei=Kiyoka kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=IshidaSaeko en-aut-sei=Ishida en-aut-mei=Saeko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 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=6 ORCID= affil-num=1 en-affil=Section of Developmental Physiology and Pathology, Faculty of Education, Okayama University kn-affil= affil-num=2 en-affil=Department of Molecular Oncology, Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=3 en-affil=Division of Epidemiology, Kobe University Graduate School of Medicine kn-affil= affil-num=4 en-affil=Otsuka Pharmaceutical kn-affil= affil-num=5 en-affil=Division of Animal Genetics, Laboratory Animal Research Center, Institute of Medical Science, University of Tokyo kn-affil= affil-num=6 en-affil=Division of Animal Genetics, Laboratory Animal Research Center, Institute of Medical Science, University of Tokyo kn-affil= en-keyword=animal model kn-keyword=animal model en-keyword=combined generalized and focal epilepsy kn-keyword=combined generalized and focal epilepsy en-keyword=oxidative stress kn-keyword=oxidative stress en-keyword=thioredoxin kn-keyword=thioredoxin END start-ver=1.4 cd-journal=joma no-vol=175 cd-vols= no-issue= article-no= start-page=105921 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2022 dt-pub=202212 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Thioredoxin deficiency increases oxidative stress and causes bilateral symmetrical degeneration in rat midbrain en-subtitle= kn-subtitle= en-abstract= kn-abstract=Thioredoxin, encoded by Txn1, acts as a critical antioxidant in the defense against oxidative stress by regulating the dithiol/disulfide balance of interacting proteins. The role of thioredoxin in the central nervous system (CNS) is largely unknown. A phenotype-driven study of N-ethyl-N-nitrosourea-mutated rats with wild-running seizures revealed the importance of Txn1 mutations in CNS degeneration. Genetic mapping identified Txn1-F54L in the epileptic rats. The insulin-reducing activity of Txn1-F54L was approximately one-third of that of the wild-type (WT). Bilateral symmetrical vacuolar degeneration in the midbrain, mainly in the thalamus and the inferior colliculus, was observed in the Txn1-F54L rats. The lesions displayed neuronal and oligodendrocytic cell death. Neurons in Txn1-F54L rats showed morphological changes in the mitochondria. Vacuolar degeneration peaked at five weeks of age, and spontaneous repair began at seven weeks. The TUNEL assay showed that fibroblasts derived from homozygotes were susceptible to cell death under oxidative stress. In five-week-old WT rats, energy metabolism in the thalamus was significantly higher than that in the cerebral cortex. In conclusion, in juvenile rats, Txn1 seems to play an essential role in reducing oxidative stress in the midbrains with high energy metabolism. 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=ImaiHirohiko en-aut-sei=Imai en-aut-mei=Hirohiko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 ORCID= en-aut-name=IshidaSaeko en-aut-sei=Ishida en-aut-mei=Saeko kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=4 ORCID= en-aut-name=ToyokuniShinya en-aut-sei=Toyokuni en-aut-mei=Shinya kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=5 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=6 ORCID= affil-num=1 en-affil=Section of Developmental Physiology and Pathology, Faculty of Education, Okayama University kn-affil= affil-num=2 en-affil=Department of Molecular Oncology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= affil-num=3 en-affil=Department of Systems Science, Kyoto University Graduate School of Informatics kn-affil= affil-num=4 en-affil=Division of Animal Genetics, Laboratory Animal Research Center, Institute of Medical Science, The University of Tokyo kn-affil= affil-num=5 en-affil=Department of Pathology and Biological Responses, Nagoya University Graduate School of Medicine kn-affil= affil-num=6 en-affil=Division of Animal Genetics, Laboratory Animal Research Center, Institute of Medical Science, The University of Tokyo kn-affil= en-keyword=Txn1 kn-keyword=Txn1 en-keyword=Thioredoxin kn-keyword=Thioredoxin en-keyword=Mitochondria kn-keyword=Mitochondria en-keyword=Vacuolar degeneration kn-keyword=Vacuolar degeneration en-keyword=Epilepsy kn-keyword=Epilepsy en-keyword=Oxidative stress kn-keyword=Oxidative stress END start-ver=1.4 cd-journal=joma no-vol=12 cd-vols= no-issue= article-no= start-page=103 end-page=110 dt-received= dt-revised= dt-accepted= dt-pub-year=2019 dt-pub=201912 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=性的マイノリティ当事者の語りは聴き手の性的マイノリティへの印象や当惑感を改善する en-subtitle= kn-subtitle= en-abstract= kn-abstract=本研究の目的は，性的マイノリティ当事者の語りが，聴講者の性的マイノリティへの態度や認識に及ぼす変化を明らかにすることである．