Faculty Profiles - OHMORI Iori

Papers - OHMORI Iori

Division display >> ／ All the affair displays 1 - 109 of about 109

Txn1mutation is a monogenic cause of chronic kidney disease associated with mitochondrial dysfunction in rats

Iori Ohmori, Mamoru Ouchida, Yoshiko Hada, Haruhito A. Uchida, Shinya Toyokuni, Tomoji Mashimo

BioRxiv 2023.8

Thioredoxin deficiency increases oxidative stress and causes bilateral symmetrical degeneration in rat midbrain. Reviewed International journal

Iori Ohmori, Mamoru Ouchida, Hirohiko Imai, Saeko Ishida, Shinya Toyokuni, Tomoji Mashimo

Neurobiology of disease 175 105921 - 105921 2022.11

Authorship：Lead author,　Corresponding author Language：English Publishing type：Research paper (scientific journal) Publisher：Elsevier BV

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.

File： 2022 Thioredoxin deficiency increases oxidative stress.pdf

DOI： 10.1016/j.nbd.2022.105921

PubMed

researchmap

Novel animal model of combined generalized and focal epilepsy. Reviewed International journal

Iori Ohmori, Mamoru Ouchida, Masakazu Shinohara, Kiyoka Kobayashi, Saeko Ishida, Tomoji Mashimo

Epilepsia 63 ( 7 ) e80 - e85 2022.7

Authorship：Lead author,　Corresponding author Language：English Publishing type：Research paper (scientific journal)

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.

File： 2022 Novel animal model of combined generalized and focal epilepsy.pdf

DOI： 10.1111/epi.17295

PubMed

researchmap

ナトリウムチャネル異常とてんかん Invited Reviewed

大守(川﨑)伊織

Epilepsy 18 ( 2 ) 33 - 40 2024.12

Large-scale animal model study uncovers altered brain pH and lactate levels as a transdiagnostic endophenotype of neuropsychiatric disorders involving cognitive impairment Reviewed

Hideo Hagihara, Hirotaka Shoji, Satoko Hattori, Giovanni Sala, Yoshihiro Takamiya, Mika Tanaka, Masafumi Ihara, Mihiro Shibutani, Izuho Hatada, Kei Hori, Mikio Hoshino, Akito Nakao, Yasuo Mori, Shigeo Okabe, Masayuki Matsushita, Anja Urbach, Yuta Katayama, Akinobu Matsumoto, Keiichi I Nakayama, Shota Katori, Takuya Sato, Takuji Iwasato, Haruko Nakamura, Yoshio Goshima, Matthieu Raveau, Tetsuya Tatsukawa, Kazuhiro Yamakawa, Noriko Takahashi, Haruo Kasai, Johji Inazawa, Ikuo Nobuhisa, Tetsushi Kagawa, Tetsuya Taga, Mohamed Darwish, Hirofumi Nishizono, Keizo Takao, Kiran Sapkota, Kazutoshi Nakazawa, Tsuyoshi Takagi, Haruki Fujisawa, Yoshihisa Sugimura, Kyosuke Yamanishi, Lakshmi Rajagopal, Nanette Deneen Hannah, Herbert Y Meltzer, Tohru Yamamoto, Shuji Wakatsuki, Toshiyuki Araki, Katsuhiko Tabuchi, Tadahiro Numakawa, Hiroshi Kunugi, Freesia L Huang, Atsuko Hayata-Takano, Hitoshi Hashimoto, Kota Tamada, Toru Takumi, Takaoki Kasahara, Tadafumi Kato, Isabella A Graef, Gerald R Crabtree, Nozomi Asaoka, Hikari Hatakama, Shuji Kaneko, Takao Kohno, Mitsuharu Hattori, Yoshio Hoshiba, Ryuhei Miyake, Kisho Obi-Nagata, Akiko Hayashi-Takagi, Léa J Becker, Ipek Yalcin, Yoko Hagino, Hiroko Kotajima-Murakami, Yuki Moriya, Kazutaka Ikeda, Hyopil Kim, Bong-Kiun Kaang, Hikari Otabi, Yuta Yoshida, Atsushi Toyoda, Noboru H Komiyama, Seth GN Grant, Michiru Ida-Eto, Masaaki Narita, Ken-ichi Matsumoto, Emiko Okuda-Ashitaka, Iori Ohmori, Tadayuki Shimada, Kanato Yamagata, Hiroshi Ageta, Kunihiro Tsuchida, Kaoru Inokuchi, Takayuki Sassa, Akio Kihara, Motoaki Fukasawa, Nobuteru Usuda, Tayo Katano, Teruyuki Tanaka, Yoshihiro Yoshihara, Michihiro Igarashi, Takashi Hayashi, Kaori Ishikawa, Satoshi Yamamoto, Naoya Nishimura, Kazuto Nakada, Shinji Hirotsune, Kiyoshi Egawa, Kazuma Higashisaka, Yasuo Tsutsumi, Shoko Nishihara, Noriyuki Sugo, Takeshi Yagi, Naoto Ueno, Tomomi Yamamoto, Yoshihiro Kubo, Rie Ohashi, Nobuyuki Shiina, Kimiko Shimizu, Sayaka Higo-Yamamoto, Katsutaka Oishi, Hisashi Mori, Tamio Furuse, Masaru Tamura, Hisashi Shirakawa, Daiki X Sato, Yukiko U Inoue, Takayoshi Inoue, Yuriko Komine, Tetsuo Yamamori, Kenji Sakimura, Tsuyoshi Miyakawa

eLife 12 2024.3

Language：English Publishing type：Research paper (scientific journal) Publisher：eLife Sciences Publications, Ltd

Increased levels of lactate, an end-product of glycolysis, have been proposed as a potential surrogate marker for metabolic changes during neuronal excitation. These changes in lactate levels can result in decreased brain pH, which has been implicated in patients with various neuropsychiatric disorders. We previously demonstrated that such alterations are commonly observed in five mouse models of schizophrenia, bipolar disorder, and autism, suggesting a shared endophenotype among these disorders rather than mere artifacts due to medications or agonal state. However, there is still limited research on this phenomenon in animal models, leaving its generality across other disease animal models uncertain. Moreover, the association between changes in brain lactate levels and specific behavioral abnormalities remains unclear. To address these gaps, the International Brain pH Project Consortium investigated brain pH and lactate levels in 109 strains/conditions of 2294 animals with genetic and other experimental manipulations relevant to neuropsychiatric disorders. Systematic analysis revealed that decreased brain pH and increased lactate levels were common features observed in multiple models of depression, epilepsy, Alzheimer’s disease, and some additional schizophrenia models. While certain autism models also exhibited decreased pH and increased lactate levels, others showed the opposite pattern, potentially reflecting subpopulations within the autism spectrum. Furthermore, utilizing large-scale behavioral test battery, a multivariate cross-validated prediction analysis demonstrated that poor working memory performance was predominantly associated with increased brain lactate levels. Importantly, this association was confirmed in an independent cohort of animal models. Collectively, these findings suggest that altered brain pH and lactate levels, which could be attributed to dysregulated excitation/inhibition balance, may serve as transdiagnostic endophenotypes of debilitating neuropsychiatric disorders characterized by cognitive impairment, irrespective of their beneficial or detrimental nature.

