| Project/Area Number |
08670874
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pediatrics
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| Research Institution | Nagoya University |
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Principal Investigator |
MORISHIMA Tsuneo School of Medicine, Nagoya University, Professor, 医学部, 教授 (90157892)
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| Co-Investigator(Kenkyū-buntansha) |
KIMURA Hiroshi School of Medicine, Assistant, 医学部, 助手 (30303621)
糸州 朝久 名古屋大学, 医学部, 医員
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| Project Period (FY) |
1996 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1998: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1997: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1996: ¥900,000 (Direct Cost: ¥900,000)
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| Keywords | acute encephalitis / acute encephalopathy / interferon-gamma / PCR / herpes simplex virus / influenza / Epstein-Barr virus / IL-6 / インフルエンザウィルス / 単純ヘルペス脳炎 / インフルエンザ |
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| Research Abstract |
The aim of this study has been to establish the diagnostic techniques in terms of early diagnosis of acute encephalitis using polymerase chain reaction (PCR) and to clarify the mechanism of brain damage during the course of illness.
(1) Herpes simplex encephalitis (HSE)
We established nested PCR assay for the early diagnosis of HSE patients. The sensitivity of PCR assay was same as that of brain biopsy, which has been a golden standard method of diagonsis in HSE.The PCR assay is also useful for monitoring the response to antiviral therapy. We also revealed that relapse of HSE could be related to the total dose and the duration of antiviral agent.
(2) In chroaic active EBV infections, calcification of basal ganglia was found frequently. We found that EBV-infected natural killer cells and hyper cytokinemia (IFN-gamma and TNF-alpha) play important roles in the pathogenesis of calcification.
(3) In 1996-1998 winter seasons, many cases with influenza-associated encephalopathy were reported among children (under l5yrs) . Several cytokines, particullariy, IL-6 may play a important role in the pathogenesis of brain damage.
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