当事者が現職の学校教員と校長を対象に50分の講話をし，講演の前後に質問紙調査を行い，印象や当惑感，理解の困難さについて数値化し，変化を調べた．調査内容は，印象の測定にはSD法を使用し，印象の「身近さ」因子に含まれる6項目について7件法で回答を求め，当惑感については8項目，理解困難については2項目の尺度を使用し，6件法で回答を求めた．その結果，参加者は性的マイノリティをより身近に感じるようになり，当惑感や理解困難等の否定的な態度や認識が有意に軽減した． en-copyright= kn-copyright= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=前本浩希 kn-aut-sei=前本 kn-aut-mei=浩希 aut-affil-num=1 ORCID= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=佐々木新 kn-aut-sei=佐々木 kn-aut-mei=新 aut-affil-num=2 ORCID= 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=3 ORCID= affil-num=1 en-affil=岡山大学特別支援教育特別専攻科 kn-affil= affil-num=2 en-affil=川崎医療福祉大学医療福祉学部 kn-affil= affil-num=3 en-affil=Graduate School of Education, Okayama University kn-affil=岡山大学大学院教育学研究科 en-keyword=自己開示 kn-keyword=自己開示 en-keyword=受容 kn-keyword=受容 en-keyword=性的マイノリティ kn-keyword=性的マイノリティ en-keyword=当事者の語り kn-keyword=当事者の語り END start-ver=1.4 cd-journal=joma no-vol=11 cd-vols= no-issue= article-no= start-page=293 end-page=306 dt-received= dt-revised= dt-accepted= dt-pub-year=2021 dt-pub=20210322 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=A Review of Interventions for Students with Dyscalculia kn-title=算数障害生徒への学習支援に関する文献レビュー en-subtitle= kn-subtitle= en-abstract=The purpose of this study was to review the interventions and practice of learning support for students with dyscalculia in regular junior high school. We conducted a literature survey focusing on the following four points: (1) learning form, (2) ICT and teaching materials, (3) learning content, and (4) motivation to learn. Based on the assessment of the disability of students, appropriate learning forms and teaching materials should be selected. It is recommended to build a support system at school. In the leaning content, there were many practical examples of individual support in the "number and formula" area. Psychological support for students with dyscalculia is needed to motivate them to learn. It was pointed out that it is necessary to support while respecting the will of the students. Future tasks are to verify new support methods and contents using ICT and their effects, and to develop learning support contents tailored to the individual characteristics of students with dyscalculia. and select flexible support methods according to the student's situation. It is important to select a flexible support method according to the student’s situation. kn-abstract=本研究の目的は、中学校通常学級での算数障害生徒への学習支援に関する研究・実践について整理し、支援の方法及び内容と今後の課題を明らかにすることである。中学校・高等学校での学習支援に関する実践論文を中心に文献調査を行い、@学習形態AICT や教材教具 B学習内容C学習意欲の４つに焦点をあてて検討した。生徒の障害特性のアセスメントをもとに適切な学習形態や教材を選択すること、支援体制を構築することの重要性が明らかになった。学習内容では、「数と式」領域に個別の支援の実践例が多いこと、学習意欲では、算数障害生徒は心理的サポートが必要であり、生徒の気持ちを尊重しながら支援する必要があることが指摘されていた。ICT を活用した新しい支援方法や内容とその効果の検証、及び算数障害生徒の個々の特性に合わせた学習支援コンテンツの開発が今後の課題であり、生徒の状況に応じた柔軟な支援法を選択していくことが重要であると言える。 en-copyright= kn-copyright= en-aut-name=SUEHIROKumiko en-aut-sei=SUEHIRO en-aut-mei=Kumiko kn-aut-name=末廣久美子 kn-aut-sei=末廣 kn-aut-mei=久美子 aut-affil-num=1 ORCID= 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=2 ORCID= affil-num=1 en-affil=Okayama University, Postgraduate Special Education Credential Program kn-affil=岡山大学教育学部特別支援教育特別専攻科 affil-num=2 en-affil=Okayama University, Graduate School of Education kn-affil=岡山大学大学院教育学研究科 en-keyword=算数障害 (Dyscalculia) kn-keyword=算数障害 (Dyscalculia) en-keyword=学習障害 (learning disability) kn-keyword=学習障害 (learning disability) en-keyword=学習支援 (learning support) kn-keyword=学習支援 (learning support) en-keyword=中学校 (Junior high school) kn-keyword=中学校 (Junior high school) END start-ver=1.4 cd-journal=joma no-vol=11 