DOI： 10.7554/elife.89376

researchmap

Other Link： https://cdn.elifesciences.org/articles/89376/elife-89376-v1.xml

重症心身障害児に関する制度の変遷と家族の生活の質に関する課題―医療的ケア児支援法との関連に注目して― Reviewed

池内由子, 大守(川﨑)伊織

日本重症心身障害学会誌 49 ( 3 ) 467 - 474 2024

The Effect of a Film Viewing Intervention Added to Lectures to Improve University Students' Attitudes toward Sexual and Gender Minorities Reviewed

Arata SASAKI, Iori OHMORI, Shawna, M. CARROLL

Kawasaki Journal of Medical Welfare 28 ( 2 ) 71 - 85 2023.3

就学時期のセクシュアルハラスメントに関する文献研究

野田夕月奈, 大守伊織

岡山大学教師教育開発センター紀要 13 315 - 325 2023.3

Difficulties and problems in teachers who educate sick children with chronic severe diseases Reviewed

20 ( 2 ) 65 - 74 2022.1

Txn1 mutation causes epilepsy associated with vacuolar degeneration in the midbrain

Iori Ohmori, Mamoru Ouchida, Hirohiko Imai, Saeko Ishida, Shinya Toyokuni, Tomoji Mashimo

bioRxiv 2021.10

Authorship：Lead author,　Corresponding author Language：English Publisher：Cold Spring Harbor Laboratory

<title>Abstract</title>Thioredoxin (TXN), encoded by <italic>Txn1</italic>, acts as a critical antioxidant in the defense against oxidative stress by regulating the dithiol/disulfide balance of interacting proteins. The role of TXN in the central nervous system (CNS) is largely unknown. A phenotype-driven study of <italic>N</italic>-ethyl-<italic>N</italic>-nitrosourea-mutated rats with running seizures at around five-week of age revealed the relevance of <italic>Txn1</italic> mutations to CNS disorders. Genetic mapping identified <italic>Txn1</italic>-F54L in epileptic rats. The insulin-reducing activity of <italic>Txn1</italic>-F54L rats was approximately one-third that of the wild-type. Vacuolar degeneration in the midbrain, mainly in the thalamus and the inferior colliculus, was observed in the <italic>Txn1</italic>-F54L rats. The lesions displayed neuronal and oligodendrocyte cell death. Neurons in <italic>Txn1</italic>-F54L rats showed morphological changes in the mitochondria. Vacuolar degeneration began at three weeks of age, and spontaneous repair began at seven weeks; a dramatic change from cell death to repair occurred in the midbrain during a restricted period. In conclusion, <italic>Txn1</italic> is essential for the development of the midbrain in juvenile rats.

File： 2021.10.07.463470v1.full_Txn1.pdf

DOI： 10.1101/2021.10.07.463470

researchmap

CUX2 mutations in temporal lobe epilepsy; increased kainate susceptibility and excitatory input to hippocampus in deficient mice

Toshimitsu Suzuki, Tetsuya Tatsukawa, Genki Sudo, Caroline Delandre, Yun Jin Pai, Hiroyuki Miyamoto, Matthieu Raveau, Atsushi Shimohata, Iori Ohmori, Shin-ichiro Hamano, Kazuhiro Haginoya, Mitsugu Uematsu, Yukitoshi Takahashi, Masafumi Morimoto, Shinji Fujimoto, Hitoshi Osaka, Hirokazu Oguni, Makiko Osawa, Atsushi Ishii, Shinichi Hirose, Sunao Kaneko, Yushi Inoue, Adrian Walton Moore, Kazuhiro Yamakawa

bioRxiv 2021.9

Language：English Publisher：Cold Spring Harbor Laboratory

<title>Abstract</title><italic>CUX2</italic> gene encodes a transcription factor that controls neuronal proliferation, dendrite branching and synapse formation, locating at the epilepsy-associated chromosomal region 12q24 that we previously identified by a genome-wide association study (GWAS) in Japanese population. A <italic>CUX2</italic> recurrent <italic>de novo</italic> variant p.E590K has been described in patients with rare epileptic encephalopathies and the gene is a candidate for the locus, however the mutation may not be enough to generate the genome-wide significance in the GWAS and whether <italic>CUX2</italic> variants appear in other types of epilepsies and physiopathological mechanisms are remained to be investigated. Here in this study, we conducted targeted sequencings of <italic>CUX2</italic>, a paralog <italic>CUX1</italic> and its short isoform <italic>CASP</italic> harboring a unique C-terminus on 271 Japanese patients with a variety of epilepsies, and found that multiple <italic>CUX2</italic> missense variants, other than the p.E590K, and some <italic>CASP</italic> variants including a deletion, predominantly appeared in patients with temporal lobe epilepsy (TLE). Human cell culture and fly dendritic arborization analyses revealed loss-of- function properties for the <italic>CUX2</italic> variants. <italic>Cux2</italic>- and <italic>Casp</italic>-specific knockout mice both showed high susceptibility to kainate, increased excitatory cell number in the entorhinal cortex, and significant enhancement in glutamatergic synaptic transmission to the hippocampus. CASP and CUX2 proteins physiologically bound to each other and co-expressed in excitatory neurons in brain regions including the entorhinal cortex. These results suggest that <italic>CUX2</italic> and <italic>CASP</italic> variants contribute to the TLE pathology through a facilitation of excitatory synaptic transmission from entorhinal cortex to hippocampus.

