| Project/Area Number |
07307031
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 総合 |
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| Research Field |
Otorhinolaryngology
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| Research Institution | Oita Medical University |
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Principal Investigator |
MOGI Goro Dept.of Otolaryngology, Oita Med.Univ., Professor, 医学部, 教授 (20035190)
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| Co-Investigator(Kenkyū-buntansha) |
KAWAUCHI Hideyuki Dept.of Otolaryngology, Shimane Med.Univ., Professor, 医学部, 教授 (50161279)
KANZAKI Jin Dept.of Otolaryngology Sch.of Med., Keio Univ., Professor, 医学部, 教授 (00051441)
TAKASAKA Tomonori Dept.of Otolaryngology, Tohoku Univ.Sch.of Med., Professor, 医学部, 教授 (80004646)
NAKAI Yoshiaki Dept.of Otolaryngology, Osaka City Univ.Med.Sch., Professor, 医学部, 教授 (10046998)
YANAGITA Noriyuki Dept.of Otorhinolaryngology, Sch of Med., Nagoya Univ., Professor, 医学部, 教授 (00023804)
高橋 光明 旭川医大, 医学部, 講師 (50094652)
富山 俊一 日本医大, 医学部, 助教授 (00094665)
久保 武 大阪大学, 医学部, 教授 (30107031)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥5,000,000 (Direct Cost: ¥5,000,000)
Fiscal Year 1996: ¥5,000,000 (Direct Cost: ¥5,000,000)
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| Keywords | autoimmune diseases / PCR (polymerase chain reaction) / HLA (human leukocyte antigen) / adhesion molecule / Na, K-ATPase / spiral ligament / endolymphatic sac / anaphylaxis / ステロイド依存性難聴 / HLA (human leukocyte antigen) / PCR法 / ICAM-1 / 血液-内耳関門 / 内リンパ曩 / 増殖期細胞 / フリーラジカル / 血管条 |
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| Research Abstract |
A.Clinical Studies
(1) The clinical features of steroid-responsive sensorineural hearing loss and acute sensorineural hearing loss with autoimmune diseases were investigated.
(2) Using a RT-PCR technique, the measles virus was detected in perilymph taken during cochlear implant surgery in patients with profound hearing loss.
(3) The frequency of HLA-Aw33 in otosclerosis patients was higher than that in the control subjects.
B.Basic Studies
(1) Secondary antigen challenge into the endolymphatic sac resulted in the cellular migration and ICAM-1 expression in the whole inner ear venules, suggesting that chemical mediators produced within the endolymphatic sac may spread into all compartments of the inner ear and lead to immunological defense and injury of the inner ear.
(2) Inner ear responses to foreign cells induced activation and invasion of natural killer cells which occur relatively late compared with those in other organs.
(3) Decreased immunoreactivity for Na, K-ATPase and connexin 26 was observed in the spiral ligament after immune injury.
(4) Study of cell proliferation revealed that the epithelium of the endolymphatic sac can regenerate after immune injury.
(5) Repeated antigen challenges into the inner ear caused an anaphylactic reaction that may disturb hearing and equilibrium.
(6) MRL/prmouse and NZB mouse were studied electrophysiologically and histopathologically to clarify the mechanism by which autoimmune inner ear diseases occur.
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