ISHII Takao

写真a

Affiliation

School of Health Science, Department of Occupational Therapy, Second Division of Occupational Therapy

Job title

Professor
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Research Experience 【 display / non-display 】

  • 2022.07
    -
    Now

    Sapporo Medical University   School of Health Sciences Department of Occupational Therapy   教授

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Research Areas 【 display / non-display 】

  • Life sciences   Psychiatry  

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Affiliation 【 display / non-display 】

  • Sapporo Medical University   School of Health Sciences Department of Occupational Therapy   教授  

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Research Interests 【 display / non-display 】

  • 気分障害

  • コンサルテーション・リエゾン精神医学

  • 精神腫瘍学

  • 慢性疼痛

  • 精神薬理学

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Papers 【 display / non-display 】

  • 【救命救急センターに搬送される自殺企図者に対する精神科医の役割】自殺企図で救命救急センターに搬送される重症患者の臨床的特徴と対応

    石井 貴男, 佐野 智章, 大江 開, 河西 千秋

    精神神経学雑誌 ( (公社)日本精神神経学会 )  125 ( 10 ) 876 - 882  2023.10

    　View Summary

    身体的に重症な状態で救急医療部門に搬入される自殺企図患者は,縊頸や高所墜落などの致死的な自殺企図手段を選択していることが多い.自殺のリスク因子は多数知られているが,最も強力な自殺リスク因子は,自殺未遂などの自損行為の既往であり,自殺企図を繰り返すごとに致死性の高い方法になるといわれている.そのため,自殺予防の観点からも,自殺未遂者に適切な介入を行うことの重要性を示す根拠にもなっている.著者らが所属する札幌医科大学附属病院は,北海道で唯一の高度救命救急センターを有している.搬入される自殺企図患者は,身体的に重症な患者が多く,自殺既遂が半数以上を占める.2016年度から2020年度までに搬入された自殺企図患者の特徴をみてみると,性別は既存の報告と同様に,自殺既遂の比率は男性のほうが高く,自殺未遂の比率は女性のほうが高い傾向がみられた.自殺企図の手段に関しては,男女とも縊頸が最多で,高所墜落が続いた.ほぼ全例で精神疾患の診断基準を満たし,男女ともICD-10の分類でF3(気分障害)が最多で全体の42%を占めていた.「自殺企図の再発防止に対する複合的ケース・マネージメントの効果-多施設共同による無作為化比較試験-」(ACTION-J研究)で開発された継続的なケース・マネージメント介入が,「自殺企図後の患者に対する継続的な指導の評価(救急患者精神科継続支援料)」として2016年に診療報酬化された.札幌医科大学附属病院神経精神科では,いち早くこの救急患者継続支援を臨床に導入した.2016年度から2020年度の5年間に58名の自殺企図患者に対して介入を行ったが,介入後6ヵ月の時点で自殺再企図はみられなかった.このように身体的に重症な自殺企図患者が多く搬入される当施設でも,ケース・マネージメント介入が実装可能であることが示された.今後も症例数を増やして検討を進めていきたい.(著者抄録)

  • Reduced sociability in a prenatal immune activation model: Modulation by a chronic blonanserin treatment through the amygdala-hippocampal axis.

    Kenta Deriha, Eri Hashimoto, Wataru Ukai, Francesca Marchisella, Emi Nishimura, Hanako Hashiguchi, Masaya Tayama, Takao Ishii, Marco A Riva, Chiaki Kawanishi

    Journal of psychiatric research   164   209 - 220  2023.08  [International journal]

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    The environmental disturbances in a critical neurodevelopmental period exert organizational effects on brain intrinsic plasticity including excitatory and inhibitory (E/I) neurotransmission those can cause the onset of psychiatric illness. We previously reported that treatment of neural precursor cells with N-methyl-D-aspartate (NMDA) receptor antagonist MK-801 induced reduction of GABAergic interneuron differentiation, and these changes recovered by atypical antipsychotic blonanserin treatment in vitro. However, it remains unclear how this treatment affects neural circuit changes in hippocampus and amygdala, which might contribute to the prevention of onset process of schizophrenia. To elucidate the pathogenic/preventive mechanisms underlying prenatal environmental adversity-induced schizophrenia in more detail, we administered poly (I:C) followed by antipsychotics and examined alterations in social/cognitive behaviors, GABA/glutamate-related gene expressions with cell density and E/I ratio, and brain-derived neurotrophic factor (Bdnf) transcript levels, particularly in limbic areas. Treatment with antipsychotic blonanserin ameliorated impaired social/cognitive behaviors and increased parvalbumin (PV)-positive (+) cell density and its mRNA levels as well as Bdnf with long 3'UTR mRNA levels, particularly in the dorsal hippocampus, in rats exposed to maternal immune activation (MIA). Low dose of blonanserin and haloperidol altered GABA and glutamate-related mRNA levels, the E/I ratio, and Bdnf long 3'UTR mRNA levels in the ventral hippocampus and amygdala, but did not attenuate behavioral impairments. These results strongly implicate changes in PV expression, PV(+) GABAergic interneuron density, and Bdnf long 3'UTR expression levels, particularly in the dorsal hippocampus, in the pathophysiology and treatment responses of MIA-induced schizophrenia and highlight the therapeutic potential of blonanserin for developmental stress-related schizophrenia.

