| Project/Area Number |
08670648
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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 |
Respiratory organ internal medicine
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| Research Institution | Akita University |
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Principal Investigator |
SHIOYA Takanobu Akita University, College of Allied Medical Science, Professor, 医療技術短期大学部, 教授 (90170852)
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| Co-Investigator(Kenkyū-buntansha) |
SASAKI Masahiro Akita University, School of Medicine, Lecturer, 医学部, 講師 (20221278)
黒川 博一 秋田大学, 医学部, 助手 (50234589)
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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: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1997: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1996: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | Neurogenic inflammation / autonomic receptor / Bronchial hyperresponsiveness / Cough sensitivity / Capsaicin / Bronchial asthma / Eosinophil / ムスカリン受容体 / セロトニン受容体 / 神経ペプチド / 抗コリン薬 |
|---|
| Research Abstract |
We have made bronchial asthma model using guinea pigs. We have also evaluated bronchial hyperresponsiveness by capsaicin-induced cough. In this bronchial asthma model, anti-histamine agent ; azelastine and terfenadine inhibited capsaicin-induced cough suggesting inhibition of neurogenic inflammation.
We have measured intracelular antigen EG2 in asthmatic patients using a technique in whole-blood flow cytometry. From this study, it is suggested that eosinophil intracellular EG2 is very important factor and correlates the pathophysiological condition of asthma.
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