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Biomedical subjects

J Soria

Publications and source records attributed to J Soria.

At least 145 records · Page 8Linked to original sources
PubMed1985

Fibrinogen synthesis by megakaryocyte rich human marrow cell concentrates.

A rapid method is described for the production of a human marrow cell suspension highly enriched in megakaryocytes. These concentrates were incubated with radiolabelled amino-acids, and cell lysates were then analysed for fibrinogen synthesis. Neosynthesized proteins were detected by immunoprecipitation, immuno-affinity chromatography and electrophoresis. Fluorography of the electrophoresis gels showed three radioactive bands corresponding to the three chains of cold fibrinogen. Immunoblotting and autoradiography of bidimensional, nonreduced-reduced electrophoresis gels showed that these three proteins were joined by disulfide bonds in the cell. These results suggest that megakaryocytes synthesize fibrinogen, and imply that platelet fibrinogen is of megakaryocytic origin.

Autoradiography↗
PubMed1985

Modulation of fibroblast-induced clot retraction by calcium channel blocking drugs and the monoclonal antibody ALB6.

Suspensions of living human fibroblast induce fibrin clot retractile activity (FCR). The efficiency is dependent on the growth phase; it is maximal during active growth and reduced in post-confluent cultures. In contrast human osteosarcoma cells constantly exhibit very low FCR efficiency. Two different calcium channel-blocking drugs Diltiazem and Verapamil inhibit, depending on the concentrations employed, FCR, and spreading within the clots of the normal cells. Intermediate FCR levels are associated with intermediate degrees of spreading. A similar dose dependent inhibition is also obtained by treating the normal cells with the calmodulin inhibitor trifluoperazine (TFP). On the other hand, treatment of the normal cells with the monoclonal antibody ALB6 which is directed at the human leukocyte differentiation antigen CD9 (p24) causes a significant increase in the FCR efficiency in post-confluent normal cells, but it has no effect on the Te85 osteosarcoma cells. Moreover ALB6 IgG reverses the FCR inhibitory effect of the calcium-channel blocking drugs but not that of TFP. This means that the ALB6 IgG target on the cellular membrane is probably the same as that of the two drugs and that ALB6 IgG is active in the regulation of the calcium flux which controls fibrin clot retractile activity of normal human fibroblasts.

Animals↗
PubMed1985

Episodes of increased fibronectin level observed in a patient suffering from recurrent thrombosis related to congenital hypodysfibrinogenaemia (fibrinogen Malmoe).

A study has been conducted in a Swedish patient with severe thrombotic disease and repeated miscarriages related to a hypodysfibrinogenaemia with defective thrombin binding to the abnormal fibrin. The hypodysfibrinogenaemia was found in several members of the family. The patient also had an increased concentration of fibronectin in her plasma at two different occasions. This would appear to be unrelated to the abnormal fibrinogen since a normal concentration of fibronectin has been found in her relatives presenting the same fibrinogen anomaly, and in the patient at two other times. In conclusion, the thrombotic disorder in this patient presenting a congenital hypodysfibrinogenaemia may be explained by the defective thrombin binding to fibrin.

Adult↗
PubMed1985

Platelet aggregation occurs in congenital afibrinogenaemia despite the absence of fibrinogen or its fragments in plasma and platelets, as demonstrated by immunoenzymology.

Platelet aggregation of an afibrinogenaemic patient's platelet rich plasma (PRP) was greatly decreased when ADP was used for stimulation. In the presence of collagen or arachidonic acid the changes in light transmission recorded during platelet aggregation of patient's PRP were similar to those observed with normal PRP but the size of aggregates appeared to be smaller in comparison with those observed with normal platelets. In addition, thrombin-induced aggregation of washed platelets was similar to normal platelets. The interpretation was made possible because the fibrinogen level in plasma and in platelets was found to be almost nil as demonstrated by both an Elisa procedure described here and the determination of fibrinopeptide A (fpA). Furthermore, fibrinogen fragments, which could result from abnormal synthesis and therefore replace fibrinogen in platelet aggregation, were undetectable by immunological analysis using specific antibodies against A alpha, B beta and gamma chains and 10 different monoclonal antibodies against fibrin degradation products.