    DOI PubMed

  • Implementations of an evidence‐based assertive case management intervention for suicide attempters: Post‐ACTION‐J Study (PACS)

    Takao Ishii, Naohiro Yonemoto, Yasushi Otaka, Kazuya Okamura, Noa Tsujii, Kotaro Otsuka, Reiji Yoshimura, Toshihiko Kinoshita, Daisuke Fujisawa, Hirokazu Tachikawa, Mitsuhiko Yamada, Yusuke Tsuyama, Satoshi Hashimoto, Chiaki Kawanishi

    Psychiatry and Clinical Neurosciences Reports    2023.06

    DOI

  • Identification of epigenetically active L1 promoters in the human brain and their relationship with psychiatric disorders.

    Risa Watanabe, Yutaka Nakachi, Hikari Matsubara, Junko Ueda, Takao Ishii, Wataru Ukai, Eri Hashimoto, Kiyoto Kasai, Siro Simizu, Tadafumi Kato, Miki Bundo, Kazuya Iwamoto

    Neuroscience research    2023.05  [International journal]

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    Long interspersed nuclear element-1 (LINE-1, L1) affects the transcriptome landscape in multiple ways. Promoter activity within its 5'UTR plays a critical role in regulating diverse L1 activities. However, the epigenetic status of L1 promoters in adult brain cells and their relationship with psychiatric disorders remain poorly understood. Here, we examined DNA methylation and hydroxymethylation of the full-length L1s in neurons and nonneurons and identified "epigenetically active" L1s. Notably, some of epigenetically active L1s were retrotransposition competent, which even had chimeric transcripts from the antisense promoters at their 5'UTRs. We also identified differentially methylated L1s in the prefrontal cortices of patients with psychiatric disorders. In nonneurons of bipolar disorder patients, one L1 was significantly hypomethylated and showed an inverse correlation with the expression level of the overlapping gene NREP. Finally, we observed that altered DNA methylation levels of L1 in patients with psychiatric disorders were not affected by the surrounding genomic regions but originated from the L1 sequences. These results suggested that altered epigenetic regulation of the L1 5'UTR in the brain was involved in the pathophysiology of psychiatric disorders.

    DOI PubMed

  • 統合失調症の社会性認知機能障害の脳基盤解析 Glutamate/GABAニューロンバランスメカニズムからの検討

    出利葉 健太, 鵜飼 渉, Riva Marco, 西村 恵美, 橋本 恵理, 木川 昌康, 橋口 華子, 古瀬 研吾, 田山 真矢, 村山 友規, 石井 貴男, 河西 千秋

    日本神経精神薬理学会年会・日本生物学的精神医学会年会・日本精神薬学会総会・学術集会合同年会プログラム・抄録集 ( 日本神経精神薬理学会・日本生物学的精神医学会・日本精神薬学会 )  50回・42回・4回   189 - 189  2020.08

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Misc 【 display / non-display 】

  • 自殺未遂者へのアサーティヴ・ケースマネジメントの実装 多施設共同コホート研究

    石井 貴男, 米本 直裕, 大高 靖史, 岡村 和哉, 辻井 農亜, 大塚 耕太郎, 吉村 玲児, 木下 利彦, 藤澤 大介, 太刀川 弘和, 山田 光彦, 津山 雄亮, 橋本 聡, 河西 千秋

    総合病院精神医学 ( (一社)日本総合病院精神医学会 )  35 ( Suppl. ) S - 166  2023.11

  • 自殺未遂者へのアサーティヴ・ケースマネジメントの実装 多施設共同コホート研究

    石井 貴男, 米本 直裕, 大高 靖史, 岡村 和哉, 辻井 農亜, 大塚 耕太郎, 吉村 玲児, 木下 利彦, 藤澤 大介, 太刀川 弘和, 山田 光彦, 津山 雄亮, 橋本 聡, 河西 千秋

