基本情報
- 所属
- 自治医科大学 医学部内科学講座 神経内科学部門 教授
- 学位
- 医学博士(新潟大学)
- J-GLOBAL ID
- 201501013641767523
- researchmap会員ID
- B000248143
Medical School-Tokyo Medical University, M.D., 1985-1991
Medical School-Graduate School-Niigata University School of Medicine, Ph.D., 1996-2000
Medical School-Graduate School-Niigata University School of Medicine, Ph.D., 1996-2000
研究分野
1論文
147-
MOVEMENT DISORDERS 22(6) 857-862 2007年4月 査読有り
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ANNALS OF NEUROLOGY 61(1) 25-36 2007年1月 査読有り
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JOURNAL OF NEURO-ONCOLOGY 81(1) 71-74 2007年1月 査読有り
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JOURNAL OF NEURO-OPHTHALMOLOGY 24(3) 273-273 2004年9月 査読有り
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Brain and Nerve 56(1) 77-81 2004年1月 査読有り
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Brain and Nerve 55(5) 443-447 2003年5月1日 査読有り
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No to shinkei = Brain and nerve 55(4) 374-375 2003年4月 査読有り
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No to shinkei = Brain and nerve 54(10) 912-913 2002年10月 査読有り
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ACTA NEUROLOGICA SCANDINAVICA 106(2) 113-116 2002年8月 査読有り
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JOURNAL OF NEUROSCIENCE RESEARCH 68(4) 442-448 2002年5月 査読有り
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ARCHIVES OF NEUROLOGY 59(4) 623-629 2002年4月 査読有り
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No to shinkei = Brain and nerve 54(1) 64-65 2002年1月 査読有り
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Brain and Nerve 53(6) 575-579 2001年 査読有り
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NATURE GENETICS 26(1) 29-36 2000年9月 査読有り
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ACTA NEUROPATHOLOGICA 99(3) 331-336 2000年3月 査読有り
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Clinical Neurology 40(6) 600-604 2000年 査読有り
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NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY 25(5) 363-368 1999年10月 査読有り
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HUMAN MOLECULAR GENETICS 8(11) 2047-2053 1999年10月 査読有り
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NEUROGENETICS 2(3) 189-190 1999年9月 査読有り
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NEUROSCIENCE LETTERS 270(2) 110-112 1999年7月 査読有り
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HUMAN MOLECULAR GENETICS 8(6) 997-1006 1999年6月 査読有り
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Human Molecular Genetics 8(1) 99-106 1999年 査読有り
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ACTA NEUROPATHOLOGICA 96(6) 547-552 1998年12月 査読有り
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AMERICAN JOURNAL OF HUMAN GENETICS 63(4) 1060-1066 1998年10月 査読有り
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NATURE GENETICS 18(2) 111-117 1998年2月 査読有り
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NATURE GENETICS 18(2) 111-117 1998年2月 査読有り
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ANNALS OF NEUROLOGY 42(6) 879-884 1997年12月 査読有り
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NEUROLOGY 49(6) 1605-1612 1997年12月 査読有り
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NATURE GENETICS 14(3) 277-284 1996年11月 査読有り
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JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY 61(1) 113-114 1996年7月 査読有り
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AMERICAN JOURNAL OF HUMAN GENETICS 58(6) 1212-1222 1996年6月 査読有り
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AMERICAN JOURNAL OF HUMAN GENETICS 58(4) 730-733 1996年4月 査読有り
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No to shinkei = Brain and nerve 48(4) 323-328 1996年4月 査読有り
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Japanese Journal of Human Genetics 41(1) 33 1996年
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ANNALS OF NEUROLOGY 37(6) 769-775 1995年6月 査読有り
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SEMINARS IN CELL BIOLOGY 6(1) 37-44 1995年2月 査読有り
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Clinical Neurology 35(2) 201-203 1995年 査読有り
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CLINICAL NEUROSCIENCE 3(1) 23-27 1995年 査読有り
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LANCET 344(8938) 1711-1712 1994年12月 査読有り
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NATURE GENETICS 6(1) 9-13 1994年1月 査読有り
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Rinsho shinkeigaku = Clinical neurology 33(8) 909-911 1993年8月 査読有り
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JAPANESE JOURNAL OF CLINICAL ONCOLOGY 14(1) 107-113 1984年 査読有り
MISC
50-
Journal of thrombosis and thrombolysis 49(4) 681-684 2020年5月Cerebral amyloid angiopathy-related inflammation is a syndrome of reversible encephalopathy with cerebral amyloid angiopathy, however the pathology is not well understood. We clear a part of the pathology through the first case of an 80-year-old man with cerebral amyloid angiopathy-related inflammation induced by relapsing polychondritis (RP) analysis. An 80-year-old man was diagnosed with RP by auricular cartilage biopsy. Almost no abnormality including intracranial microbleeding was detected by cranial magnetic resonance image (MRI) at diagnosis. However, he developed a headache and hallucination after five months. Seven-month cranial MRI showed novel, multiple, intracranial microbleeding, especially in the bilateral but asymmetry posterior, temporal, and parietal lobes. 123I-N-isopropyl-p-iodoamphetamine single-photon emission computed tomography showed increased cerebral blood flow in the bilateral posterior lobes. After treatment, both of his neurological symptoms and increased cerebral blood flow improved to mild. Photon emission computed tomography using Pittsburgh compound B (PiB) for evaluation of brain amyloidosis at 12 months after onset showed an amyloid deposit in the bilateral frontal lobes, but a lack of uptake corresponded to the RP lesions. Our case suggests that inflammation coupled with an amyloid deposit, induced the multiple intracranial bleeding, and resulted in the lack of PiB uptake. Findings from our case show that inflammation including excess blood flow coupled with an amyloid deposit synergistically facilitate intracranial bleeding.
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Journal of obstetrics and gynaecology : the journal of the Institute of Obstetrics and Gynaecology 40(1) 135-136 2020年1月
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Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association 27(7) e132-e134 2018年7月Some stroke patients with the acute aortic dissection receiving thrombolysis treatment resulted in fatalities. Thus, the concurrent acute aortic dissection is the contraindication for the intravenous recombinant tissue-type plasminogen activator. However, the safety and the effectiveness of the intravenous recombinant tissue-type plasminogen activator therapy are not known in patients with stroke some days after acute aortic dissection treatment. Here, we first report a case of a man with a cardioembolism due to the nonvalvular atrial fibrillation, who received the intravenous recombinant tissue-type plasminogen activator therapy 117 days after the traumatic Stanford type A acute aortic dissection operation. Without the intravenous recombinant tissue-type plasminogen activator therapy, the prognosis was expected to be miserable. However, the outcome was good with no complication owing to the intravenous recombinant tissue-type plasminogen activator therapy. Our case suggests the effectiveness and the safety of the intravenous recombinant tissue-type plasminogen activator therapy to the ischemic stroke some days after acute aortic dissection treatment.