File： 2021.09.17.460803v1.full_CUX2.pdf

DOI： 10.1101/2021.09.17.460803

researchmap

CUX2 deficiency causes facilitation of excitatory synaptic transmission onto hippocampus and increased seizure susceptibility to kainate Reviewed

Sci Rep. 12 ( 6505 ) 2021.9

Language：English Publishing type：Research paper (scientific journal) Publisher：Cold Spring Harbor Laboratory

CUX2 gene encodes a transcription factor that controls neuronal proliferation, dendrite branching and synapse formation, locating at the epilepsy-associated chromosomal region 12q24 that we previously identified by a genome-wide association study (GWAS) in Japanese population. A CUX2 recurrent de novo variant p.E590K has been described in patients with rare epileptic encephalopathies and the gene is a candidate for the locus, however the mutation may not be enough to generate the genome-wide significance in the GWAS and whether CUX2 variants appear in other types of epilepsies and physiopathological mechanisms are remained to be investigated. Here in this study, we conducted targeted sequencings of CUX2, a paralog CUX1 and its short isoform CASP harboring a unique C-terminus on 271 Japanese patients with a variety of epilepsies, and found that multiple CUX2 missense variants, other than the p.E590K, and some CASP variants including a deletion, predominantly appeared in patients with temporal lobe epilepsy (TLE). The CUX2 variants showed abnormal localization in human cell culture analysis. While wild-type CUX2 enhances dendritic arborization in fly neurons, the effect was compromised by some of the variants. Cux2- and Casp-specific knockout mice both showed high susceptibility to kainate, increased excitatory cell number in the entorhinal cortex, and significant enhancement in glutamatergic synaptic transmission to the hippocampus. CASP and CUX2 proteins physiologically bound to each other and co-expressed in excitatory neurons in brain regions including the entorhinal cortex. These results suggest that CUX2 and CASP variants contribute to the TLE pathology through a facilitation of excitatory synaptic transmission from entorhinal cortex to hippocampus.

DOI： 10.1101/2021.09.17.460803

researchmap

The Effects of Taking a Class on Knowledge about Sexual and Gender Minorities and Homophobia

Bulletin of Center for Teacher Education and Development, Okayama University, 11 ( 11 ) 75 - 88 2021.3

A Review of Interventions for Students with Dyscalculia

( 11 ) 293 - 306 2021

学校教員や心理職になり得る大学生の性的マイノリティへの態度に及ぼす講義の効果 Reviewed

佐々木新, 大守伊織

GID(性同一性障害)学会雑誌 13 ( 1 ) 63 - 73 2020.12

Scn1a and Cacna1a mutations mutually alter their original phenotypes in rats. Reviewed International journal

Iori Ohmori, Kiyoka Kobayashi, Mamoru Ouchida

Neurochemistry international 141 104859 - 104859 2020.12

Authorship：Lead author,　Corresponding author Language：English Publishing type：Research paper (scientific journal) Publisher：Elsevier BV

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.

File： 2020 Scn1a and Cacna1a mutations mutually alter their original phenotypes in rats.pdf

DOI： 10.1016/j.neuint.2020.104859

PubMed

researchmap

Thinking about Ways to Support Autonomy for Children with Cancer and Their Families using the Movie “My Sister’s Keeper”

( 174 ) 15 - 23 2020.7

A recurrent PJA1 variant in trigonocephaly and neurodevelopmental disorders Reviewed International journal

Toshimitsu Suzuki, Toshifumi Suzuki, Matthieu Raveau, Noriko Miyake, Genki Sudo, Yoshinori Tsurusaki, Takaki Watanabe, Yuki Sugaya, Tetsuya Tatsukawa, Emi Mazaki, Atsushi Shimohata, Itaru Kushima, Branko Aleksic, Tomoko Shiino, Tomoko Toyota, Yoshimi Iwayama, Kentaro Nakaoka, Iori Ohmori, Aya Sasaki, Ken Watanabe, Shinichi Hirose, Sunao Kaneko, Yushi Inoue, Takeo Yoshikawa, Norio Ozaki, Masanobu Kano, Takeyoshi Shimoji, Naomichi Matsumoto, Kazuhiro Yamakawa

Annals of Clinical and Translational Neurology 7 ( 7 ) 1117 - 1131 2020.7

Language：English Publishing type：Research paper (scientific journal) Publisher：Wiley

OBJECTIVE: Neurodevelopmental disorders (NDDs) often associate with epilepsy or craniofacial malformations. Recent large-scale DNA analyses identified hundreds of candidate genes for NDDs, but a large portion of the cases still remain unexplained. We aimed to identify novel candidate genes for NDDs. METHODS: We performed exome sequencing of 95 patients with NDDs including 51 with trigonocephaly and subsequent targeted sequencing of additional 463 NDD patients, functional analyses of variant in vitro, and evaluations of autism spectrum disorder (ASD)-like phenotypes and seizure-related phenotypes in vivo. RESULTS: We identified de novo truncation variants in nine novel genes; CYP1A1, C14orf119, FLI1, CYB5R4, SEL1L2, RAB11FIP2, ZMYND8, ZNF143, and MSX2. MSX2 variants have been described in patients with cranial malformations, and our present patient with the MSX2 de novo truncation variant showed cranial meningocele and partial epilepsy. MSX2 protein is known to be ubiquitinated by an E3 ubiquitin ligase PJA1, and interestingly we found a PJA1 hemizygous p.Arg376Cys variant recurrently in seven Japanese NDD patients; five with trigonocephaly and one with partial epilepsy, and the variant was absent in 886 Japanese control individuals. Pja1 knock-in mice carrying p.Arg365Cys, which is equivalent to p.Arg376Cys in human, showed a significant decrease in PJA1 protein amount, suggesting a loss-of-function effect of the variant. Pja1 knockout mice displayed moderate deficits in isolation-induced ultrasonic vocalizations and increased seizure susceptibility to pentylenetetrazole. INTERPRETATION: These findings propose novel candidate genes including PJA1 and MSX2 for NDDs associated with craniofacial abnormalities and/or epilepsy.

