| Project/Area Number |
13576013
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 海外学術 |
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| Research Field |
Bacteriology (including Mycology)
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| Research Institution | OKAYAMA UNIVERSITY |
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Principal Investigator |
KURAZONO Hisao Okayama University Medical School, Professor, 医学部, 教授 (90186487)
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| Co-Investigator(Kenkyū-buntansha) |
MAKINO Sou-ichi Obihiro University of Agriculture and Veterinary Medicine, Assistant Professer, 畜産学部, 助教授 (30181621)
HIRAYAMA Toshiya Nagasaki University, Institute of Tropical Medicine, Professor, 熱帯医学研究所, 教授 (50050696)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥13,200,000 (Direct Cost: ¥13,200,000)
Fiscal Year 2002: ¥6,200,000 (Direct Cost: ¥6,200,000)
Fiscal Year 2001: ¥7,000,000 (Direct Cost: ¥7,000,000)
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| Keywords | Salmonella oranienburg / STEC / Helicobacter pylori / morphine / bead-ELISA / RPTP β / Salmonella Oranienburg / Salmonella enteritidis / タイ王国 / インド |
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| Research Abstract |
Salmonella Oranienburg strains which had isolated from the patient in 1999 were VNC and sensitive to NaCl osmotic stress. After the passage of these strains in mice, they became resistant to NaCl osmotic stress. VNC Salmonella Oranienburg would be potentially dangerous contaminants of NaCl-preserved foods. VNC Salmonella showed high pathogenicity to morphine-treated mice. The morphine-treated mouse is the good bioassay model for VNC Salmonella.
We investigated the secretion of STEC from the sheep for 15 months. Once a sheep had STEC, it maintained STEC and secreted it for a long time. A sheep might be important as a reservoir of STEC.
We found the homologue of the B-subunit of Cholera toxin and E. coli LT toxin in Citrobacter freundii and determined the sequence of the gene.
We constructed the highly sensitive bead-ELISA system for Helicovacter pylori VacA and succeeded to detect VacA directly in the gastric juice of the gastric ulcer patients.
The mice deficient in RPTP β do not show mucosal damage by VacA of Helicobacter pylori. This result indicates that erroneous RPTP β signaling induced gastric ulcers.
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