    総合病院精神医学 ( (一社)日本総合病院精神医学会 )  35 ( Suppl. ) S - 166  2023.11

  • 難治性精神疾患と周産期メンタルヘルス異常の病態・治療法探索 漢方薬と幹細胞を用いた社会性/共感性の行動・脳神経回路変動の解析

    鵜飼 渉, 出利葉 健太, 西村 恵美, 橋本 恵理, 山田 美佐, 橋口 華子, 廣瀬 奨真, 望月 真里菜, 桃木 幸彦, 古瀬 研吾, 石井 貴男, リーバ・マルコ, 河西 千秋

    日本神経精神薬理学会年会プログラム・抄録集 ( (一社)日本神経精神薬理学会 )  53回   151 - 151  2023.09

  • 発達期環境ストレス誘発統合失調症の病態生理の探索 抗精神病薬によるパルブアルブミン陽性細胞変異に焦点を当てた発症予防法開発を目指す試み

    出利葉 健太, 鵜飼 渉, 西村 恵美, 橋本 恵理, 橋口 華子, 廣瀬 奨真, 望月 真里菜, 桃木 幸彦, 古瀬 研吾, 石井 貴男, Riva Marco A., 河西 千秋

    日本神経精神薬理学会年会プログラム・抄録集 ( (一社)日本神経精神薬理学会 )  53回   153 - 153  2023.09

  • 性欲の異常亢進と誤診されていたrestless genital syndromeの1例

    廣瀬 奨真, 大江 開, 野呂 孝徳, 石井 貴男, 河西 千秋

    精神神経学雑誌 ( (公社)日本精神神経学会 )  124 ( 12 ) 894 - 894  2022.12

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Research Projects 【 display / non-display 】

  • 血小板のBDNF放出能の変化に着目した慢性疼痛とうつ病のバイオマーカー開発

    基盤研究(C)

    Project Year :

    2022.04
    -
    2025.03
     

    石井 貴男

  • Recovery of occupational functions in schizophrenia: significance of empathy behavior enhancement by synchronizer neuron activation

    Grant-in-Aid for Scientific Research (C)

    Project Year :

    2022.04
    -
    2025.03
     

    鵜飼 渉, 仲地 ゆたか, 橋本 恵理, 石井 貴男, 館農 勝, 森元 隆文

  • Neural basis of recovery of social cognitive impairment in mental disorder: significance of enhancing for synchronizer neurons

    Grant-in-Aid for Scientific Research (C)

    Project Year :

    2019.04
    -
    2022.03
     

    Ukai Wataru

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    First, we used animal model of schizophrenia produced by exposing rats to poly (I:C) during fetal period. We showed that treatment with a drug that has been reported to improve occupational and social dysfunction in schizophrenic patients in clinical practice recovered social behavior deficits in this model, involving the mechanism of increase in the number of parvalbumin (PV)-positive cells in the hippocampus and amygdala. Next, we conducted analysis of the molecular changes in the social/cognitive recovery, and found that treatment with the therapeutic drug increased PV and Bdnf long 3'UTR mRNA levels in the dorsal hippocampus, and that these were strongly implicated in the onset, pathogenesis, and treatment response of developmental stress-related schizophrenia.

  • Social function recovery in schizophrenia: brain mechanism of empathy/concerning function using stem cells and oxytocin

    Grant-in-Aid for Scientific Research (C)

    Project Year :

    2014.04
    -
    2017.03
     

    Ukai Wataru, Iwamoto Kazuya, Morimoto Takafumi

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    First, we analyzed the social functioning behavior of model animals administered with stem cells and the distribution of cells in the brain. We detected that the patient-derived stem cells was difficult to become GAD67 and Parvalbumin-positive GABA interneurons in the brain after administration, and social interaction behavior was decreased in the patient-derived stem cell administered group compared to the control and healthy-derived stem cell administered group. Next, the synapse forming ability of the GABAergic interneuron was analyzed by the actin motility of the precursor structure filopodia, and found the reduction of the filopodia movement in the patient-derived cells. We also found that the possibility of the influence of decreased expression of the transcription factor TBX1 against it.

  • The develpoment of biological marker for alcohol-induced mood disorders: focusing on the functional alteration of platelet and neural stem cell

    Grant-in-Aid for Scientific Research (C)

    Project Year :

    2013.04
    -
    2016.03
     

    ISHII Takao, HASHIMOTO ERI, MATSUYAMA KIYOJI, UKAI WATARU, SOUMA HITOSHI

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    In this study, we investigated the common pathophysiology of alcohol-induced brain damage and mood disorders, focusing on the functional alteration of platelet and neural stem cell. We examine the effects of ethanol and antidepressants on the platelet BDNF release. Ethanol suppressed platelet BDNF release and the promotive effect of antidepressant on BDNF release. Furthermore, we investigated the transfer of BDNF derived from serum (or platelet) to the brain using fluorescent-labeled BDNF. We have detected BDNF-FITC in the cells at dentate gyrus in the hippocampus in which adult neurogenesis occurs.

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