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医学部 附属病院 麻酔科 |
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透析用バスキュラーアクセスカテーテルが上行腰静脈に迷入し腸腰筋血腫を呈した1症例 査読あり
古澤 高廣, 矢野 武志, 菓子野 里奈, 吉海 瑞穂, 越田 智広, 與那覇 哲, 谷口 正彦, 恒吉 勇男
日本集中治療医学会雑誌 30 ( 1 ) 23 - 24 2023年1月
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Maruta T., Hidaka K., Kouroki S., Koshida T., Kurogi M., Kage Y., Mizuno S., Shirasaka T., Yanagita T., Takahashi S., Takeya R., Tsuneyoshi I.
PLoS ONE 17 ( 10 October ) e0275751 2022年10月
記述言語：英語 掲載種別：研究論文（学術雑誌） 出版者・発行元：PLoS ONE
In small and large spinal dorsal root ganglion neurons, subtypes of voltage-gated sodium channels, such as NaV1.7, NaV1.8, and NaV1.9 are expressed with characteristically localized and may play different roles in pain transmission and intractable pain development. Selective stimulation of each specific subtype in vivo may elucidate its role of each subtype in pain. So far, this has been difficult with current technology. However, Optogenetics, a recently developed technique, has enabled selective activation or inhibition of specific neural circulation in vivo. Moreover, optogenetics had even been used to selectively excite NaV1.8-expressing dorsal root ganglion neurons to induce nocifensive behavior. In recent years, genetic modification technologies such as CRISPR/Cas9 have advanced, and various knock-in mice can be easily generated using such technology. We aimed to investigate the effects of selective optogenetic activation of NaV1.7-expressing afferents on mouse behavior. We used CRISPR/Cas9-mediated homologous recombination to generate bicistronic NaV1.7–iCre knock-in mice, which express iCre recombinase under the endogenous NaV1.7 gene promoter without disrupting NaV1.7. The Cre-driver mice were crossed with channelrhodopsin-2 (ChR2) Cre-reporter Ai32 mice to obtain NaV1.7iCre/+;Ai32/+, NaV1.7iCre/iCre;Ai32/+, NaV1.7iCre/+;Ai32/Ai32, and NaV1.7iCre/iCre;Ai32/Ai32 mice. Compared with wild–type mice behavior, no differences were observed in the behaviors associated with mechanical and thermal stimuli exhibited by mice of the aforementioned genotypes, indicating that the endogenous NaV1.7 gene was not affected by the targeted insertion of iCre. Blue light irradiation to the hind paw induced paw withdrawal by mice of all genotypes in a light power-dependent manner. The threshold and incidence of paw withdrawal and aversive behavior in a blue-lit room were dependent on ChR2 expression level; the strongest response was observed in NaV1.7iCre/iCre;Ai32/Ai32 mice. Thus, we developed a non-invasive pain model in which peripheral nociceptors were optically activated in free-moving transgenic NaV1.7–ChR2 mice.
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Hidaka K., Maruta T., Koshida T., Kurogi M., Kage Y., Kouroki S., Shirasaka T., Takeya R., Tsuneyoshi I.