cd-vols= no-issue= article-no= start-page=75 end-page=88 dt-received= dt-revised= dt-accepted= dt-pub-year=2021 dt-pub=20210322 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=The E?ects of Taking a Class on Knowledge about Sexual and Gender Minorities and Homophobia kn-title=性的マイノリティに関する授業が性的マイノリティへの知識や受容感に及ぼす影響 : 性的マイノリティに関する授業の前後で en-subtitle= kn-subtitle= en-abstract=The purpose of this study is to clarify the effects of taking a class on knowledge about sexual and gender minorities, confidence in one's own knowledge, and levels of homophobia. We measured the amount of knowledge students had about sexual and gender minorities, students’ confidence in answering the questionnaires correctly, and their levels of homophobia. The results showed that taking a class about sexual and gender minorities significantly increased the amount of knowledge students had about sexual and gender minorities and decreased their homophobia. However, the effect size in the level of homophobia was very small. As for the students’ confidence of their correct answers, before the class, those who had incorrect knowledge about sexual and gender minorities were more confident in their knowledge, but after the class, those who had correct knowledge were more confident in their knowledge, a positive correlation. Based on these results, it is necessary to find an effective way to decrease homophobia. kn-abstract=本研究の目的は，性的マイノリティへの関心やレディネスが備わっていない場合であっても授業を受けることにより性的マイノリティへの受容感や知識及び自身の知識に対する自信が変化するかどうかを明らかにすることである。方法は，教員志望の学生を対象に 100分の授業を実施した。調査項目は，性的マイノリティに関する知識量および正答確信度と同性愛者受容感尺度であった。結果は，授業を受けることで，有意に性的マイノリティに関する知識量が増え，同性愛者への受容感が高まることが分かった。しかし，受容感に対する授業の効果量は僅かであった。正答確信度に関しては，授業前は，誤った知識をもっている人ほど自分の知識に自信をもっていたが，授業後は，正しい知識を持っている人ほど自分の知識に自信を持っているという正の相関へ転じた。以上の結果から，性的マイノリティに対する受容感を高める効果的な授業の方法を模索していく必要があると考えられた。 en-copyright= kn-copyright= en-aut-name=NODAYukina en-aut-sei=NODA en-aut-mei=Yukina kn-aut-name=野田夕月奈 kn-aut-sei=野田 kn-aut-mei=夕月奈 aut-affil-num=1 ORCID= en-aut-name=YAMADATsuyoshi en-aut-sei=YAMADA en-aut-mei=Tsuyoshi kn-aut-name=山田剛史 kn-aut-sei=山田 kn-aut-mei=剛史 aut-affil-num=2 ORCID= 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=3 ORCID= affil-num=1 en-affil=Student at the Graduate School of Education, Okayama University kn-affil=岡山大学大学院教育学研究科大学院生 affil-num=2 en-affil=Graduate School of Urban Social and Cultural Studies, Yokohama City University kn-affil=横浜市立大学都市社会文化研究科 affil-num=3 en-affil=Graduate School of Education, Okayama University kn-affil=岡山大学大学院教育学研究科 en-keyword=性的マイノリティ (sexual and gender minority) kn-keyword=性的マイノリティ (sexual and gender minority) en-keyword=性の多様性 (diversity of sexuality) kn-keyword=性の多様性 (diversity of sexuality) en-keyword=教育 (education) kn-keyword=教育 (education) END start-ver=1.4 cd-journal=joma no-vol=69 cd-vols= no-issue=2 article-no= start-page=153 end-page=160 dt-received= dt-revised= dt-accepted= dt-pub-year=2020 dt-pub=2020 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Poor mother-offspring relationships in rats with Cacna1a mutation en-subtitle= kn-subtitle= en-abstract= kn-abstract=Homozygous Groggy dams, which carry a Cacna1a missense mutation, often show no interest in their offspring, leading to frequent offspring deaths due to lack of nurturing. The present study aimed to clarify whether the Cacna1a mutation contributes to impaired attachment behaviors between dam and offspring. The open field test showed that homozygous female rats exhibited markedly short travel distance, whereas no difference was found between the motor activity of heterozygous females and that of wild types (WT). A series of behavioral tests was performed to compare the mother?offspring relationship between WT and heterozygous rats. Performance in the pup retrieval test was significantly less successful in heterozygous than WT dams. During the experiment, heterozygous dams spent significantly less time licking and crouching than WT dams. The offspring dam-seeking behavior test revealed that heterozygous pups’ vocalizations were significantly less frequent and shorter than those of WT pups. Although no significant difference was found between WT and heterozygous offspring