| Project/Area Number |
12672239
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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 |
Laboratory medicine
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| Research Institution | Kanazawa University |
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Principal Investigator |
MORISHITA Eriko Kanazawa University, School of Medicine, Assistant professor, 医学部, 助教授 (50251921)
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| Co-Investigator(Kenkyū-buntansha) |
MASAHIDE Yamazaki Kanazawa University, School of Medicine, Assistant, 医学部, 助手 (50242558)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2001: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2000: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | Leukemia / Mac-1 / Fibrinolysis / Neutrophilic elastase / Plasminogen / DIC / Acute promyelocytic leukemia / 組織因子 / CD14 / 凝固亢進 / TAT / PIC / 急性白血病 / FDP / プラスミン / エラスターゼ |
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| Research Abstract |
The aim of this study was to assess the expression of Mac-1 (CD11b/CD18 integrin adhension molecules) on the leukemic cells, and to evaluate the plasmin activity in leukemic cell homoginates and the concentration of elastase-α 1-proteinaseinhibitor (E-α IPI) complex. A total of 14 patients were examined : 11 with acute leukemia (AML 7, ALL 3, LGL leukemia 1) ; 1 with myelodysplasia syndrome (RAEB-T) ; 2 with chronic myelocytic leukemia (CML).
Mac-1 on leukemic cell was detected by flow cytometory, whereas plasmin activity was measured using chromogenic assay by S2251, and concentrations of E-α IPI complex were assayed using a sandwich-type immunoassay.
Mac-1 expression was found to be higher in the patients with acute myelomonocytic leukemia (AMMoL) than other leukemic patients, especially acute promyelocytic leukemia (APL). On the other hand, plasmin activation markedly increased in APL patients with DIC. Marked to moderate elevation of E-E_0 IPI complex levels was observed in patients with APL, AMMoL or CML. The concentrations of E- a IPI complex did not show any significant differences between patients with DIC and patients without DIC.
From these results, it is suggested that hyperfibrinolysis in leukemia, especially APL, participates in leukocyte elastase rather than Mac-1.
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