Molecular Pain 18 17448069221089784 2022年3月
記述言語：英語 掲載種別：研究論文（学術雑誌） 出版者・発行元：Molecular Pain
Pulsed radiofrequency (PRF) therapy is one of the most common treatment options for neuropathic pain, albeit the underlying mechanism has not been hitherto elucidated. In this study, we investigated the efficacy and mechanism of PRF therapy on resiniferatoxin (RTX)-induced mechanical allodynia, which has been used as a model of postherpetic neuralgia (PHN). Adult male rats were intraperitoneally injected with a vehicle or RTX. Furthermore, PRF current was applied on a unilateral sciatic nerve in all RTX-treated rats. On both ipsilateral and contralateral sides, the paw mechanical withdrawal thresholds were examined and L4-6 dorsal root ganglia (DRG) were harvested. In the DRG of rats with RTX-induced mechanical allodynia, NaV1.7, a voltage-gated Na+ channel, was upregulated following the enhancement of extracellular signal-regulated kinase phosphorylation. Early PRF therapy, which was applied 1 week after RTX exposure, suppressed this NaV1.7 upregulation and showed an anti-allodynic effect; however, late PRF therapy, which was applied after 5 weeks of RTX exposure, failed to inhibit allodynia. Interestingly, late PRF therapy became effective after daily tramadol administration for 7 days, starting from 2 weeks after RTX exposure. Both early PRF therapy and late PRF therapy combined with early tramadol treatment suppressed NaV1.7 upregulation in the DRG of rats with RTX-induced mechanical allodynia. Therefore, NaV1.7 upregulation in DRG is related to the development of RTX-induced neuropathic pain; moreover, PRF therapy may be effective in the clinical management of patients with PHN via NaV1.7 upregulation inhibition.
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Upregulation of ERK phosphorylation in rat dorsal root ganglion neurons contributes to ozaliplatin-induced chronic neuropathic pain. 査読あり
Toyoaki Maruta, Takayuki Nemoto, Koutaro Hidaka, Tomohiro Koshida, Tetsuro Shirasaka, Toshihiko Yanagita, Ryu Takeya Isao Tsuneyoshi
PLoS ONE 14 ( 11 ) e0225586 2019年11月
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低体温療法中の小児の気管チューブ固定にアンカーファストを使用した経験 査読あり
矢野 武志, 宮里 岳志, 長濱 真澄, 越田 智広, 長野 健彦, 與那覇 哲, 押川 満雄, 谷口 正彦, 白阪 哲朗, 恒吉 勇男
麻酔 63 ( 1 ) 84 - 87 2014年1月
記述言語：日本語 掲載種別：研究論文（学術雑誌）
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帯状疱疹後神経痛モデルラットにおける高周波パルス療法の作用機序の検討．
日髙康太郎，丸田豊明，越田智広，興梠聡志，白阪哲朗，恒吉勇男
第43回日本疼痛学会
開催年月日： 2021年12月10日 - 2021年12月11日
記述言語：日本語 会議種別：口頭発表（一般）
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ECMOの抗凝固剤としてナファモスタットを使用したHIT抗体陽性COVID-19肺炎の１症例（優秀演題）．
與那覇 哲，村社瑞穂，深尾麻由，古澤高廣，越田智広，矢野武志，山下幸貴，谷口正彦，恒吉勇男
日本集中治療医学会第５回九州支部学術集会
開催年月日： 2021年7月24日
記述言語：日本語 会議種別：口頭発表（一般）
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NutriVentTMを使用し呼吸管理を行った侵襲性肺アスペルギルス症の一例．
村社瑞穂，與那覇 哲，深尾麻由，古澤高廣，越田智広，矢野武志，山下幸貴，谷口正彦
日本集中治療医学会第５回九州支部学術集会
開催年月日： 2021年7月24日
記述言語：日本語 会議種別：口頭発表（一般）
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レシニフェラトキシン誘発性疼痛ラットでのトラマドール治療後の高周波パルス療法の有効性と作用機序の検討（優秀演題）．
日髙康太郎，丸田豊明，門田瑶子，興梠聡志，越田智広，渡部由美，山賀昌治，恒吉勇男
日本ペインクリニック学会第55回大会
開催年月日： 2021年7月22日 - 2021年7月24日
記述言語：日本語 会議種別：口頭発表（一般）
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オプトジェネティクスを用いた末梢神経疼痛モデル動物の開発
丸田豊明，越田智広，日髙康太郎，黒木未央，白阪哲朗，恒吉勇男
第42回日本疼痛学会 (Web開催) 日本疼痛学会
開催年月日： 2020年12月
記述言語：日本語 会議種別：口頭発表（一般）
開催地：Web開催