in the olfactory sense test, using a piece of chocolate, heterozygous pups took significantly longer to reach a sample of the dam’s bedding. Taken together, these findings suggest that the Cacna1a mutation impairs both the dam’s maternal behavior and the offspring’s attachment behavior toward the dam en-copyright= kn-copyright= en-aut-name=KawakamiNozomi en-aut-sei=Kawakami en-aut-mei=Nozomi kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=1 ORCID= en-aut-name=KobayashiKiyoka en-aut-sei=Kobayashi en-aut-mei=Kiyoka kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=2 ORCID= en-aut-name=NishimuraAyumu en-aut-sei=Nishimura en-aut-mei=Ayumu 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= 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=Okayama University kn-affil= affil-num=4 en-affil=Department of Physiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= en-keyword=attachment kn-keyword=attachment en-keyword=Cacna1a kn-keyword=Cacna1a en-keyword=calcium channel kn-keyword=calcium channel en-keyword=mother-offspring relationship kn-keyword=mother-offspring relationship en-keyword=rat model kn-keyword=rat model END start-ver=1.4 cd-journal=joma no-vol=141 cd-vols= no-issue= article-no= start-page=104859 end-page= dt-received= dt-revised= dt-accepted= dt-pub-year=2020 dt-pub=202012 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Scn1a and Cacna1a mutations mutually alter their original phenotypes in rats en-subtitle= kn-subtitle= en-abstract= kn-abstract=This study aimed to examine the effects of Cacna1a mutation on the phenotype of Scn1a-associated epilepsy in rats. We used rats with an N1417H missense mutation in the Scn1a gene and others with an M251K mutation in the Cacna1a gene. Scn1a/Cacna1a double mutant rats were generated by mating both Scn1a and Cacna1a mutants. We investigated general health and the epileptic phenotype in all these genotypes. The onset threshold of hyperthermia-induced seizures was examined at 5 weeks and spontaneous seizures were monitored using video-EEG recordings from 6 to 12 weeks of age. Scn1a/Cacna1a double mutants showed significantly reduced threshold for hyperthermia-sensitive seizures onset compared with the Scn1a mutants and had absence seizures having 6?7 c/s spike-wave bursts with changes in the spike-wave pattern, whereas Cacna1a mutants had regular 6?7 c/s spike-wave bursts. In Scn1a/Cacna1a double mutants, 6?7 c/s spike-wave bursts were accompanied with eyelid myoclonia and continuously shifting generalized clonic seizures, which were not observed in either Scn1a or Cacna1a mutants. Although a curvature of the spine was observed in rats of all these genotypes, the degree of curvature was more pronounced in Scn1a/Cacna1a double mutants, followed by Cacna1a and Scn1a mutants. Our results indicate that Cacna1a and Scn1a mutations mutually alter their original phenotypes in rats. The phenotype of absence seizures with eyelid myoclonia, generalized clonic seizures, and of spine curvature in the Scn1a/Cacna1a double mutants were similar to that observed in patients with Dravet syndrome. 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=KobayashiKiyoka en-aut-sei=Kobayashi en-aut-mei=Kiyoka 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= affil-num=1 en-affil=Graduate School of Education, 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 Molecular Oncology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University kn-affil= en-keyword=Scn1a kn-keyword=Scn1a en-keyword=Cacna1a kn-keyword=Cacna1a en-keyword=GEFS+ kn-keyword=GEFS+ en-keyword=Dravet syndrome kn-keyword=Dravet syndrome en-keyword=Absence seizure kn-keyword=Absence seizure en-keyword=Hyperthermia-sensitive seizure kn-keyword=Hyperthermia-sensitive seizure en-keyword=Skeletal abnormality kn-keyword=Skeletal abnormality en-keyword=GABAergic interneuron kn-keyword=GABAergic interneuron en-keyword=Parvalbumin-positive cell kn-keyword=Parvalbumin-positive cell END start-ver=1.4 cd-journal=joma no-vol=174 cd-vols= no-issue= article-no= start-page=15 end-page=23 dt-received= dt-revised= dt-accepted= dt-pub-year=2020 dt-pub=20200727 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=映画「私の中のあなた」から考える　終末期小児がんの子どもと家族がより良く生きるための支援 en-subtitle= kn-subtitle= en-abstract= kn-abstract=本研究の目的は，終末期小児がんの子どもと家族の思いを知り，彼らがより良く生きるための課題を明らかにすることである。