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Biomedical subjects

J Soria

Publications and source records attributed to J Soria.

At least 163 records · Page 9Linked to original sources
PubMed1983

Characteristics of platelet aggregation induced by the monoclonal antibody ALB6 (acute lymphoblastic leukemia antigen p 24). Inhibition of aggregation by ALB6Fab.

The leukemia-associated cell surface antigen p 24 is found on normal platelets as well as on Bernard Soulier syndrome and thrombasthenia type I platelets. ALB6 IgG (a monoclonal antibody against p 24) induces the aggregation of platelets from normal donors but not from thrombasthenia. In contrast, ALB6 Fab inhibits platelet aggregation induced by collagen, ADP, thrombin, ionophore A 23187 and ALB6 IgG. The results suggest that ALB6 interferes with a mechanism common to all aggregation pathways; the possible mechanisms are discussed.

Antibodies, Monoclonal↗
PubMed1983

Fibrinogen binding on human platelets. Influence of different heparins and of pentosane polysulfate.

Unfractionated heparin increased the binding of fibrinogen on ADP-treated platelets. The results varied according to both, the platelets of the donor and the kind of heparin preparation used. Beef lung heparin was more active than porcine intestinal mucosa heparin (p less than 0.02). A fraction of low molecular weight low sulfated heparin, did not significantly increase the binding of fibrinogen, except in one case for which the binding of fibrinogen to platelets was largely increased by standard heparin. On the contrary, pentosane polysulfate, a sulfated polysaccharide (of low molecular weight) significantly increased the binding of fibrinogen (p less than 0.01).

Animals↗
PubMed1983

A new type of congenital dysfibrinogenaemia with defective fibrin lysis--Dusard syndrome: possible relation to thrombosis.

Congenital dysfibrinogenaemia is described in three members of a family presenting with recurrent thrombosis and in two other young members not yet affected. An abnormality in the polymerization of fibrin monomers was noted. In addition, the pathological fibrin clots were found to be less sensitive to degradation by a post venous occlusion euglobulin solution than normal fibrin. After fibrin clot incubation with lys-plasminogen at different concentrations, the biological activity of plasminogen in patient fibrin clot on S 2251 after SK-addition, was less than that observed with normal fibrin. It is speculated that defective in vivo thrombolysis might explain the recurrent thrombosis observed in this family. This finding represents a new concept in understanding thromboembolic diseases.

Adolescent↗
PubMed1982

The amidolytic activity of the SK-plasminogen complex is enhanced by a potentiator which is generated in the presence of vascular plasminogen activator--role of fibrin degradation products.

In the presence of an excess of streptokinase (SK) the amidolytic activity of the plasminogen-SK complex on chromogenic substrates is 12% lower in serum than in the corresponding plasma. However, in subjects in whom venous stasis lead to a shortening of the euglobulin lysis time to less than 60 min (high responders), the amidolytic activity of the plasminogen-SK complex in serum was 60% higher than in the corresponding plasma. Attempts to find alterations of the plasminogen molecule itself which would account for the enhanced activity in high responder serum were negative. No free plasmin was present and the plasminogens isolated from plasma and serum before and after venous stasis had the same amidolytic activity as gluplasminogen in the presence of an excess of SK. N-terminal analysis of these four plasminogens revealed in each instance glutamic acid. The enhancement of the amidolytic activity of the SK-plasminogen complex in serum of high responders (potentiator activity) could be reproduced by adding purified tissue plasminogen activator (TA) to native blood before clotting, but not if TA was added to plasma or to prestasis serum. Removal of fibrin degradation products from poststasis serum resulted in the disappearance of potentiator activity. These experiments suggest that fibrin degradation products, generated during clotting in the presence of vascular or tissular plasminogen activator act as a potentiator of the amidolytic activity of the plasminogen SK-complex.

Amides↗
PubMed1981

[Is glycosylated haemoglobin subject to rapid variations? Changes in insulin-dependent diabetic patients under a 24-hour artificial pancreas treatment (author's transl)].

According to recent studies, glycosylated haemoglobin (HbA1) is subject to rapid variations. In order to verify this point, nine insulin-dependent diabetic patients underwent a 24-hour normalization of glycaemia with an artificial pancreas. There was a non-significant decrease of HbA1 from 9.26 +/- 1.03 p. cent to 8.69 +/- 0.84 p. cent (mean +/- s.d.). An explanation to the apparent discrepancies between the different studies is proposed. The variations observed could largely be due to the inclusion or non inclusion in the assay methods of a subfraction of glycosylated haemoglobin: a Schiff's base likely to undergo glysosylation in a rapidly reversible manner.

Diabetes Mellitus↗
PubMed1981

Heterogeneity of human prekallikrein deficiency (Fletcher trait): evidence that five of 18 cases are positive for cross-reacting material.

