○種別 (必須): | □ | 学術論文 (審査論文)
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○言語 (必須): | □ | 英語
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○招待 (推奨): |
○審査 (推奨): |
○カテゴリ (推奨): |
○共著種別 (推奨): |
○学究種別 (推奨): |
○組織 (推奨): | 1. | 徳島大学.工学部.電気電子工学科.電気電子システム講座
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| 2. | 徳島大学.医学部
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○著者 (必須): | 1. | 池原 敏孝 ([徳島文理大学])
○役割 (任意): |
○貢献度 (任意): |
○学籍番号 (推奨): |
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| 2. | 朴 基豪 (University of Medicine and Dentistry of New Jersey)
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○貢献度 (任意): |
○学籍番号 (推奨): |
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| 3. | 山口 久雄 ([徳島文理大学])
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○貢献度 (任意): |
○学籍番号 (推奨): |
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| 4. | 細川 敬子
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○学籍番号 (推奨): |
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| 5. | 吉﨑 和男
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| 6. | 宮本 博司 ([徳島文理大学])
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○貢献度 (任意): |
○学籍番号 (推奨): |
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| 7. | (英) Aizawa Katsuo (日) 會沢 勝夫 (読) あいざわ かつお
○役割 (任意): |
○貢献度 (任意): |
○学籍番号 (推奨): |
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| 8. | 木内 陽介
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○題名 (必須): | □ | (英) Effects on Rb+(K+) Uptake of HeLa Cells in a High K+ Medium of Exposure to a Switched 1.7 Tesla Magnetic Field (日)
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○副題 (任意): |
○要約 (任意): | □ | (英) Effects of a switched, time-varying 1.7 T magnetic field on Rb(+)(K+) uptake by HeLa S3 cells incubated in an isosmotic high K(+) medium were examined. The magnetic flux density was varied intermittently from 0.07-1.7 T at an interval of 3 s. K(+) uptake was activated by replacement of normal medium by high K(+) medium. A membrane-permeable Ca(2+) chelating agent (BAPTA-AM) and Ca(2+)-dependent K(+) channel inhibitors (quinine, charibdotoxin, and iberiotoxin) were found to reduce the Rb(+)(K+) uptake by about 30-40%. Uptake of K(+) that is sensitive to these drugs is possibly mediated by Ca(2+)-dependent K(+) channels. The intermittent magnetic field partly suppress ed the drug-sensitive K(+) uptake by about 30-40% (P < 0.05). To test the mechanism of inhibition by the magnetic fields, intracellular Ca(2+) concentration ([Ca(2+)]c) was measured using Fura 2-AM. When cells were placed in the high K(+) medium, [Ca(2+)]c increased to about 1.4 times the original level, but exposure to the magnetic fields completely suppressed the increase (P < 0.01). Addition of a Ca(2+) ionophore (ionomycin) to the high K(+) medium increased [Ca(2+)]c to the level of control cells, regardless of exposure to the magnetic field. But the inhibition of K(+) uptake by the magnetic fields was not restored by addition of ionomycin. Based on our previous results on magnetic field-induced changes in properties of the cell membrane, these results indicate that exposure to the magnetic fields partly suppresses K(+) influx, which may be mediated by Ca(2+)-dependent K(+) channels. The suppress ion of K(+) fluxes could relate to a change in electric properties of cell surface and an inhibition of Ca(2+) influx mediated by Ca(2+) channels of either the cell plasma membrane or the inner vesicular membrane of intracellular Ca(2+) stores. (日)
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○キーワード (推奨): | 1. | カルシウム (calcium)
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| 2. | (英) Cell Membrane (日) (読)
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| 3. | (英) Charybdotoxin (日) (読)
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| 4. | (英) Chelating Agents (日) (読)
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| 5. | (英) Culture Media (日) (読)
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| 6. | (英) Egtazic Acid (日) (読)
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| 7. | (英) Electromagnetic Fields (日) (読)
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| 8. | 電気生理学 (electrophysiology)
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| 9. | (英) Environmental Exposure (日) (読)
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| 10. | (英) Fluorescent Dyes (日) (読)
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| 11. | (英) Fura-2 (日) (読)
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| 12. | (英) HeLa Cells (日) (読)
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| 13. | (英) Humans (日) (読)
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| 14. | (英) Intracellular Membranes (日) (読)
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| 15. | (英) Ionomycin (日) (読)
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| 16. | (英) Ionophores (日) (読)
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| 17. | (英) Magnetics (日) (読)
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| 18. | (英) Peptides (日) (読)
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| 19. | カリウム (potassium)
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| 20. | (英) Potassium Channel Blockers (日) (読)
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| 21. | (英) Potassium Channels (日) (読)
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| 22. | (英) Quinine (日) (読)
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| 23. | (英) Rubidium (日) (読)
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○発行所 (推奨): |
○誌名 (必須): | □ | Bioelectromagnetics ([The Bioelectromagnetics Society])
(pISSN: 0197-8462, eISSN: 1521-186X)
○ISSN (任意): | □ | 0197-8462
ISSN: 0197-8462
(pISSN: 0197-8462, eISSN: 1521-186X) Title: BioelectromagneticsTitle(ISO): BioelectromagneticsSupplier: Bioelectromagnetics SocietyPublisher: Wiley (NLM Catalog)
(Wiley)
(Scopus)
(CrossRef)
(Scopus information is found. [need login])
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○巻 (必須): | □ | 21
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○号 (必須): | □ | 3
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○頁 (必須): | □ | 228 237
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○都市 (任意): |
○年月日 (必須): | □ | 西暦 2000年 4月 10日 (平成 12年 4月 10日)
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○URL (任意): |
○DOI (任意): |
○PMID (任意): | □ | 10723022 (→Scopusで検索)
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○備考 (任意): | 1. | (英) Article.PublicationTypeList.PublicationType: Journal Article (日)
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| 2. | (英) Article.PublicationTypeList.PublicationType: Research Support, Non-U.S. Gov't (日)
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