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外文期刊>Arthritis and Rheumatism
>Platelet‐activating activity in synovial fluids of patients with rheumatoid arthritis, juvenile rheumatoid arthritis, gout, and noninflammatory arthropathies
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Platelet‐activating activity in synovial fluids of patients with rheumatoid arthritis, juvenile rheumatoid arthritis, gout, and noninflammatory arthropathies
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机译：Platelet‐activating activity in synovial fluids of patients with rheumatoid arthritis, juvenile rheumatoid arthritis, gout, and noninflammatory arthropathies
AbstractThe predominant activating activity in rheumatoid synovial fluid for human platelets, as assessed by the release of11C serotonin, was previously isolated and shown to be a complex of IgG of molecular weight 450,000. Thus, a pooled 5 ml concentrate of the 450,000 molecular weight fraction obtained by Sepharose 66 gel filtration of 1 ml of synovial fluid was used to compare the platelet‐activating activity (PAA) of fluids from 28 patients with inflammatory and noninflammatory ar‐thropathies. One unit of PAA was arbitrarily defined as that volume of the 5 ml concentrate required to obtain release equal to that obtained with a standard dose of thrombin, and total units per milliliter of synovial fluid were calculated as the reciprocal of the volume of concentrate in milliliters containing one unit multiplied by five. A platelet‐activating activity of>766 units/ml of synovial fluid was arbitrarily defined as elevated, since this value represents two standard deviations above the mean for the noninflammatory synovial fluids. Each of 7 noninflammatory fluids (range<50 to 695) and 3 of 4 gouty fluids (range<50 to 1,250) fell within the normal range, whereas 9 of 13 adult rheumatoid fluids (range<50 to 11,880), and 4 of 4 JRA fluids (range 1,299 to 5,100) had elevated levels of PAA per ml of synovial fluid. The finding that the purified synovial fluid 450,000 molecular weight complex of IgG was inhibited in its platelet‐activating capacity by purified monoclonal rheumatoid factor suggests that a role for IgM rheumatoid factor could be to block IgG complex Fc receptor‐dependent proinflammatory effects on platelets, and perhaps ot
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