File： 2020 A recurrent PJA1 variant in trigonocephaly and neurodevelopmental disorders.pdf

DOI： 10.1002/acn3.51093

PubMed

researchmap

Other Link： https://onlinelibrary.wiley.com/doi/full-xml/10.1002/acn3.51093

Poor mother-offspring relationships in rats with Cacna1a mutation Reviewed

Nozomi Kawakami, Kiyoka Kobayashi, Ayumu Nishimura, Iori Ohmori

Experimental Animals 69 ( 2 ) 153 - 160 2020.4

Authorship：Last author,　Corresponding author Language：English Publishing type：Research paper (scientific journal) Publisher：Japanese Association for Laboratory Animal Science

File： 2020 Poor mother-offspring relationships in rats with Cacna1a mutation.pdf

DOI： 10.1538/expanim.19-0086

researchmap

Action of antiepileptic drugs on neurons Reviewed

Katsuhiro Kobayashi, Fumika Endoh, Iori Ohmori, Tomoyuki Akiyama

Brain and Development 42 ( 1 ) 2 - 5 2020.1

Adherence to Medication among Children with ADHD and their Parents

( 174 ) 9 - 14 2020

PRRT2 mutations in Japanease patients with benign infantile epilepsy and paroxysmal kinesigenic dyskinesia Reviewed International journal

Okumura A, Shimojima K, Kurahashi H, Numoto S, Shimada S, Ishii A, Ohmori I, Takahashi S, Awaya T, Kubota T, Sakakibara T, Ishihara N, Hattori A, Torisu H, Tohyama J, Inoue T, Haibara A, Nishida T, Yuhara Y, Miya K, Tanaka R, Hirose S, Yamamoto T

Seizure 71 1 - 5 2019.10

Language：English Publishing type：Research paper (scientific journal)

PURPOSE: This study was performed to clarify the clinical features of Japanese patients with PRRT2 mutations. METHODS: The PRRT2 gene was analyzed in 135 patients with benign infantile epilepsy (BIE) or paroxysmal kinesigenic dyskinesia (PKD) using a direct sequencing method: 92 patients had BIE alone, 25 had both BIE and PKD, and 18 had PKD alone. Of the cases, 105 were familial, and 30 were sporadic. Clinical information was collected using a structured questionnaire. RESULTS: PRRT2 mutations were identified in 104 patients. Among the familial cases, PRRT2 mutations were found in at least one individual in 21 of 28 families with BIE alone, in 26 of 27 families with infantile convulsions and choreoathetosis, and in 2 of 3 families with PKD alone. Among the sporadic cases, PRRT2 mutations were observed in 7 of 25 patients with BIE alone, in 1 of 1 patient with BIE and PKD, and in 3 of 4 patients with PKD alone. The c.649dupC mutation was the most frequent, followed by the c.981C > G mutation. Among the patients with epilepsy, the median age at BIE onset was 5 months, the median age at the last seizure was 6 months, and the median number of seizures was 5. CONCLUSION: PRRT2 mutations were found in 68% of Japanese probands with BIE or PKD. The phenotypes of BIE associated with PRRT2 mutations were consistent with those of BIE diagnosed clinically.

DOI： 10.1016/j.seizure.2019.05.017

PubMed

researchmap

Difficulties in school life can be seen from the medical records of patients with gender dysphoria Reviewed

Amano Yumi, Sasaki Arata, Matsumoto Yosuke, Ohmori Iori

( 20 ) 39 - 48 2019.3

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

佐々木新, 天野佑美, 大守伊織

岡山大学大学院教育学研究科研究集録 ( 171 ) 39 - 46 2019

年齢依存性てんかん性脳症の分子病態解析

大内田守, 真下知士, 豊國伸哉, 大守伊織

てんかん治療研究振興財団 30 37 - 44 2019

Is Same-sex Marriage Acceptable in Japan? Reference to Same-sex Marriage Acceptance in Other Countries

2019

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 Reviewed

前本浩希, 佐々木新, 大守伊織

GID (性同一性障害) 学会雑誌 ( 12 ) 103 - 110 2019

学校教員や心理職になり得る大学生の性的マイノリティへの態度と関連する要因 Reviewed

佐々木新, 大守伊織

GID(性同一性障害)学会雑誌 ( 12 ) 41 - 49 2019

Trends in research concerning school re-entry support for children with chronic illness.

Murakami R, Ohmori I

Bulletin of center for teacher education 8 181 - 191 2018

A case of Dravet syndrome with cortical myoclonus indicated by jerk-locked back-averaging of electroencephalogram data Reviewed

Yoshinori Kobayashi, Yoshiyuki Hanaoka, Tomoyuki Akiayma, Iori Ohmori, Mamoru Ouchida, Toshiyuki Yamamoto, Makio Oka, Harumi Yoshinaga, Katsuhiro Kobayashi

BRAIN & DEVELOPMENT 39 ( 1 ) 75 - 79 2017.1

PRRT2遺伝子変異を認めたepisodic ataxiaの女児

柴田敬, 岡牧郎, 小林勝弘, 大内田守, 大守伊織

脳と発達 48 ( 6 ) 446 - 446 2016.11

Cytokine-related and sodium channel polymorphism as candidate predisposing factors for childhood encephalopathy FIRES/AERRPS Reviewed

M. Saitoh, K. Kobayashi, I. Ohmori, Y. Tanaka, K. Tanaka, T. Inoue, A. Horino, K. Ohmura, A. Kumakura, Y. Takei, S. Hirabayashi, M. Kajimoto, T. Uchida, S. Yamazaki, T. Shiihara, T. Kumagai, M. Kasai, H. Terashima, M. Kubota, M. Mizuguchi

JOURNAL OF THE NEUROLOGICAL SCIENCES 368 272 - 276 2016.9

日本におけるPRRT2関連てんかんの臨床的様相(A clinical picture of PRRT2-related epilepsy in Japan)

Kurahashi Hirokazu, 奥村彰久, 五十嵐鮎子, 安部信平, 高須倫彦, 小林勝弘, 大守伊織, 大内田まもる, 石井敦士, 廣瀬伸一, 高橋悟, 粟屋智就, 山本俊至

てんかん研究 34 ( 2 ) 395 - 395 2016.9

医療機器の臨床研究に関するアンケート調査と新指針対応の研究計画書定型書式の作成

住谷昌彦, 清水公治, 伊藤達也, 倉田真由美, 戸田聡一郎, 川上浩司, 岩江荘介, 大守伊織, 戸高浩司, 村山敏典, 山本晴子

医療機器学 86 ( 2 ) 252 - 252 2016.4

Survey results on the implementation of clinical research using the medical equipment Reviewed