方法として小児がん患児の発病から終末期までを描いた映画「私の中のあなた」を用い，患児や家族の気持ちが表れる場面をとりあげ，その各場面について研究論文を基に詳しく読み解いた。子どもが終末期により良く生きるために必要とされていることは，子どもの希望を尊重し，意思決定を支援すること，家族の苦悩に寄り添い，子どもと家族の意思が異なり葛藤する時には合意形成を支援すること，兄弟姉妹の抱える困難を理解し支援することが考えられた。 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= affil-num=1 en-affil=Graduate School of Education, Okayama University kn-affil=岡山大学大学院教育学研究科 en-keyword=end-of-life care kn-keyword=end-of-life care en-keyword=terminal care kn-keyword=terminal care en-keyword=childhood cancer kn-keyword=childhood cancer en-keyword=decision-making process kn-keyword=decision-making process en-keyword=autonomy kn-keyword=autonomy END start-ver=1.4 cd-journal=joma no-vol=174 cd-vols= no-issue= article-no= start-page=9 end-page=14 dt-received= dt-revised= dt-accepted= dt-pub-year=2020 dt-pub=20200727 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=ADHD患児とその保護者の服薬アドヒアランス調査 en-subtitle= kn-subtitle= en-abstract= kn-abstract=【目的】注意欠如・多動症（ADHD）の患児とその保護者が薬物治療をどのように評価し，治療に向き合っているのかを明らかにする。【方法】ADHDの診断を受け，メチルフェニデート徐放剤およびアトモキセチンを処方された小１から高３までの患児94 人と保護者106人に質問紙調査と半構造化面接を行った。【結果】90％以上で服薬は規則正しく行われており，薬物治療に対する肯定的な評価は，患児・保護者で約80 〜 90％と高かった。一方で，全面的に賛成しているわけではなく，約80％の保護者が否定的な意見も持っていた．否定的評価をする要因は，保護者は副作用を含めた長期的な影響への不安，患児は服薬の煩わしさや胃腸症状が多かった。定期的な薬物治療を続けているにも関わらず，効果と不安等を天秤にかけて治療を継続することへの積極的な支持は，患児・保護者で約50 〜 60％であった。【結論】小児では，低年齢のため客観的に自身の状況を判断し，見通しをもって治療に参加することが難しい場合がある。患児へは胃腸症状への対処を，保護者へは治療の見通しや副作用について丁寧な説明を繰り返すことによって，薬物治療への否定的評価が軽減され，服薬アドヒアランスが向上する可能性がある。 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=MinamiKyoko en-aut-sei=Minami en-aut-mei=Kyoko kn-aut-name=南恭子 kn-aut-sei=南 kn-aut-mei=恭子 aut-affil-num=2 ORCID= en-aut-name=OhnoShigeru en-aut-sei=Ohno en-aut-mei=Shigeru kn-aut-name=大野繁 kn-aut-sei=大野 kn-aut-mei=繁 aut-affil-num=3 ORCID= en-aut-name=OkaMakio en-aut-sei=Oka en-aut-mei=Makio kn-aut-name=岡牧郎 kn-aut-sei=岡 kn-aut-mei=牧郎 aut-affil-num=4 ORCID= affil-num=1 en-affil=Graduate School of Education, Okayama University kn-affil=岡山大学大学院教育学研究科 affil-num=2 en-affil=Ex-Division of Developmental Studies and Support, Graduate School of Education (Master’s Course), Okayama University kn-affil=前　岡山大学大学院教育学研究科修士課程 affil-num=3 en-affil=Ohno Hagukumi Clinic kn-affil=医療法人大野はぐくみクリニック affil-num=4 en-affil=Department of Child Neurology, Okayama University Medical School kn-affil=岡山大学医学部附属病院小児神経 en-keyword=注意欠如・多動性症 kn-keyword=注意欠如・多動性症 en-keyword=ADHD kn-keyword=ADHD en-keyword=アドヒアランス kn-keyword=アドヒアランス en-keyword=メチルフェニデート kn-keyword=メチルフェニデート en-keyword=アトモキセチン kn-keyword=アトモキセチン END start-ver=1.4 cd-journal=joma no-vol=172 cd-vols= no-issue= article-no= start-page=49 end-page=56 dt-received= dt-revised= dt-accepted= dt-pub-year=2019 dt-pub=20191127 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Is Same-sex Marriage Acceptable in Japan? Reference to Same-sex Marriage Acceptance in Other Countries kn-title=同性婚は日本で容認されるか？ : 他国の同性婚容認を参考に en-subtitle= kn-subtitle= en-abstract= kn-abstract=　日本において同性愛，異性愛等の性的指向に関わらず，全ての人が希望すれば婚姻に伴う幸福や利益を享受できる時代がくるかを問う。研究方法は，CiNii Articles とGoogle Scholarを利用して「同性婚」「憲法」等のキーワードで検索し，47 本の論文を検討した。同性婚が認められていない日本では，日本国憲法第24 条の「両性」の意味がどのように解釈されるか議論がなされている。同性婚が容認されている米国では，「人間の基本権」として認められてきた「婚姻の自由」が当事者の性的指向や性自認により否定されないという考えから容認された。スペインでは，同性婚が社会的に受け入れられていること等の考えより，容認されている。同性カップルが子どもを持つ時の子どもの不利益については，多くの研究が，子どもにとって大切なのは「親の性的指向」ではなく，「親の愛情」であると述べていた。画一的な家族のありようから離れ，多様な家族の幸せへの希求が始まっている。 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=AMAKAWAAkari en-aut-sei=AMAKAWA en-aut-mei=Akari kn-aut-name=天川あかり kn-aut-sei=天川 kn-aut-mei=あかり aut-affil-num=2 ORCID= affil-num=1 en-affil=Graduate School of Education, Okayama University kn-affil=岡山大学大学院教育学研究科 affil-num=2 en-affil=Faculty of Education, Okayama University kn-affil=岡山大学 教育学部 en-keyword=同性婚 kn-keyword=同性婚 en-keyword=LGBT kn-keyword=LGBT en-keyword=憲法 kn-keyword=憲法 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= cd-vols= no-issue=20 article-no= start-page=39 end-page=48 dt-received= dt-revised= dt-accepted= dt-pub-year=2019 dt-pub=201903 