| Project/Area Number |
07558113
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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 | 展開研究 |
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| Research Field |
Laboratory animal science
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| Research Institution | HIROSAKI UNIVERSITY |
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Principal Investigator |
KAMIYA Haruo Hirosaki University, School of Medicine, Professor, 医学部, 教授 (70002079)
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| Co-Investigator(Kenkyū-buntansha) |
ITO Mamoru CENTRAL RESEARCH INSTITUTE FOR ANIMAL EXPERIMENT,HEAD OF RESEARCHER, 実験動物中央研究所, 主任研究員 (00176364)
OZAKI Toshihiro Hirosaki University, School of Medicine, Instructor, 医学部, 助手 (30194541)
SATO Hiroshi Hirosaki University, School of Medicine, Instructor, 医学部, 助手 (90211945)
INABA Takashi Hirosaki University, School of Medicine Associate Professor, 医学部, 講師 (60003612)
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| Project Period (FY) |
1995 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥9,500,000 (Direct Cost: ¥9,500,000)
Fiscal Year 1997: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 1996: ¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 1995: ¥5,000,000 (Direct Cost: ¥5,000,000)
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| Keywords | Schistosoma mansoni / Trichinella britovi / Echinococcus multilocularis / Trypanosoma cruzi / Trypanosomagrosi / SCID mouse / drug resistance / infection kinetic / Trypanosoma spp. / Trichimella spiralis / Trichinella spiralis |
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| Research Abstract |
Drug resistance against parasitic diseases, such as malaria, became critical issues in developing countries. Doenhoff et al.(1982) were the first report that the praziquantel (PZQ) was less active against schistosomes in immuncompromized than in normal hosts. This issue provides the conception that the possible establishment of animal model using SCID mice for analysis of the generation of drug resistance against parasitic diseases. The summarized results of present research project are as follows : 1. Schistosoma mansoni : a) SCID mice exhibited the innate resistance against the infection. b) Parasites in SCID mice were not killed by praziquantel. c) Efficacy of drugs was also affected by the immune status of the host. d) Female mirracidia in infected SCID mice treated with PZQ were killed selectively. e) Dendritic cells play the important role for the induction of protective immunity in vaccine model of the disease. 2. Echinococcus multilocularis. Mebebdazole were used for the treatm
… More
ent of the disease, although the drug resistance was not evident. Subcutaneous echinococcosis was established in SCID mice. 3. Trichinella britovi : Several passage of T.britovi life cycle in SCID mice treated with mebendazole could generate the drug resistant isolate, although the resistance nature disappeared in subsequent passages in ICR mice. 4. Trypanosoma spp. : T cruzi was maintained in SCID mice through consecutive passage for 4 years. Possible change of its nature is now under the investigation by means of PCR.A new laboratory model of non-pathogenic trypanosome (T.grosi)-Mongolian gerbil was established. 5. Intermediate filaments (IFs) : IFs make up the cytoskelton of most eukaryotic cells. Monoclonal antibodies against IFs were produced. These probes clarified the cross reactivity with IFs of parasites and also the increase of autoantibody against IFs in rats infected with T.britovi and treated with mebendazole. 6. Immunosurpressive acidic protein (LAP) : Information about IAP in parasitic infection was limited, although SCID mice infected with those parasites showed the distinct increase of IAP.
These results need further investigation to know its more detailed involvement in drug resistance. Less
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