Adenosine Diphosphate↗
PubMed1985

Inhibition of some activities of thrombin by a collagen-derived octapeptide.

The effect of a collagen-derived octapeptide on some properties of thrombin is presented. This peptide provoked a dose- and time-dependent prolongation of the thrombin-induced plasma and fibrinogen clotting time and inhibited the polymerization of fibrin generated from fibrinogen by thrombin. It did not affect the polymerization of fibrin monomers; it was also without effect on the coagulation of plasma or fibrinogen by reptilase. The prolongation of the fibrinogen clotting time depended on the duration of the incubation of thrombin and the octapeptide and not on the duration of the incubation of fibrinogen and the octapeptide. The inhibition was therefore ascribed to an interference with thrombin, rather than with fibrinogen. A preincubation of the octapeptide with thrombin resulted in an inhibition of the thrombin-induced platelet aggregation. The effect of the octapeptide on thrombin has been related to the presence of positively and negatively charged groups, because uncharged analogue sequences were without effect on these activities of thrombin.

Adult↗
PubMed1985

Psychopathological aspects of the toxic oil syndrome catastrophe.

In May 1981 a new disease caused by widespread food-poisoning (probably with adulterated rape-seed oil) appeared in Spain. More than 20000 people were affected, and about 350 patients have died. The clinical syndrome consisted of pulmonary, neuromuscular and systemic symptoms, which evolved to produce mild or severe physical disabilities. Although the disease is not primarily a psychiatric condition, more than 6000 TOS patients have been referred to a psychiatrist: these patients show a well-defined 'reactive disaster syndrome', vulnerability being associated with female sex, low income and class, and a personal history of 'nervous' disorders. The enormous public repercussions of the disease and the specific administrative measures it provoked are discussed and evaluated. This unique experience of a specific disaster can contribute to our knowledge of the psychological and psychiatric aspects of disasters in general; and it suggests that teams of psychologists and psychiatrists should play a significant role in managing the effects of major catastrophes.

Adolescent↗
PubMed1985

Aggregation of chymotrypsin-treated thrombasthenic platelets is mediated by fibrinogen binding to glycoproteins IIb and IIIa.

Previous experiments demonstrated that chymotrypsin, but not adenosine diphosphate (ADP), exposed fibrinogen binding sites on platelets from patients with Glanzmann's thrombasthenia. Three of these patients have been reexamined, and previous observations were confirmed. The quantity of iodine 125-labeled glycoprotein IIb (GPIIb) and glycoprotein IIIa (GPIIIa) on the platelets of these patients was considerably less than normal but was detectable by immunoprecipitation, sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and autoradiography. The amount of residual GPIIb and GPIIIa as measured by binding studies with radiolabeled monoclonal antibodies was between 3% and 12% of the normal value. Platelet suspensions from these patients did not aggregate with fibrinogen and did not bind 125I-fibrinogen on stimulation with ADP. However, incubation of these platelets with chymotrypsin or pronase resulted in fibrinogen binding and platelet aggregation. Monoclonal antibodies specific for the GPIIb-GPIIIa complex blocked both the fibrinogen binding and the aggregation of enzyme-treated platelets. The treatment of washed platelets of a fourth thrombasthenic patient with ADP or with chymotrypsin failed to result in fibrinogen binding and aggregation. However, the level of GPIIb and GPIIIa on these platelets as measured by a Western blot technique and by monoclonal antibody binding amounted to less than 0.35% to 0.5% of normal values. In conclusion, fibrinogen binding sites exposed on thrombasthenic platelets by chymotrypsin are derived from GPIIb-GPIIIa molecules. Aggregation of chymotrypsin-treated thrombasthenic platelets by fibrinogen appears to represent a sensitive test for detection of functionally active GPIIb-GPIIIa complex on the platelet surface.

Antibodies, Monoclonal↗
PubMed1984

Importance of the interaction between plasminogen and fibrin for plasminogen activation by tissue-type plasminogen activator.