Iryou kikigaku (The Japanese journal of medical instrumentation) 86 ( 5 ) 482 - 488 2016

Action potentials contribute to epileptic high-frequency oscillations recorded with electrodes remote from neurons Reviewed

Katsuhiro Kobayashi, Tomoyuki Akiyama, Iori Ohmori, Harumi Yoshinaga, Jean Gotman

CLINICAL NEUROPHYSIOLOGY 126 ( 5 ) 873 - 881 2015.5

Methylphenidate improves learning impairments and hyperthermia-induced seizures caused by an Scn1a mutation Reviewed

Iori Ohmori, Nozomi Kawakami, Sumei Liu, Haijiao Wang, Ikuko Miyazaki, Masato Asanuma, Hiroyuki Michiue, Hideki Matsui, Tomoji Mashimo, Mamoru Ouchida

EPILEPSIA 55 ( 10 ) 1558 - 1567 2014.10

遺伝学的検査をめぐる国際動向―欧米と中国の動き Reviewed

岩江荘介, 大守伊織, 小杉眞司

こころの科学「遺伝診断の未来と罠」pp.58-63 日本評論社 58 - 63 2014.9

The transdermal inhibition of melanogenesis by a cell-membrane-permeable peptide delivery system based on poly-arginine Reviewed

Nanako Ookubo, Hiroyuki Michiue, Mizuki Kitamatsu, Maho Kamamura, Tei-ichi Nishiki, Iori Ohmori, Hideki Matsui

BIOMATERIALS 35 ( 15 ) 4508 - 4516 2014.5

The acceleration of boron neutron capture therapy using multi-linked mercaptoundecahydrododecaborate (BSH) fused cell-penetrating peptide Reviewed

Hiroyuki Michiue, Yoshinori Sakurai, Natsuko Kondo, Mizuki Kitamatsu, Feng Bin, Kiichiro Nakajima, Yuki Hirota, Shinji Kawabata, Tei-ichi Nishiki, Iori Ohmori, Kazuhito Tomizawa, Shin-ichi Miyatake, Koji Ono, Hideki Matsui

BIOMATERIALS 35 ( 10 ) 3396 - 3405 2014.3

Novel multi-linked mercaptoundecahydrododecaborate (BSH) fused cellpenetrating peptide accelerated boron neutron capture therapy (BNCT)

H.Michiue, Y.Sakurai, N.Kondo, M.Kitamatsu, F.Bin, K.Nakajima, Y.Hirota, S.Kawabata, T.Nishiki, I.Ohmori, K.Tomizawa, S.Miyatake, K.Ono, H.Matsui

Book of Abstracts for 16th International Congress on Neutron Capture Therapy, Cancer Society of Finland 187 - 188 2014

乳児期早期に皮質性ミオクローヌスを認めたDravet症候群の一例

小林由典, 秋山倫之, 中尻智史, 柴田敬, 井上拓志, 小林勝弘, 大守伊織, 大内田守, 吉永治美

臨床神経生理学 41 ( 5 ) 490 - 490 2013.10

Inhalation of 10% carbon dioxide rapidly terminates Scn1a mutation-related hyperthermia-induced seizures Reviewed

Iori Ohmori, Keiichiro Hayashi, Haijiao Wang, Mamoru Ouchida, Naohiro Fujita, Takushi Inoue, Hiroyuki Michiue, Teiichi Nishiki, Hideki Matsui

EPILEPSY RESEARCH 105 ( 1-2 ) 220 - 224 2013.7

ICCA症候群および乳児期発症良性痙攣性疾患におけるPRRT2遺伝子解析

大内田守, 小林勝弘, 榎日出夫, 横田卓也, 伊予田邦昭, 吉永治美, 大守伊織

脳と発達 45 ( Suppl. ) S375 - S375 2013.5

CACNA1A遺伝子変異/多型がドラベ症候群の臨床症状に及ぼす影響

大守伊織, 小林勝弘, 大内田守, 大塚頌子

脳と発達 45 ( Suppl. ) S320 - S320 2013.5

症候の異なる発作性ジスキネジアにおけるPRRT2遺伝子変異の有無

榎日出夫, 横田卓也, 大守伊織, 大内田守, 小林勝弘

脳と発達 45 ( Suppl. ) S374 - S374 2013.5

ドラベ症候群で検出されるCACNA1A遺伝子変異の電気生理学的特性

大守伊織, 大内田守

脳と発達 45 ( Suppl. ) S349 - S349 2013.5

ICCA症候群に片麻痺性片頭痛を合併した1家系

大守伊織, 大内田守, 小林勝弘, 吉永治美

脳と発達 45 ( Suppl. ) S378 - S378 2013.5

CACNA1A variants may modify the epileptic phenotype of Dravet syndrome Reviewed

Iori Ohmori, Mamoru Ouchida, Katsuhiro Kobayashi, Yoshimi Jitsumori, Akiko Mori, Hiroyuki Michiue, Teiichi Nishiki, Yoko Ohtsuka, Hideki Matsui

NEUROBIOLOGY OF DISEASE 50 209 - 217 2013.2

High-frequency EEG oscillations in hyperthermia-induced seizures of Scn1a mutant rats Reviewed

Katsuhiro Kobayashi, Iori Ohmori, Keiichiro Hayashi, Yuichiro Kitagawa, Mamoru Ouchida, Takushi Inoue, Yoko Ohtsuka

EPILEPSY RESEARCH 103 ( 2-3 ) 161 - 166 2013.2

脳波異常から診断に至ったAngelman症候群とRett症候群の4症例

桃木恵美子, 吉永治美, 林裕美子, 岡牧郎, 小林勝弘, 大守伊織, 斎藤伸治

日本小児科学会雑誌 117 ( 2 ) 407 - 407 2013.2

Acute encephalopathy with a novel point mutation in the SCN2A gene Reviewed

Katsuhiro Kobayashi, Hiroki Ohzono, Mayu Shinohara, Makiko Saitoh, Iori Ohmori, Yoko Ohtsuka, Masashi Mizuguchi

EPILEPSY RESEARCH 102 ( 1-2 ) 109 - 112 2012.11

Combining poly-arginine with the hydrophobic counter-anion 4-(1-pyrenyl)-butyric acid for protein transduction in transdermal delivery Reviewed

