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Biomedical subjects

N Semeraro

Publications and source records attributed to N Semeraro.

At least 109 records · Page 6Linked to original sources
PubMed1978

Inhibition of plasmin by antithrombin-heparin complex. II. During thrombolytic therapy in man.

The role of antithrombin as an inhibitor of plasmin in the presence and absence of heparin was studied during thrombolytic therapy in 12 patients with vascular occlusive disease. The extent of plasmin-antithrombin-(heparin) complex formation was studied by intravenous injection of iodine-labelled antithrombin (5-20 muCi) and quantitation of the amount of antithrombin bound to plasmin. In the absence of heparin, less than 0.8% of the labelled antithrombin was recovered in the plasmin-antithrombin complex but between 1.2 and 4.8% following injection of 5000 iu of heparin. Thus only between 3 and 11% of the in vivo formed plasmin is neutralized by antithrombin-heparin complex. Repeated activation of the fibrinolytic system resulted in a shortening of the plasma radioactivity half-life of labelled antithrombin from 2.45 to 2.03 d in the absence of heparin (three patients), and from 3.13 to 2.35 d following heparin administration (two patients). This increased turnover does not result in a decrease of the plasma antithrombin level.

Adult↗
PubMed1977

Turnover of fibrinogen, plasminogen, and prothrombin during exercise in man.

The turnover of biologically intact high-purity 125I- and 131I-labeled fibrinogen, plasminogen, and/or prothrombin was studied in 16 untrained healthy subjects before and during strenuous physical exercise on a bicycle ergometer (repeated 4 times/day for 2 days). The exertion resulted in the well-known changes in the coagulation and fibrinolytic tests but did not induce changes in the concentration of fibrinogen, plasminogen, or prothrombin in the plasma. A significantly increased catabolism of fibrinogen and plasminogen but not of prothrombin was observed. The extent of Aalpha-chain degradation of fibrinogen in the plasma was quantitated before and 2 h after exercise, and a significant increase in degraded Aalpha chains was found in the postexercise samples. Immunochemical estimation of plasmin-antiplasmin complex in four subjects revealed a small increase after exercise in three of them. All these data support the concept that plasminogen activation and plasmin-induced fibrinogen degradation occur to some extent in man following strenuous physical exercise.

Adult↗
PubMed1976

Platelet-endotoxin interaction: a review.

The studies reviewed in the present manuscript outline the effects of bacterial endotoxins on human and animal platelets. In animals the endotoxin administration is followed by thrombocytopenia, presence of platelet aggregates in the blood vessels of several organs, appearance of appreciable quantities of serotonin in plasma and increased platelet factor 3 availability. These in vivo effects can readily be explained by the in vitro demonstration that endotoxin aggregates platelets, induces release of vasoactive amines and adenine nucleotides and activates platelet factor 3. There is substantial evidence suggesting that the mechanism of this animal platelet-endotoxin interaction is immunological and complement dependent. In humans thrombocytopenia is frequently observed in endotoxemia as encountered during Gram-negative sepsis indicating that platelets are involved in some of the biological effects endotoxin. In vitro experiments demonstrate that several endotoxin preparations significantly enhance a weak procoagulant activity of human platelets different from platelet factor 3.

Animals↗
PubMed1973

Detection of fibrinogen antigens with two latex techniques applied to urine concentrates.

Fibrinogen antigens were measured either with an agglutination inhibition method (using latex particles coated with fibrinogen; Diagen test) or with a direct agglutination technique (using latex particles coated with a mixture of anti-D and anti-E antibodies; Thrombo-Wellcotest). Both methods were compared with the tanned red cell haemagglutination inhibition immunoassay (TRCHII) during progressive degradation of fibrinogen with plasmin and using purified fibrinogen fragments or urine concentrates from chronic glomerulonephritis or transplanted patients. Due to the different sensitivity of the two latex techniques to fibrinogen and its plasmin derivatives, their combined use may be helpful to distinguish the nature of the fibrinogen-like material excreted in urine.

Agglutination↗
PubMedDate not supplied

Disseminated intravascular coagulation associated with disseminated cryptococcosis in a patient with acquired immunodeficiency syndrome.

Disseminated intravascular coagulation (DIC) is uncommon in acquired immunodeficiency syndrome (AIDS), despite the high incidence of infectious diseases. We describe an HIV-infected patient presenting with disseminated cryptococcosis, who had clear-cut laboratory evidence of progressively worsening DIC (thrombocytopenia, prolonged prothrombin time and partial thromboplastin time, hypofibrinogenemia, increased fibrin(ogen) degradation products and D-Dimer, reduced antithrombin III), although the clinical signs of the disease were rather scarce. The patient died despite intense treatment, which included heparin and fresh frozen plasma, and DIC was confirmed histologically. It is suggested that, in a patient with AIDS presenting with an opportunistic infection, laboratory signs of DIC should be carefully checked to early recognize this complication and promptly initiate the required therapy.

Acquired Immunodeficiency Syndrome↗
PubMedDate not supplied

DMSO-induced changes in the procoagulant and fibrinolytic activity of B16 melanoma cells: influence on lung colony formation.

In this study DMSO (dimethylsulphoxide) was used as a tool to test the significance of in vitro modifications of procoagulant and fibrinolytic activity of tumor cells for their in vivo metastatic ability. B16 melanoma cells were chosen as the experimental model. After four days' treatment DMSO increased both the procoagulant and fibrinolytic (plasminogen activator) activity of B16 melanoma cells in a dose-related manner. DMSO treated cells showed significantly greater lung colonizing ability than untreated cells. Our results indicate that DMSO treatment in vitro can modulate procoagulant and fibrinolytic activity and the metastatic ability of B16 melanoma cells; however a direct causal relationship between these in vitro and in vivo effects remains to be established.

Animals↗