Prolonged clot lysis time and absence of platelet gamma M-globulin in patients with thrombasthenia.
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Biomedical subjects
Publications and source records attributed to F B Taylor.
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The addition of plasminogen and streptokinase to rabbit serum results in appearance of chemotactic activity which is relatively heat-labile and dialyzable. Generation of this activity requires heat-labile factors in serum, but not the sixth component of complement. The optimal mole ratio for generation of chemotactic activity is 1:1 to 1:3 for plasminogen to streptokinase. Neither material alone is sufficient to generate the activity in fresh serum. Generation of chemotactic activity can be blocked by the presence of epsilon-aminocaproic acid. This plasmin-generated chemotactic factor sediments slowly in a sucrose density gradient during ultracentrifugation. The addition of plasminogen and streptokinase to rabbit serum containing the preformed chemotactic factor (activated trimolecular complex of C'5, C'6, C'7) causes destruction of the chemotactic factor and loss of hemolytic activity of the sixth component of complement. The same mole ratio of reactants for optimal expression of the phenomenon holds as for plasmin generation of chemotactic activity in untreated serum.
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By means of a photodynamic bioassay, with Paramecium caudatum, photosensitizing compounds have been demonstrated in extracts of finished drinking water in the United States. These findings are of interest in view of a demonstrated association between photodynamic toxicity and carcinogenicity. Neither the origin nor the identity of these compounds has been determined.
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Shiga toxin (Stx) and lipopolysaccharide (LPS) both participate in the pathogenesis of post-diarrheal hemolytic uremic syndrome (HUS), yet little is known about the factors that modulate the host response to these toxins. We have previously shown that the baboon develops HUS if 100 ng/kg of purified Stx-1 is administered rapidly as a single bolus, but not if it is given as four 25-ng/kg doses every 12 h. We therefore used this baboon model to study the response to small intravenous doses of Stx-1, with and without the co-administration of LPS. The co-administration of two 1-mg/kg doses of LPS (given at 0 and 24 h) and four 25-ng/kg doses of Stx-1 (given at 0, 12, 24, and 36 h) resulted in HUS, but the administration of either toxin separately did not. The development of HUS was associated with a rise in urinary, but not plasma concentrations of TNF, and a rise in both urinary and plasma concentrations of IL-6 and IL-8. We speculate that LPS is not required for disease expression in the human, but that it can augment the response to otherwise subtoxic amounts of Stx and this augmentation may be mediated by LPS-induced cytokine release.
The recently developed coagulolysis assay was utilized in conjuction with fibrinogen uptake scanning to monitor 91 of 111 consecutive orthopedic patients scheduled for hip surgery or total knee replacement. Sixteen patients had abnormal coagulolysis assays and positive scans. Venography was performed in 15 of these patients, and deep vein thrombosis was documented in 12. Five patients developed pulmonary emboli, including one with negative venogram. Thus, over 80% of the patients in which both the coagulolysis assay and the fibrinogen scan were abnormal had additional documentation of deep vein thrombosis. In 41 patients, the coagulolysis assay was negative. Venograms were not routinely performed in this group. However, 3 patients developed pulmonary emboli indicating that deep vein thrombosis developed in this group. Only one patient had a normal coagulolysis with a positive fibrinogen scan. Venography documented a deep vein thrombosis. Thirty-three patients who had normal coagulolysis assays and negative fibrinogen scans also had no evidence of deep vein thrombosis or pulmonary embolism. The coagulolysis assay appears to be a safe, noninvasive study for the detection of deep vein thrombosis. There was only a one per cent false-negative incidence.