We studied the plasma of 18 patients with a functional deficiency of plasma prekallikrein (Fletcher trait). Samples from 13 subjects contained less than 1 per cent of normal levels of prekallikrein antigen recognized by a specific antiserum (cross-reacting-material negative [CRM-]). In the five other subjects, however, nonfunctional material immunologically indistinguishable from normal prekallikrein was detected by radioimmunoassays at concentrations of 13 to 30 per cent (CRM+ variant). None of the plasma samples contained detectable circulating anticoagulants against prekallikrein. On immunodiffusion against antiserum to kallikrein, each of the five CRM+ samples formed a single precipitin line of complete identity with normal plasma or purified prekallikrein. On immunoelectrophoresis, the precipitin line had the same mobility as that for normal prekallikrein. These studies demonstrate the molecular heterogeneity of human prekallikrein deficiency and show that persons with the CRM+ variant have a nonfunctional form of prekallikrein in their plasma.

Blood Coagulation Disorders↗
PubMed1981

Hemoglobin Hotel-Dieu beta 99 Asp replaced by Gly (g1). A new abnormal hemoglobin with high oxygen affinity.

Hemoglobin Hotel-Dieu was detected by isoelectric focusing during investigation of a patient who had erythrocytosis. This variant migrates on cellulose acetate electrophoresis to a cathodic position relative to Hb F. In hemoglobin Hotel-Dieu, aspartic acid is substituted by glycine in position 99 of the beta chain. As in other abnormal hemoglobins in which substitution of this residue has occurred, Hb Hotel-Dieu exhibits a high oxygen affinity and is associated with familial erythrocytosis.

Adult↗
PubMed1981

[Clinical studies of the erythrocytosis produced by a new hemoglobin with oxygen affinity : Hb Hôtel-Dieu alpha 2A beta 2 Asp replaced by Gly (author's transl)].

A new case of erythrocytosis associated with a high oxygen affinity hemoglobin is reported : the substitution of beta 99 of aspartic acid by glycine, characterized this abnormal hemoglobin, named "hemoglobin Hôtel-Dieu". An important associated smoking habit, probably responsible of an abnormal lung X-ray and of a disturbed CO transport, contributed to increase the difficulty of diagnosis. Familial inquiry, the search of an abnormal hemoglobin by standard or isoelectrofocusing electrophoresis, and the 2,3-DPG assay should be systematically performed in case of polycythemia in young people or in the absence of obvious aetiology. A corpuscular abnormality can be thus detected in about 10 p. cent of such polycythemias.

Adult↗
PubMed1980

[Metabolic control in 107 maturity onset diabetic out patients (author's transl)].

Hemoglobin A1c concentrations were measured in 107 out patients with non insulin treated diabetes. A good correlation was observed between Hb A1c and random post-prandial plasma glucose levels. Mean Hb A1c concentrations were slightly higher in these diabetics than in controls but markedly lower than values observed in insulin treated patients. Sixty three per cent of the patients had Hb a1c levels below three standard deviations above our normal mean value. Random post-prandial plasma insulin levels were correlated to the degree of overweight but not other parameters. The best results were observed in patients treated by diet alone (31 % of the whole population) and in those on diet and sulfonylureas (30 %) who were also the less older and the less overweight subjects.

Biguanides↗
PubMed1980

Diabetic control in 102 insulin-treated out-patients.

Haemoglobin AIc concentrations were measured in 102 insulin-treated diabetic outpatients. Only 19% had Hb AIc levels below three standard deviations above the normal mean value (5.23 +/- 0.05%). There were no correlations between Hb AIc levels, random C-peptide immunoreactivity or age. A significant correlation (r = 0.49; p < 0.001) was, however, observed between HbAIc and random plasma glucose levels. The mean random plasma glucose value was normal (89 +/- 18 mg/100 ml; 5 +/- 1 mmol/l) in the patients on insulin three times a day who had received short acting insulin 160 +/- 6 min before the sampling. --A significant inverse correlation was found (r = -0.26; p < 0.01) between the number of daily insulin injections and the HbAIc concentration. --These results suggest that the use of multiple daily insulin injections improves diabetic control. It should however be emphasised that the patients receiving multiple insulin injections were younger than those on the single injection regime and had lower plasma insulin antibody titres, different social and psychological status and a shorter duration of the disease.

Adult↗
PubMed1980

Fibrinogen Marseille. A new case of congenital dysfibrinogenaemia.

A new case of congenital dysfibrinogenaemia was found in 2 members of the same family. The anomaly was characterized by an abnormal polymerization of fibrin monomers, whereas the release of fibrinopeptides by thrombin and fibrin stabilization by F XIII were normal. Investigation of the fibrinogen molecule did not lead to localizing the structural abnormality.

Adult↗