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Biomedical subjects

G Leone

Publications and source records attributed to G Leone.

At least 469 records · Page 26Linked to original sources
PubMed1976

Platelet aggregation by thimerosal: role of ADP and SH groups.

Thimerosal, a sulphydryl inhibitor, induces aggregation of normal platelet rich plasma over a wide range of concentrations. Low doses induce a monophasic response preceded by a lag phase, high doses produce an immediate biphasic response. Thimerosal induces platelet aggregation through its binding by sulphydryl groups. Thimerosal induced aggregation is not mediated by ADP, it is not influenced by fibrinogen, von Willebrand factor, calcium, and magnesium ions of the medium. Thimerosal induced platelet aggregation is normal in patients affected by thrombocytopathia (defect of ADP release) but not in patients affected by Glanzmann's thrombasthenia. Mercaptopropionglycine, a substance which tends to preserve SH groups, inhibits platelet aggregation induced by thimerosal, thrombin, collagen, and ADP. A mechanism is proposed for thimerosal induced aggregation and the role of SH groups also in ADP, thrombin and collagen induced aggregation is indicated.

Adenosine Diphosphate↗
PubMed1976

Pretreatment with heparin in thrombolytic therapy with Urokinase. Heparin-urokinase therapy.

Initially, we administered urokinase to five patients according to the following schedule: 500,000 CTA U during the first 10 min, then 250,000 CTA U/h for 12 h. Using this modality, we noted the appearance, during the first hours of treatment, of hypercoagulability. We then choose to modify the schedule by pretreatment with 7,500 U. i.v. of heparin, followed promptly by 250,000 CTA U/h of urokinase (without a loading dose). This obviate the appearance of hypercoagulability without reducing the fibrinolytic effect of treatment and without producing hemorrhagic complications.

Blood Coagulation↗
PubMed1974

Discrepancies between immunological and caseinolytic plasma plasminogen assays in health and hyperfibrinolytic states.

A sensitive immunological assay for plasminogen and/or plasmin was developed by using a haemagglutination inhibition technique. Plasma and the corresponding euglobulin fraction of healthy subjects and of patients with hyperfibrinolysis (liver cirrhosis, thrombolytic treatment) were assayed for plasminogen using immunological and caseinolytic techniques. In hyperfibrinolytic states discrepancies were found between immunoreactive and caseinolytic plasma plasminogen whereas a good correlation was observed between immunoreactive and caseinolytic euglobulin plasminogen. Experiments in vitro suggested that these discrepancies might depend on the presence in hyperfibrinolytic plasma of variable amounts of plasmin(ogen)-related antigen which has no caseinolytic activity and is not precipitated with euglobulin.

Adolescent↗