Gerile Candan, Hiroyuki Michiue, Sanae Ishikawa, Atsushi Fujimura, Keiichiro Hayashi, Atsuhito Uneda, Akiko Mori, Iori Ohmori, Tei-ichi Nishiki, Hideki Matsui, Kazuhito Tomizawa

BIOMATERIALS 33 ( 27 ) 6468 - 6475 2012.9

SCN9A遺伝子変異/多型がドラベ症候群の臨床型に及ぼす影響

大守伊織, Wang Haijiao, 大内田守, 小林勝弘, 松井秀樹

てんかん研究 30 ( 2 ) 358 - 358 2012.9

Therapy for hyperthermia-induced seizures in Scn1a mutant rats

124 ( 2 ) 115 - 117 2012.8

A protein transduction method using oligo-arginine (3R) for the delivery of transcription factors into cell nuclei Reviewed

Takashi Hitsuda, Hiroyuki Michiue, Mizuki Kitamatsu, Atsushi Fujimura, Feifei Wang, Takahiro Yamamoto, Xiao-Jian Han, Hiroshi Tazawa, Atsuhito Uneda, Iori Ohmori, Tei-ichi Nishiki, Kazuhito Tomizawa, Hideki Matsui

BIOMATERIALS 33 ( 18 ) 4665 - 4672 2012.6

RGS2 mediates the anxiolytic effect of oxytocin Reviewed

Naoki Okimoto, Oliver J. Bosch, David A. Slattery, Konstanze Pflaum, Hiroaki Matsushita, Fan-Yan Wei, Masayasu Ohmori, Tei-ichi Nishiki, Iori Ohmori, Yuji Hiramatsu, Hideki Matsui, Inga D. Neumann, Kazuhito Tomizawa

BRAIN RESEARCH 1453 26 - 33 2012.5

P/Q型電位依存性カルシウムチャネル変異に伴う発達障害

大内田守, 大守伊織

脳と発達 44 ( Suppl. ) S302 - S302 2012.5

Scn1a遺伝子変異ラットにおける発達障害

大守伊織, 大内田守

脳と発達 44 ( Suppl. ) S205 - S205 2012.5

熱性けいれん既往患者におけるSCN9A遺伝子解析

大守伊織, 小林勝弘, 大内田守

脳と発達 44 ( Suppl. ) S232 - S232 2012.5

Additional information regarding "Dravet syndrome: Inroads into understanding epileptic encephalopathies" Reviewed

Katsuhiro Kobayashi, Yoko Ohtsuka, Iori Ohmori

JOURNAL OF PEDIATRICS 160 ( 3 ) 532 - 533 2012.3

Ca2+-independent syntaxin binding to the C2B effector region of synaptotagmin Reviewed

Toshio Masumoto, Koichiro Suzuki, Iori Ohmori, Hiroyuki Michiue, Kazuhito Tomizawa, Atsushi Fujimura, Tei-ichi Nishiki, Hideki Matsui

MOLECULAR AND CELLULAR NEUROSCIENCE 49 ( 1 ) 1 - 8 2012.1

Acute encephalopathy in children with Dravet syndrome Reviewed

Akihisa Okumura, Mitsugu Uematsu, George Imataka, Manabu Tanaka, Tohru Okanishi, Tetsuo Kubota, Akira Sudo, Jun Tohyama, Megumi Tsuji, Iori Ohmori, Misako Naiki, Ayako Hiraiwa-Sofue, Hitoshi Sato, Shinji Saitoh, Toshiaki Shimizu

EPILEPSIA 53 ( 1 ) 79 - 86 2012.1

ANTIDEPRESSANT-LIKE EFFECT OF SILDENAFIL THROUGH OXYTOCIN-DEPENDENT CYCLIC AMP RESPONSE ELEMENT-BINDING PROTEIN PHOSPHORYLATION Reviewed

H. Matsushita, M. Matsuzaki, X-J. Han, T. -I. Nishiki, I. Ohmori, H. Michiue, H. Matsui, K. Tomizawa

NEUROSCIENCE 200 13 - 18 2012.1

Dravet syndrome with an exceptionally good seizure outcome in two adolescents Reviewed

Katsuhiro Kobayashi, Iori Ohmori, Mamoru Ouchida, Yoko Ohtsuka

EPILEPTIC DISORDERS 13 ( 3 ) 340 - 344 2011.9

Scn1a遺伝子変異による熱性けいれんの二酸化炭素吸入療法

大守伊織, 大内田守, 王海こう, 林桂一郎, 松井秀樹

てんかん研究 29 ( 2 ) 251 - 251 2011.9

Scn1a変異ラットの高体温誘発発作における高周波振動

小林勝弘, 大守伊織, 林桂一郎, 大内田守, 井上拓志, 大塚頌子

てんかん研究 29 ( 2 ) 251 - 252 2011.9

代謝性および呼吸性アシドーシスはCacna1a変異ラットの欠神発作を抑制する

大内田守, 改田祐子, 大守伊織, 上原孝, 松井秀樹

てんかん研究 29 ( 2 ) 382 - 382 2011.9

Therapy for hyperthermia-induced seizures in Scn1a mutant rats Reviewed

Keiichiro Hayashi, Satoshi Ueshima, Mamoru Ouchida, Tomoji Mashimo, Teiichi Nishiki, Toshiaki Sendo, Tadao Serikawa, Hideki Matsui, Iori Ohmori

EPILEPSIA 52 ( 5 ) 1010 - 1017 2011.5

Expression of a Constitutively Active Calcineurin Encoded by an Intron-Retaining mRNA in Follicular Keratinocytes Reviewed

Atsushi Fujimura, Hiroyuki Michiue, Tei-ichi Nishiki, Iori Ohmori, Fan-Yan Wei, Hideki Matsui, Kazuhito Tomizawa

PLOS ONE 6 ( 3 ) e17685 2011.3

Regulation of Mitochondrial Dynamics and Neurodegenerative Diseases Reviewed

Xiao-Jian Han, Kazuhito Tomizawa, Atsushi Fujimura, Iori Ohmori, Tei-ichi Nishiki, Masayuki Matsushita, Hideki Matsui

ACTA MEDICA OKAYAMA 65 ( 1 ) 1 - 10 2011.2

遺伝子検査が診断に有用であった非典型的Rett症候群の1例

松岡剛司, 葛原誠人, 大塚頌子, 清水憲二, 大内田守, 大守伊織

日本小児科学会雑誌 114 ( 11 ) 1756 - 1756 2010.11

Oxytocin mediates the antidepressant effects of mating behavior in male mice Reviewed

