| Project/Area Number |
62570164
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Experimental pathology
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| Research Institution | Yamaguchi University |
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Principal Investigator |
UCHINO Fumiya Yamaguchi University School of Medicine, Professor, 医学部, 教授 (20034902)
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| Co-Investigator(Kenkyū-buntansha) |
YOKOTA Tadaaki Yamaguchi University School of Medicine, Assistant, 医学部, 助手 (40144927)
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| Project Period (FY) |
1987 – 1988
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1988: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1987: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | Synthesized peptide / Monoclonal antibody / Amyloid / Amyloidosis / AA / SAA / アミロイドーシス発症促進因子 / AA蛋白 |
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| Research Abstract |
O. Monoclonal antibody against AA protein A monoclonal antibody (KM-268) was raised against the synthesized shor to 37-47 residues in amino acid sequence of human amyloid A (AA) protein. T immunohistchemically to amyloid tissues from cow, mouse, swan and human AA was useful for the identification of AA type amyloidosis of various species
II. Monoclonal antibody against SAA protein A monoclonal antibody (KM-503) was raised the synthesized peptides cor residues in amino acid sequence of murine serum amyloid A (SAA) protein. Thimmunohistochemically to SAA protein in the hepatocytes of mice after an am but not to the amyloid deposits in various organs. Positive immunoreaction the uriniferous tubles. The finding suggests that SAA is filterered through urine and is reabsorbed in the epithelium of the uriniferous tubule, and mi
III. amyloid enhancing factor (AEF) a) AEF in aging mice; AEF activity was tested in spleen homogenates f and 9-week-old mice. Strong AEF activity was present in the supernatant of from the 52-week-old mice. Only weak activity was observed in the homogenat mice, and none was from the 9-week-old mice. The findings suggest that AEF with aging. b) An immunocytochemical evidence of AEF in neutrophils; AEF was extr recieved an amyloidogenic stimulation. An antiserum against AEF was raised antiserum reacted strongly with the neutrophils in the organs of mice with stimulation, and weakly in normal mice. The findings suggest that AEF might neutrophils, and that AEF activity in the neutrophils increases with the am
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