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Faculty of Medicine College Hospital Anesthesiology |
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Assistant Professor |
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Related SDGs |
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KOROKI Satoshi
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Papers 【 display / non-display 】
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Kouroki S., Maruta T., Hidaka K., Koshida T., Kurogi M., Kage Y., Miura A., Nakagawa H., Yanagita T., Takeya R., Tsuneyoshi I.
Plos One 20 ( 5 May ) e0323628 2025.5
Language：English Publishing type：Research paper (scientific journal) Publisher：Plos One
Neuropathic pain has a significant social impact, with high morbidity and reduced productivity, the underlying mechanisms of neuropathic pain remain poorly understood, and effective therapeutic strategies remain elusive. The development of animal models of neuropathic pain that stimulate only the nociceptors and not the other sensory receptors or motor nerves is desirable for elucidating the complex pathogenesis of neuropathic pain. We have previously reported the generation of Na<inf>V</inf>1.7−channelrhodopsin-2 (ChR2), Na<inf>V</inf>1.8−ChR2, and Na<inf>V</inf>1.9−ChR2 mice. Optogenetics was employed in these light-responsive pain mice for generating nociceptive pain by specifically exciting the spinal dorsal root ganglion neurons, in which the respective Na<sup>+</sup> channels are expressed through exposure to blue light. This study aimed to compare the neuropathic pain produced by the prolonged exposure of light-responsive pain mice to blue light. A reversible neuropathic pain state was established persisting for a minimum of 24 hours when each light-responsive pain mouse was irradiated with light of an intensity that consistently elicited pain. Furthermore, the mice also showed pain sensitivity to light irradiation and mechanical stimulation. The expression of c-Fos, a marker for neuronal activity following noxious stimulation, was increased in the dorsal horn of the spinal cord on the light irradiated side. DS-1971a, a selective Na<inf>V</inf>1.7 inhibitor, was effective in attenuating neuropathic pain in all light-responsive pain mice. In conclusion, optogenetics helps elucidate the specific functions of sodium channel subtypes in pain signaling, thereby advancing our understanding and paving the way for the development of further effective treatments for pain disorders in the future.
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Maruta T., Kouroki S., Kurogi M., Hidaka K., Koshida T., Miura A., Nakagawa H., Yanagita T., Takeya R., Tsuneyoshi I.
Journal of Neuroscience Research 102 ( 10 ) e25386 2024.10
Language：English Publishing type：Research paper (scientific journal) Publisher：Journal of Neuroscience Research
Voltage-gated sodium channels, including NaV1.7, NaV1.8, and NaV1.9, play important roles in pain transmission and chronic pain development. However, the specific mechanisms of their action remain unclear, highlighting the need for in vivo stimulation studies of these channels. Optogenetics, a novel technique for targeting the activation or inhibition of specific neural circuits using light, offers a promising solution. In our previous study, we used optogenetics to selectively excite NaV1.7-expressing neurons in the dorsal root ganglion of mice to induce nocifensive behavior. Here, we further characterize the impact of nocifensive behavior by activation of NaV1.7, NaV1.8, or NaV1.9-expressing neurons. Using CRISPR/Cas9-mediated homologous recombination, NaV1.7–iCre, NaV1.8–iCre, or NaV1.9–iCre mice expressing iCre recombinase under the control of the endogenous NaV1.7, NaV1.8, or NaV1.9 gene promoter were produced. These mice were then bred with channelrhodopsin-2 (ChR2) Cre–reporter Ai32 mice to obtain NaV1.7–ChR2, NaV1.8–ChR2, or NaV1.9–ChR2 mice. Blue light exposure triggered paw withdrawal in all mice, with the strongest response in NaV1.8–ChR2 mice. These light sensitivity differences observed across NaV1.x–ChR2 mice may be dependent on ChR2 expression or reflect the inherent disparities in their pain transmission roles. In conclusion, we have generated noninvasive pain models, with optically activated peripheral nociceptors. We believe that studies using optogenetics will further elucidate the role of sodium channel subtypes in pain transmission.
DOI： 10.1002/jnr.25386
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症例報告 胸腺腫による心圧排所見を伴う発作性心房細動に対してランジオロールが奏効した1症例 Reviewed
興梠 聡志, 矢野 武志, 村社 瑞穂, 長嶺 佳弘, 古澤 高廣, 長濵 真澄, 與那覇 哲, 谷口 正彦, 恒吉 勇男
麻酔 72 ( 3 ) 285 - 290 2023.3
Publishing type：Research paper (scientific journal) Publisher：克誠堂出版
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Kouroki S., Maruta T., Tsuneyoshi I.
