Biomedical subjects
R B Andersen
Publications and source records attributed to R B Andersen.
Degradation of fibrinogen in vitro. Demonstration of several antigenic intermediates by specific anti-D and anti-E serum.
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Immunofluorescent demonstration of intracellular fibrin in synovial tissue.
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Protease activity in synovial tissue extracts.
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Metabolism of fibrinogen in patients with rheumatoid arthritis and in a control group.
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[Dimethyl sulphoxide. Review of the literare].
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[Dimethyl sulfoxide in the treatment of humeroscapula periarthrosis].
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Fibrinolytic and fibrin stabilizing activity of synovial membranes.
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Fibrin dissolution in synovial fluid.
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Blood-fibrinolysis and activity of rheumatoid arthritis.
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Tenosteochondrosis of the pubis.
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[Atrophic skin and osteoporosis in patients with rheumatoid arthritis and osteoarthrosis].
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[The role of the retrogastric space in the diagnosis of pancreatic diseases. A radiographic study with special reference to variations due to respiration].
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Blood-fibrinolysis during chrysotherapy.
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[Primary ulceration of the small intestine].
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[Changes in the blood potassium content in acute coronary occlusion].
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Fibrinogen-fibrin breakdown products in pathologic synovial fluids. An immunologic study.
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The primary plasmin inhibitor in rheumatoid synovial fluid.
In 20 consecutive rheumatoid arthritis patients, 14 women and 6 men, age 26--76, average 62 years, the concentration of the recently found "primary plasmin inhibitor" and phase proteins was estimated in plasma and synovial fluid. In 12 patients a complex between the inhibitor and plasmin could be demonstrated by crossed immunoelectrophoresis into immunoglobulins against the primary plasmin inhibitor and immunoglobulin against plasminogen. Only free inhibitor was found in corresponding plasma. All plasminogen present in synovial fluid could be activated to plasmin upon addition of urokinase (24 nM/1). In those patients where enzyme-inhibitor complex in synovial fluid was present, a higher concentration of phase proteins in synovial fluid was found, indicating an increased degree of inflammation despite identical scores in the Lansbury clinical index in the two groups. From these experiments it was concluded that the fibrinolytic capacity in rheumatoid synovial fluid is not decreased. It is suggested that the fibrin-like material in synovial tissue and upon the synovial membrane is a poor substrate for plasmin.