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Difficulties in school life can be seen from the medical records of patients with gender dysphoria kn-title=性別違和をもつ患者の診療録から見える学校生活場面での困難さ en-subtitle= kn-subtitle= en-abstract= kn-abstract= A school should be a place where every child can feel comfortable and safe. We aimed to shed light upon difficulties in school life in children with gender dysphoria (GD) and find a way to support them. We extracted the episodes in school life from the medical records of 59 patients with GD. They suffered from using gender segregated bookbags, school uniforms, swimming wears, and bathrooms. Sex education was not enough for them to understand GD. Children with male-to-female GD were bullied at school more often than those with female-to-male GD. Teachers should take note of children with GD, and should provide necessary supports in their school life, including the facilities and their relationships with their peers. en-copyright= kn-copyright= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=天野佑美 kn-aut-sei=天野 kn-aut-mei=佑美 aut-affil-num=1 ORCID= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=佐々木 新 kn-aut-sei=佐々木 kn-aut-mei= 新 aut-affil-num=2 ORCID= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=松本洋輔 kn-aut-sei=松本 kn-aut-mei=洋輔 aut-affil-num=3 ORCID= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=大守伊織 kn-aut-sei=大守 kn-aut-mei=伊織 aut-affil-num=4 ORCID= affil-num=1 en-affil= kn-affil= affil-num=2 en-affil= kn-affil= affil-num=3 en-affil=Okayama University hospital Gender Center kn-affil=岡山大学病院ジェンダーセンター affil-num=4 en-affil=Okayama University kn-affil=岡山大学大学院教育学研究科 en-keyword=gender dysphoria kn-keyword=gender dysphoria en-keyword=gender identity disorder kn-keyword=gender identity disorder en-keyword=school education kn-keyword=school education en-keyword=gender and sexual diversity kn-keyword=gender and sexual diversity en-keyword=difficulties kn-keyword=difficulties END start-ver=1.4 cd-journal=joma no-vol=171 cd-vols= no-issue= article-no= start-page=39 end-page=46 dt-received= dt-revised= dt-accepted= dt-pub-year=2019 dt-pub=20190726 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=What Sexual Minorities in Adulthood Want for the Present School Education kn-title=成人期以降の性的マイノリティ当事者が学校生活を振り返って，学校教育に求めること en-subtitle= kn-subtitle= en-abstract= kn-abstract=　本研究の目的は，カミングアウトが難しい性的マイノリティ当事者が学校教育にどのような支援を望んでいるのか明らかにすることである。方法として質問紙調査を行った。質問紙作成にあたり，当事者への学校での支援について文献検索を行い，主に授業外で取り組む支援例を収集した。収集した支援例の評価を当事者18 名に依頼した。学校教育に求めていることは，相談してきた児童生徒の気持ちに寄り添うこと，第三者に知られないよう配慮すること，性の多様性と正しい知識を教えることであった。また，「開示しようとしまいと，いることを前提とする」学校になってほしいと希望していることが伺えた。教員は性的マイノリティの児童生徒が抱える困難さを重要な課題と捉え，いつでも誰でも相談できる環境づくりや，児童生徒の気持ちを尊重する努力が必要とされていると考える。 en-copyright= kn-copyright= en-aut-name=SASAKIArata en-aut-sei=SASAKI en-aut-mei=Arata kn-aut-name=佐々木新 kn-aut-sei=佐々木 kn-aut-mei=新 aut-affil-num=1 ORCID= en-aut-name=AMANOYumi en-aut-sei=AMANO en-aut-mei=Yumi kn-aut-name=天野佑美 kn-aut-sei=天野 kn-aut-mei=佑美 aut-affil-num=2 ORCID= 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=3 ORCID= affil-num=1 en-affil=The Joint Graduate School in Science of School Education (Doctor’s Course), Hyogo University of Teacher Education kn-affil=兵庫教育大学大学院連合学校教育学研究科 affil-num=2 en-affil=Graduate School of Education (Master’s Course), Okayama University kn-affil=岡山大学大学院教育学研究科（修士課程）　 affil-num=3 en-affil=Division of Developmental Studies and Support, Graduate School of Education, Okayama University kn-affil=岡山大学大学院教育学研究科 en-keyword=性的マイノリティ kn-keyword=性的マイノリティ en-keyword=学校教育 kn-keyword=学校教育 en-keyword=環境的整備 kn-keyword=環境的整備 en-keyword=支援 kn-keyword=支援 END start-ver=1.4 cd-journal=joma no-vol=8 cd-vols= no-issue= article-no= start-page=181 end-page=191 dt-received= dt-revised= dt-accepted= dt-pub-year=2018 dt-pub=20180320 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=慢性疾患患児に対する復学支援の研究動向 kn-title=Trends in Research Concerning School Re-entry Support for Children with Chronic Illness en-subtitle= kn-subtitle= en-abstract=本研究では、慢性疾患患児の復学支援に関する研究を概観し、研究の動向と課題を明らかにした。「復学」「支援」「小児がん」「慢性疾患」をキーワードとする36文献を分析した。その結果、保護者、医療関係者、教師など、患児に関わる人たちの思いや復学支援における役割、他職種連携、連携の具体例、高校生や思春期における復学支援の現状と課題などについて研究されていた。