Hiroaki Matsushita, Kazuhito Tomizawa, Naoki Okimoto, Tei-ichi Nishiki, Iori Ohmori, Hideki Matsui

NEUROSCIENCE RESEARCH 68 ( 2 ) 151 - 153 2010.10

Genetic seizure susceptibility underlying acute encephalopathies in childhood Reviewed

Katsuhiro Kobayashi, Mamoru Ouchida, Akihisa Okumura, Yoshihiro Maegaki, Itsuko Nishiyama, Hideki Matsui, Yoko Ohtsuka, Iori Ohmori

EPILEPSY RESEARCH 91 ( 2-3 ) 143 - 152 2010.10

Nationwide survey (incidence, clinical course, prognosis) of Rasmussen's encephalitis Reviewed

Ayako Muto, Hirokazu Oguni, Yukitoshi Takahashi, Yukiyoshi Shirasaka, Yukio Sawaishi, Tamami Yano, Toru Hoshida, Hitoshi Osaka, Satoru Nakasu, Noriyuki Akasaka, Kenji Sugai, Akie Miyamoto, Satoru Takahashi, Motomasa Suzuki, Iori Ohmori, Shin Nabatame, Makiko Osawa

BRAIN & DEVELOPMENT 32 ( 6 ) 445 - 453 2010.6

A Missense Mutation of the Gene Encoding Voltage-Dependent Sodium Channel (Na(v)1.1) Confers Susceptibility to Febrile Seizures in Rats Reviewed

Tomoji Mashimo, Iori Ohmori, Mamoru Ouchida, Yukihiro Ohno, Toshiko Tsurumi, Takafumi Miki, Minoru Wakamori, Shizuka Ishihara, Takashi Yoshida, Akiko Takizawa, Megumi Kato, Masumi Hirabayashi, Masashi Sasa, Yasuo Mori, Tadao Serikawa

JOURNAL OF NEUROSCIENCE 30 ( 16 ) 5744 - 5753 2010.4

てんかん関連変異型ナトリウムチャネルNav1.1に対する抗てんかん薬の薬理効果

大守伊織, 林桂一郎

てんかん治療研究振興財団研究年報 21 43 - 48 2010

2種類のチャネル機能異常をもつ乳児重症ミオクロニーてんかん

大守伊織, 御牧信義, 大内田守

脳と発達 41 ( Suppl. ) S241 - S241 2009.5

Hyperthermia-induced seizure-susceptible rats: a novel model of febrile seizures

Tomoji Mashimo, Iori Ohmori, Mamoru Ouchida, Yukihiro Ohno, Toshiko Tsurumi, Takafumi Miki, Minoru Wakamori, Yasuo Mori, Tadao Serikawa

NEUROSCIENCE RESEARCH 65 S47 - S47 2009

Ca(v)2.1 DYSFUNCTION MAY BE A GENETIC MODIFIER OF SEVERE MYOCLONIC EPILEPSY IN INFANCY

Iori Ohmori, Mamoru Ouchida, Takafumi Miki, Nobuyoshi Mimaki, Shigeki Kiyonaka, Teiichi Nishiki, Kazuhito Tomizawa, Yasuo Mori, Hideki Matsui

JOURNAL OF PHYSIOLOGICAL SCIENCES 59 515 - 515 2009

A CACNB4 mutation shows that altered Ca(v)2.1 function may be a genetic modifier of severe myoclonic epilepsy in infancy Reviewed

Iori Ohmori, Mamoru Ouchida, Takafumi Miki, Nobuyoshi Mimaki, Shigeki Kiyonaka, Teiichi Nishiki, Kazuhito Tomizawa, Yasuo Mori, Hideki Matsui

NEUROBIOLOGY OF DISEASE 32 ( 3 ) 349 - 354 2008.12

Novel SCN5A Mutations and SNP in Patients with Brugada Syndrome

Kazufumi Nakamura, Daiji Miura, Kaoru Kobayashi, Mamoru Ouchida, Kenji Shimizu, Iori Ohmori, Nobuhiro Nishii, Satoshi Nagase, Hiroshi Morita, Yoshiki Hata, Takefumi Oka, Kengo Kusano, Tohru Ohe

CIRCULATION 118 ( 18 ) S981 - S981 2008.10

MECP2遺伝子エキソン1およびプロモーター領域に変異をもつレット症候群

大内田守, 吉永治美, 大守伊織, 大塚頌子, 岡えい次

脳と発達 40 ( Suppl. ) S288 - S288 2008.5

A screening test for the prediction of Dravet syndrome before one year of age Reviewed

Junri Hattori, Mamoru Ouchida, Junko Ono, Susumu Miyake, Satoshi Maniwa, Nobuyoshi Mimaki, Yoko Ohtsuka, Iori Ohmori

EPILEPSIA 49 ( 4 ) 626 - 633 2008.4

Rasmussen encephalitis associated with SCN1A mutation Reviewed

Iori Ohmori, Mamoru Ouchida, Katsuhiro Kobayashi, Yoshimi Jitsumori, Takushi Inoue, Kenji Shimizu, Hideki Matsui, Yoko Ohtsuka, Yoshihiro Maegaki

EPILEPSIA 49 ( 3 ) 521 - 526 2008.3

Development of bionanocapsules targeting brain tumors Reviewed

Yumi Tsutsui, Kazuhito Tomizawa, Mana Nagita, Hiroyuki Michiue, Tei-ichi Nishiki, Iori Ohmori, Masaharu Seno, Hideki Matsui

JOURNAL OF CONTROLLED RELEASE 122 ( 2 ) 159 - 164 2007.9

A Cdk5 inhibitor enhances the induction of insulin secretion by exendin-4 both in vitro and in vivo Reviewed

Kohsuke Kitani, Shigeo Oguma, Tei-Ichi Nishiki, Iori Ohmori, Herve Galons, Hideki Matsui, Laurent Meijer, Kazuhito Tomizawa

JOURNAL OF PHYSIOLOGICAL SCIENCES 57 ( 4 ) 235 - 239 2007.8

Truncations of amphiphysin I by calpain inhibit vesicle endocytosis during neural hyperexcitation Reviewed

Yumei Wu, Shuang Liang, Yoshiya Oda, Iori Ohmori, Tei-Ichi Nishiki, Kohji Takei, Hideki Matsui, Kazuhito Tomizawa

