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Biomedical subjects

S Sherry

Publications and source records attributed to S Sherry.

At least 73 records · Page 4Linked to original sources
PubMed1976

Interrelationships between platelets and coagulation in the pathogenesis of venous thrombosis.

The relationship between platelets and coagulation in the pathogenesis of venous thrombosis is reviewed. Platelet coagulant activities, coagulation factors and platelet numbers were measured pre- and postoperatively in patients who underwent hip surgery. About 50% of patients developed venous thrombosis. No significant pre-operative differences were observed in platelet coagulant activities between the group of patients who developed thrombosis and the group who did not. However, platelet counts and coagulation activities were significantly higher postoperatively in patients with thrombosis. The postoperative increase in platelet activity preceded venographically observable thrombosis. The author concludes that in patients with thrombosis there may be an increase of young platelets which are 'hyperactive' and which may trigger thrombosis in areas of stasis. It is not impossible that the increased platelet coagulation activity was the result rather than the cause of thrombosis. However, the temporal sequence of effects observed militate against this possibility.

Blood Cell Count↗
PubMed1976

Preventing pulmonary embolism with heparin in low doses.

The introduction of low-dose heparin prophylaxis of thrombosis in deep leg veins represents a major advance in clinical medicine. It approaches an ideal form of prophylaxis in that it can be given easily to large numbers of patients at risk, requires no monitoring, is relatively safe, and, used widely, should save many lives. Conservative estimates are that 5,000 postoperative deaths and a comparable number of medical deaths can be avoided in the United States alone. Further inroads on this important problem will require additional developments, some of which are well under way.

Abdomen↗
PubMed1976

The relationship of platelet coagulant activities to venous thrombosis following hip surgery.

Platelets have recently been shown to trigger intrinsic coagulation by two alternative pathways, protect active clotting factors from inactivation by plasma inhibitors and catalyse intrinsic coagulation reactions on the platelet surface to form fibrin. To determine whether these platelet coagulant activities (PCA) might have a role in the pathogenesis of DVT, 29 patients have been studied before and after arthroplasty or other surgery for fractured hip or degenerative hip disease. The occurrence of DVT was detected by [125I]fibrinogen uptake in the legs and confirmed by venography. In patients who developed DVT, all PCA increased progressively and significantly on day 1 (mean rise, 146% of baseline), day 3 (228%) and day 5 (298%) after surgery before isotopic evidence of DVT appeared (mean 3.27 days postoperatively). In patients without DVT no changes in PCA were observed. Plasma coagulation factor assays were no different in patients with a without DVT. Platelet counts and total platelet antiheparin activity increased during the early postoperative period in DVT patients but not in patients without DVT. It is suggested that progressive increases in PCA concerned with triggering and catalysing intrinsic coagulation reactions may play a pathogenetic role in DVT after hip surgery.

Arthroplasty↗
PubMed1975

The phase II urokinase-streptokinase pulmonary embolism trial: a national cooperative study.

The controlled clinical trials of thrombolytic agents in the United States have been carried out in two phases, under the auspices of the National Heart and Lung Institute. Phase I was devoted to the comparison of 12-hour Urokinase (12h-UK) followed by heparin (H) with heparin alone in patients with acute pulmonary embolism (Walsh et al. 1969). The results showed that pateints treated with UK had more rapid and gretaer resolution of pulmonary thromboemboli in the first twenty-four hours of therapy than patients treated with H alone, as assessed by serial pulmonary angiography, hemodynamics and lung scanning (The Urokinase Pulmonary Embolism Trial, 1970, 1973; Hyers et al. 1970). Because of the ralatively small size of the Trial and the low mor tality of treated pulmonary embolism, mortality differences were not sought-nor was one found. Although there was early difference in amount of clot resolution, patients treated with H alone showed similar improvement by two weeks. The phase II Urokinase-Streptokinase Pulmonary Embolism Trial (USPET) was begun to assess the comparative results of UK and Streptokinase (SK) therapy. Because of favorable results obtained with SK in other countries, it was deemed necessary to make this comparison (Browse and James, 1964; Hirsh et al. 1968; Miller et al. 1969, 1971; Chesterman et al. 1969). A third group, 12-hour UK, was added to relate this study (24-hour UK and SK) with the Phase I results which employed only a 12-hour infusion of UK. This Phase II Trial represents the first controlled, randomized study of UK and SK in thromboembolic disorders.

Angiography↗
PubMed1975

Reaction of plasmic degradation products of fibrinogen in the radioimmunoassay of human fibrinopeptide A.

A radioimmunoassay (RIA) technique has been devised for the measurement of human fibrinopeptide A (FPA). The system utilizes rabbit antiserum to native human FPA and a synthetic fibrinopeptide, with tyrosine substituted for phenylanine in amino acid position 8. The test detects native human FPA at a concentration of 0.1 ng/ml, but does not cross react with human fibrinopeptide B or with fibrinopeptides A from canine, porcine, or bovine fibrinogen. Fibrinogen and chemical or plasmic degradation products with 2 moled of FPA per mole react fully in this test system. This includes the large-molecular-weight intermediate fragments X and Y and the NH2-terminal disulfide knot, and indicates that this antibody recognizes and reacts with FPA in the presence of the contiguous peptide structures present in fibrinogen. Fragment E, which is derived from the NH-2-terminal portion of fibrinogen, loses most of its FPA content after its liberation from its precursor derivative and reacts to a lesser extent in the RIA than do fragments X and Y. This correlated with the recovery of FPA-positive material from ultrafilitrates of extensive but not partial plasmic digests of fibrinogen. Although FPA immunoreactivity liberated from fibrinogen does not necessarily reflect thrombin activity and/or fibrin formation, only extensive plasmic degradation yields peptide material which reacts in this RIA system. This should not be a serious limitation to the application of the RIA in the detection of venous thrombosis.

Amino Acid Sequence↗