2016 Fiscal Year Final Research Report
Transmission and risk of Amyloid A amyloidosis as a protein misfolding disease in intra- and cross-species animals
| Project/Area Number |
25292171
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Partial Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Veterinary medical science
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| Research Institution | Gifu University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
猪島 康雄 岐阜大学, 応用生物科学部, 准教授 (20355184)
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| Co-Investigator(Renkei-kenkyūsha) |
YANAI Tokuma 岐阜大学, 応用生物科学部, 教授 (10242744)
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| Research Collaborator |
MURAKAMI Tomoaki
NAEEM Muhammad
SHIGEMURA Hiroaki
KAWASHIRI Momoka
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| Project Period (FY) |
2013-04-01 – 2017-03-31
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| Keywords | アミロイド / 伝播 / マウス / ウシ / ニワトリ / ミスフォールデング |
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| Outline of Final Research Achievements |
Amyloid A (AA) amyloidosis is induced with protein misfolding of serum amyloid protein A, and characterized by extracellular deposition of AA fibrils in several organs. The AA amyloidosis is also transmitted to intra- and cross-species animals. In this study, heterologous (bovine and poultry) as well as homologous (murine) AA fibrils were injected intraperitoneally to mice, and the transmission mechanism and heat stability of the AA fibrils were histologically examined. Severity of AA amyloidosis was low in mice inoculated with heterologous AA fibrils than homologous AA fibrils. Clearance of AA fibrils in spleen was gradually observed after first inoculation, but the deposition of AA fibrils was rapidly increased after the second stimulus. The level of IL-6 was increased after first inoculation, while the level of IL-10 was increased after second inoculation of AA fibrils. The AA fibrils isolated from animal amyloidosis appear to be relatively resistant to several heat treatments.
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| Free Research Field |
獣医学
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