EMBO JOURNAL 26 ( 12 ) 2981 - 2990 2007.6

SCN1A遺伝子変異I1616Tの臨床型

服部旬里, 御牧信義, 大守伊織, 大野順子, 大内田守, 大塚頌子

脳と発達 39 ( Suppl. ) S154 - S154 2007.6

Nonfunctional SCN1A is common in severe myoclonic epilepsy of infancy Reviewed

Iori Ohmori, Kristopher M. Kahlig, Thomas H. Rhodes, Dao W. Wang, Alfred L. George

EPILEPSIA 47 ( 10 ) 1636 - 1642 2006.10

Sodium channel dysfunction in intractable childhood epilepsy with generalized tonic-clonic seizures Reviewed

TH Rhodes, CG Vanoye, Ohmori, I, Ogiwara, I, K Yamakawa, AL George

JOURNAL OF PHYSIOLOGY-LONDON 569 ( 2 ) 433 - 445 2005.12

Mutation screen of GABRA1, GABRB2 and GABRG2 genes in Japanese patients with absence seizures Reviewed

M Ito, Ohmori, I, T Nakahori, M Ouchida, Y Ohtsuka

NEUROSCIENCE LETTERS 383 ( 3 ) 220 - 224 2005.8

Methyl-CpG binding protein 2 gene (MECP2) variations in Japanese patients with Rett syndrome: pathological mutations and polymorphisms Reviewed

T Fukuda, Y Yamashita, S Nagamitsu, K Miyamoto, JJ Jin, I Ohmori, Y Ohtsuka, K Kuwajima, S Endo, T Iwai, H Yamagata, Y Tabara, T Miki, T Matsuishi, Kondo, I

BRAIN & DEVELOPMENT 27 ( 3 ) 211 - 217 2005.4

Relationship between severity of epilepsy and developmental outcome in Angelman syndrome Reviewed

Y Ohtsuka, K Kobayashi, H Yoshinaga, T Ogino, I Ohmori, K Ogawa, E Oka

BRAIN & DEVELOPMENT 27 ( 2 ) 95 - 100 2005.3

Relation between typical and borderline severe myoclonic epilepsy in infancy. Reviewed

Y Ohtsuka, Ohmori, I, T Ogino, K Kobayashi, E Oka

EPILEPSIA 46 11 - 12 2005

EEG in childhood absence epilepsy Reviewed

H Yoshinaga, Y Ohtsuka, K Tamai, Tamura, I, M Ito, Ohmori, I, E Oka

SEIZURE-EUROPEAN JOURNAL OF EPILEPSY 13 ( 5 ) 296 - 302 2004.7

Clinical and electroencephalographic characteristics of children with febrile seizures plus Reviewed

K Kobayashi, Y Ohtsuka, I Ohmori, Y Nishio, M Fujiwara, M Ito, E Oka

BRAIN & DEVELOPMENT 26 ( 4 ) 262 - 268 2004.6

Initiation of treatment and selection of antiepileptic drugs in childhood epilepsy Reviewed

E Oka, T Murakami, T Ogino, T Kobayashi, Ohmori, I, T Akiyama, M Ito

EPILEPSIA 45 17 - 19 2004

Is phenotype difference in severe myoclonic epilepsy in infancy related to SCN1A mutations? Reviewed

Ohmori, I, Y Ohtsukaa, M Ouchida, T Ogino, S Maniwa, K Shimizu, E Oka

BRAIN & DEVELOPMENT 25 ( 7 ) 488 - 493 2003.10

Paroxysmal movement disorders in severe myoclonic epilepsy in infancy Reviewed

Y Ohtsuka, Ohmori, I, T Ogino, M Ouchida, K Shimizu, E Oka

BRAIN & DEVELOPMENT 25 ( 6 ) 401 - 405 2003.9

Significant correlation of the SCN1A mutations and severe myoclonic epilepsy in infancy Reviewed

Ohmori, I, M Ouchida, Y Ohtsuka, E Oka, K Shimizu

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 295 ( 1 ) 17 - 23 2002.7

The relationship between paroxysmal kinesigenic choreoathetosis and epilepsy Reviewed

Ohmori, I, Y Ohtsuka, T Ogino, H Yoshinaga, K Kobayashi, E Oka

NEUROPEDIATRICS 33 ( 1 ) 15 - 20 2002.2

てんかんを伴う結節性硬化症の表現型と遺伝型の関連性 Invited

大守伊織, 大塚頌子, 岡えい次, 濃野勉

てんかん治療研究振興財団研究年報 13 125 - 130 2001.11

A population-based neuroepidemiological survey of West syndrome in Okayama Prefecture, Japan Reviewed

E Oka, N Murakami, Ohmori, I, T Ogino

BRAIN & DEVELOPMENT 23 ( 7 ) 580 - 583 2001.11

Clinical spectrum of epileptic spasms associated with cortical malformation Reviewed

K Kobayashi, Y Ohtsuka, S Ohno, Ohmori, I, T Ogino, H Yoshinaga, A Tanaka, Y Hiraki, E Oka

NEUROPEDIATRICS 32 ( 5 ) 236 - 244 2001.10

Analysis of ictal EEGs of epilepsy associated with tuberous sclerosis Reviewed

Ohmori, I, Y Ohtsuka, S Ohno, E Oka

EPILEPSIA 39 ( 12 ) 1277 - 1283 1998.12

Long-term follow-up of childhood epilepsy associated with tuberous sclerosis Reviewed

Y Ohtsuka, Ohmori, I, E Oka

EPILEPSIA 39 ( 11 ) 1158 - 1163 1998.11

Electroclinical study of localization-related epilepsies in early infancy Reviewed

Ohmori, I, Y Ohtsuka, E Oka, T Akiyama, S Ohtahara

PEDIATRIC NEUROLOGY 16 ( 2 ) 131 - 136 1997.2

Estimation of obscure ictal epileptic activity in scalp EEG Reviewed

Katsuhiro Kobayashi, Tomoyuki Nakahori, Iori Ohmori, Harumi Yoshinaga, Yoko Otsuka, Eiji Oka, Shunsuke Ohtahara

Brain Topography 9 ( 2 ) 125 - 134 1996

　 PREV - NEXT 　

< OHMORI Iori >

Papers - OHMORI Iori