課題としては、「学習保障」および「関係維持」を挙げることができ、患児の学籍が変更になっても一定の教育機会を設けることのできるシステムの確保と、患児が発病前からつながっている人間関係を維持し、発病後に関わることになった医療関係者や教師と復学後もつながり続けられるような支援が必要と考えられた。 kn-abstract= The principle aim of the present study was to elucidate research trends and issues related to school re-entry. We reviewed past studies concerning school re-entry support for children with chronic illness. A total of 36 papers were analyzed for the keywords of "school re-entry," "support," "pediatric cancer," and "chronic illness." The results revealed that the concerns regarding the children and school re-entry support roles of legal guardians, healthcare providers, teachers, etc., and specific examples of collaboration with other occupations. "Guaranty a right to learn " and "relationship maintenance" were noted as issues, and ensuring a system that can establish certain learning opportunities even if the enrollment status of the child changes, continued maintenance of relationships of the patient before the onset of disease, and support to maintain the relationship of healthcare providers and teachers who are involved after onset of the disease are necessary even after school re-entry. en-copyright= kn-copyright= en-aut-name=MurakamiRie en-aut-sei=Murakami en-aut-mei=Rie kn-aut-name=村上理絵 kn-aut-sei=村上 kn-aut-mei=理絵 aut-affil-num=1 ORCID= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=大守伊織 kn-aut-sei=大守 kn-aut-mei=伊織 aut-affil-num=2 ORCID= affil-num=1 en-affil=Division of Special Education, Faculty of Education Okayama University kn-affil=岡山大学大学院教育学研究科 affil-num=2 en-affil=Division of Special Education, Faculty of Education Okayama University kn-affil=岡山大学大学院教育学研究科 en-keyword=school re-entry (復学) kn-keyword=school re-entry (復学) en-keyword=support (支援) kn-keyword=support (支援) en-keyword=chronic illness (慢性疾患) kn-keyword=chronic illness (慢性疾患) 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=33 cd-vols= no-issue=27 article-no= start-page=6468 end-page=6475 dt-received= dt-revised= dt-accepted= dt-pub-year=2012 dt-pub=201209 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=Combining poly-arginine with the hydrophobic counter-anion 4-(1-pyrenyl)-butyric acid for protein transduction in transdermal delivery en-subtitle= kn-subtitle= en-abstract= kn-abstract=Topical therapy is the most favored form of treatment for whitening against hyperpigmentation and sunburn because it lends itself to self-administration, patient compliance, and absence of systemic adverse effects. However, transdermal delivery of hydrophilic chemicals is difficult. The main purpose of this study is to develop a delivering system of hydrophilic drugs and proteins across the skin. Hydroquinone (HQ), a well-known tyrosinase inhibitor and antimelanogenesis compound, and enhanced green fluorescent protein (EGFP) were fused with eleven poly-arginine (11R). Both HQ-11R and EGFP-11R were efficiently delivered in B16 cells, a mouse melanoma cell line. HQ-11R was as effective as HQ alone at inhibiting melanin synthesis in B16 cells. EGFP-11R was efficiently delivered into cells of the epidermis with 4-(1-pyrenyl)-butyric acid (PB), a counteranion bearing an aromatic hydrophobic moiety, in vivo, but EGFP alone or EGFP-11R without PB was not. Finally, topical application of HQ-11R with PB significantly inhibited UV irradiation-induced pigmentation in guinea pigs compared with HQ alone. These results suggest that topical therapy using poly-arginine in combination with PB is useful for the delivery of hydrophilic drugs and proteins by the transdermal route. en-copyright= kn-copyright= en-aut-name=CandanGerile en-aut-sei=Candan en-aut-mei=Gerile 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=IshikawaSanae en-aut-sei=Ishikawa en-aut-mei=Sanae kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=3 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=4 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=5 ORCID= en-aut-name=UnedaAtsuhito en-aut-sei=Uneda en-aut-mei=Atsuhito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=6 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=7 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=8 