基本情報
- 所属
- 自治医科大学 医学部総合医学第1講座 教授 (医学博士)救命救急センター長救急部長
- 学位
- 博士(医学)(日本大学)
- 研究者番号
- 50267069
- J-GLOBAL ID
- 200901099931827043
- researchmap会員ID
- 1000313428
研究キーワード
4経歴
6-
2023年1月 - 現在
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2016年4月 - 現在
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2014年11月 - 現在
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2013年2月
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2006年8月
学歴
1-
- 1988年
委員歴
9-
2023年10月 - 現在
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2023年3月 - 現在
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2017年4月 - 現在
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2016年4月 - 現在
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2019年4月
受賞
3-
2008年11月
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2002年8月
主要な論文
125-
BRAIN HYPOTHERMIA: PATHOLOGY, PHARMACOLOGY, AND TREATMENT OF SEVERE BRAIN INJURY 103-108 2000年To evaluate the significance of an electrophysiologic monitoring system during brain hypothermia, we measured the brainstem auditory evoked potentials (BAEPs), somatosensory evoked potentials (SEPs), and topographic electroencephalography (EEG) in 29 critically ill patients (15 with severe head injury and 14 with encephalopathy following cardiopulmonary resuscitation). When the temperature measured in the internal jugular vein fell from 36 degrees C to 33 degrees C, the prolongation of latency in BAEPs was 0.1 +/-: 0.06 ms in wave I, 0.5 +/- 0.23 ms in wave III, and 0.92 +/- 0.86 ms in wave V. In addition, the prolongation of latency in SEPs was 1.2 +/- 0.2 ms in N13 and 2.1 +/- 0.4 ms in N20. The bifrontal fast wave responses, except for those of primary injured lesions, in the topographic EEG were recognized in 9 of 13 patients within 30 min after the injection of midazolam which was used as a sedative. When the temperature fell from 36 degrees C to 33 degrees C, the ratio of the delta and theta waves to the alpha waves recorded from 12 scalp electrodes increased. An electrophysiologic evaluation in critically ill patients should thus be considered an effective real-time monitoring system in patients experiencing brain hypothermia.
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The society for treatment of coma 9 159-161 2000年
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The society for treatment of coma (8) 111-114 1999年
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JOURNAL OF NEUROTRAUMA 11(3) 255-263 1994年6月 査読有りThe role of Ca2+ in cellular injury has received particular attention in studies of acute spinal cord trauma. In this context, the spatial and temporal distribution of extracellular Ca2+ ([Ca2+](e)) may have an important bearing on the development of secondary tissue injury. We therefore studied the spatial-temporal distribution of [Ca2+](e) following moderate (25 g-cm) contusive injury to the rat thoracic (T9-T11) spinal cord. Double-barreled, Ca2+-selective microelectrodes were used to measure the magnitude and time course of [Ca2+](e) at increasing depths from the dorsal spinal cord surface. After 2 h, the tissue was frozen and later analyzed for total Ca concentration using atomic absorption spectroscopy. [Ca2+](e) fell at all depths, but the decrease was maximal at 250 and 500 mu m from the dorsal surface, where, at 0-10 min after injury, [Ca2+](e) averaged 0.09 +/- 0.03 and 0.06 +/- 0.03 mM respectively. By 2 h postinjury, [Ca2+](e) recovered to nearly 1 mM across all depths. Over this time, total tissue calcium concentration ([Ca](t)) was 4.54 +/- 0.16 mu mol/g in injured cords vs 2.75 +/- 0.1 mu mol/g in sham-operated controls. These data place emphasis on the dorsal gray matter as a principal site of ionic derangement in acute spinal cord injury. The implications of these findings are discussed with reference to secondary injury processes.
MISC
59共同研究・競争的資金等の研究課題
8-
日本学術振興会 科学研究費助成事業 2021年4月 - 2026年3月
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日本学術振興会 科学研究費助成事業 2014年4月 - 2018年3月
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日本学術振興会 科学研究費助成事業 2011年 - 2013年
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2006年 - 2008年
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2003年 - 2005年