JA Clinical Reports 8 ( 1 ) 27 2022.12
Language：English Publishing type：Research paper (scientific journal) Publisher：JA Clinical Reports
Background: Cryoprecipitate, which contains fibrinogen and factor VIII in large quantities, is concentrated from fresh frozen plasma, and it has hemostatic effects in severe bleeding. We retrospectively examined the effects of cryoprecipitate on the increase in fibrinogen levels in patients with excessive intraoperative blood loss. Methods: Ninety-seven patients who were administered cryoprecipitate during surgery between June 2014 and May 2019 were enrolled in our study and categorized according to the volume of intraoperative blood loss as follows: group A, 2000–5000 mL; group B, 5000–10,000 mL; group C, > 10,000 mL. Data were extracted from electronic medical records and electronic anesthesia records. The primary endpoint was an increase in the fibrinogen level after the administration of cryoprecipitate. Results: Nine patients with no fibrinogen data and four patients with a bleeding volume of less than 2000 mL were excluded; thus, 84 patients (A: n = 36, B: n = 37, C: n = 11) were evaluated. The mean intraoperative blood loss (mL) in groups A, B, and C were 3348 ± 791, 6688 ± 1225, and 14,281 ± 5142, respectively. The fibrinogen levels (mg/dL) before cryoprecipitate administration in groups A, B, and C were 189 ± 94, 113 ± 42, and 83 ± 29, respectively (p < 0.05 among the groups). The increase in fibrinogen level (mg/dL) after cryoprecipitate administration in group C was significantly greater than that in group A (84 ± 34 versus 50 ± 36, p < 0.01). Conclusions: The results of this study indicate that the effect of cryoprecipitate on the increase in fibrinogen level was most apparent in patients with excessive intraoperative blood loss ≥ 10,000 mL. In addition, most patients with intraoperative blood loss ≥ 5000 mL had fibrinogen levels < 150 mg/dL which improved to ≥ 150 mg/dL after cryoprecipitate administration in approximately 70% of patients. Therefore, cryoprecipitate administration should be considered for patients with hypofibrinogenemia (≤ 150 mg/dL) experiencing severe bleeding (e.g., ≥ 5000 mL) and rapid administration of cryoprecipitate is necessary to maximize the hemostatic effect, especially when the bleeding volume exceeds 10,000 ml.
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Toyoaki Maruta, Kotaro Hidaka, Satoshi Kouroki, Tomohiro Koshida, Mio Kurogi, Yohko Kage, Seiya Mizuno, Tetsuro Shirasaka, Toshihiko Yanagita, Satoru Takahashi, Tyu Takeya, Isao Tsunesyoshi
PLoS One 17 ( 10 ) e0275751 2022.10
Language：English Publishing type：Research paper (scientific journal) Publisher：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.
Presentations 【 display / non-display 】
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選択的血漿交換療法が奏効した抗体陰性視神経脊髄炎の１症例
越田智広，山下幸貴，與那覇 哲，内村修二，興梠聡志，米良 舞
第52回日本集中治療医学会学術集会
Event date： 2025.3.14 - 2025.3.16
Language：Japanese Presentation type：Poster presentation
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光応答性疼痛マウスに持続的な光照射をすることで作製した神経障害性疼痛モデルの検討．
興梠聡志，丸田豊明，日髙康太郎，越田智広，恒吉勇男
第46回日本疼痛学会 2024.11.17
Event date： 2024.11.16 - 2024.11.17
Language：Japanese Presentation type：Oral presentation (general)
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高度肥満が原因で緊急開腹術後に呼吸管理に難渋した１例．
丸田豊明、興梠聡志、米良舞、内村修二、越田智広、與那覇哲、山下幸貴、谷口正彦、恒吉勇男
第39回日本救命医療学会総会・学術集会 2024.9.21
Event date： 2024.9.21
Language：Japanese Presentation type：Oral presentation (general)
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V-V ECMO管理中に胸腔ドレナージを契機とした大量血胸を発症しIVRで止血し得た１例．
山下幸貴，古澤高廣，永田悠紀子，興梠聡志，内村修二,谷口正彦，恒吉勇男
日本集中治療医学会第８回九州支部学術集会 2024.7.27
Event date： 2024.7.27
Language：Japanese Presentation type：Oral presentation (general)
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意識障害が遷延し診断に難渋した持続性副腎不全の１症例．
興梠聡志，與那覇 哲，永田悠紀子，内村修二，古澤高廣，山下幸貴，谷口正彦，恒吉勇男
日本集中治療医学会第８回九州支部学術集会 2024.7.27
Event date： 2024.7.27
Language：Japanese Presentation type：Oral presentation (general)