The potentiating effect of fibrin monomer on plasminogen activation by tissue-type plasminogen activator is much more important with lys-plasminogen than with mini-plasminogen (which lacks the high affinity lysine-binding site important for binding to fibrin). Furthermore, this potentiating effect is totally abolished when lys-plasminogen is eluted from fibrin by the addition of 1 mM epsilon-amino caproic acid. Binding does however not seem to be the only condition required since it was found that fragment D is a much stronger potentiator of the activation of plasminogen by tissue-type plasminogen activator than fragment E although plasminogen binds to both fragment D and fragment E. Furthermore, fragment E has the same effect on the activation of lys-and mini-plasminogen by tissue-type plasminogen activator. Therefore, it is suggested that binding of plasminogen to fibrin involves a conformational change in the plasminogen molecule, facilitating its activation by tissue-type plasminogen activator.

Aminocaproic Acid↗
PubMed1984

Dysfibrinogenemia (fibrinogen Dusard) associated with impaired fibrin-enhanced plasminogen activation.

The fibrin-mediated enhancement of the activation of plasminogen by tissue-type plasminogen activator observed with normal fibrin, is strongly decreased with fibrin Dusard, although the binding of tissue-type plasminogen activator to this fibrin is normal. This impaired fibrin-mediated plasminogen activation is most likely related to the history of recurrent thrombosis and pulmonary embolism observed in this family.

Blood Coagulation Disorders↗
PubMed1984

Interactions of platelets with standard heparin and low molecular weight fractions.

The availability of fibrinogen receptors on platelets after ADP stimulation, was investigated in order to analyze platelet hyperaggregability induced by heparin. Unfractionated heparin increased the binding of fibrinogen on ADP-treated platelets. The results varied according to both the donor platelets and the kind of heparin preparation used. Beef lung heparin was more active than porcine intestinal mucosa heparin (P less than 0.001). Low molecular weight (LMW) heparin fractions however did not significantly increase the binding of fibrinogen to ADP-treated platelets. The effect of standard heparin and LMW heparin on the aggregation of normal platelets induced by the addition of plasma from patients with heparin-induced immune thrombocytopenia was also studied. Concerning heparin-induced immune thrombocytopenia we have shown that the plasma cofactor present in some patient plasma may induce platelet aggregation both in the presence of standard-heparin and in the presence of LMW heparin fractions. Therefore, one has to be careful when replacing standard heparin by LMW heparin or heparinoids since each patient may react differently.

Adenosine Diphosphate↗
PubMed1983

Plasminogen Paris I: congenital abnormal plasminogen and its incidence in thrombosis.

An abnormal plasminogen was discovered because of a decreased level of plasminogen activity in plasma contrasting with a normal level of plasminogen antigen concentration. The same discrepancy was found in the purified plasminogen. The molecular abnormality seems to be inherited. The patient is a heterozygote. The experimental findings can be explained by assuming that half of the plasminogen is normal, while the other half is an inactive mutant protein, without catalytic activity after SK or UK addition. There was no binding of labeled DFP and a decreased binding of TLCK to the abnormal plasminogen. The role of the abnormal plasminogen in thrombotic tendency is uncertain since the patient is the only one who has suffered a thrombotic accident, while her relatives who present the same defective plasminogen have not had thrombotic problems.

Blood Coagulation↗
PubMed1983

[Congenital dysfibrinogenemia. Apropos of 13 cases].

Approximately 100 families with congenital dysfibrinogenemia have already been reported in the literature. We have had the opportunity to study 13 affected families in France. The study of these dysfibrinogenemias has two purposes: 1) analysis of the relationships between the structural and functional abnormalities of the fibrinogen defect, since it appears that, in a significant percentage of dysfibrinogenemias, recurrent thrombosis has been observed. The diagnosis of dysfibrinogenemia is easily presumed in hemostasis laboratories since it rests upon prolonged thrombin and/or reptilase clotting times and the discrepancy between the fibrinogen levels obtained by an immunological method and a coagulation method. Many studies have been carried out during the last few years, and in at least seven cases the fibrinogen molecular defect has been elucidated.

Adolescent↗