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=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=TomizawaKazuhito en-aut-sei=Tomizawa en-aut-mei=Kazuhito kn-aut-name= kn-aut-sei= kn-aut-mei= aut-affil-num=11 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=Ohmori affil-num=9 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Physiol affil-num=10 en-affil= kn-affil=Okayama Univ, Grad Sch Med Dent & Pharmaceut Sci, Dept Physiol affil-num=11 en-affil= kn-affil=Kumamoto Univ, Fac Life Sci, Dept Mol Physiol en-keyword=Transdermal delivery kn-keyword=Transdermal delivery en-keyword=Protein transduction kn-keyword=Protein transduction en-keyword=Poly-arginine kn-keyword=Poly-arginine en-keyword=Tat kn-keyword=Tat en-keyword=Hydroquinone kn-keyword=Hydroquinone en-keyword=Tyrosinase inhibitor kn-keyword=Tyrosinase inhibitor END start-ver=1.4 cd-journal=joma no-vol=124 cd-vols= no-issue=2 article-no= start-page=115 end-page=117 dt-received= dt-revised= dt-accepted= dt-pub-year=2012 dt-pub=20120801 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=Therapy for hyperthermia-induced seizures in Scn1a mutant rats kn-title=Scn1a遺伝子変異ラットを用いた抗てんかん薬の熱性けいれん抑制効果 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name=HayashiKeiichiro en-aut-sei=Hayashi en-aut-mei=Keiichiro kn-aut-name=林桂一郎 kn-aut-sei=林 kn-aut-mei=桂一郎 aut-affil-num=1 ORCID= 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=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= 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　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 en-keyword=febrile seizures kn-keyword=febrile seizures en-keyword=animal model kn-keyword=animal model 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=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=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=107 cd-vols= no-issue=7-8 article-no= start-page=99 end-page=109 dt-received= dt-revised= dt-accepted= dt-pub-year=1995 dt-pub=19950831 dt-online= en-article= kn-article= en-subject= kn-subject= en-title=An electroclinical study of localization-related epilepsies occurring before 6 months of age kn-title=生後6ヵ月未満発症の局在関連性てんかんに関する研究 en-subtitle= kn-subtitle= en-abstract= kn-abstract=To clarify the characteristics of localization-related epilepsies occurring before 6 monthes of age, I carried out an electroclinical study on 28 cases which had been followed up for more than one year after the onset. The subjects were divided into two groups : the controlled group (8 cases) and the refractory group (20 cases). The controlled group was defined as the subjects whose seizures were suppressed within one year after the onset and the other subjects were classified into the refractory group. The characteristies of the refractory group were as follows : Most cases had serious underlying pathologies. The seizure type of most cases was simple partial seizure or complex partial seizure or complex partial seizure without secondary generalization. The inter-ictal EEG showed focal abnormalities and severe dysrrythmia on the basic pattern associated with mulitifocal spikes in most cases. Some cases developed West syndrome after localization-related epilepsies, and generalized seizures or pseudoabsences appeared later in some other cases. In conclusion, a comprehensive assessment and an intensive follow-up of clinical and EEG manifestations are of great value for determining the prognosis localization-related epilepsies occurring in early infancy. 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= affil-num=1 en-affil= kn-affil=岡山大学医学部小児神経学教室 en-keyword=局在関連性てんかん kn-keyword=局在関連性てんかん en-keyword=難治てんかん kn-keyword=難治てんかん en-keyword=予後 kn-keyword=予後 en-keyword=脳波 kn-keyword=脳波 en-keyword=乳児期 kn-keyword=乳児期 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=1995 dt-pub=19950331 dt-online= en-article= kn-article= en-subject= kn-subject= en-title= kn-title=生後6ヵ月未満発症の局在関連性てんかんに関する研究 en-subtitle= kn-subtitle= en-abstract= kn-abstract= en-copyright= kn-copyright= en-aut-name= en-aut-sei= en-aut-mei= kn-aut-name=大守伊織 kn-aut-sei=大守 kn-aut-mei=伊織 aut-affil-num=1 ORCID= affil-num=1 en-affil= kn-affil=岡山大学 END