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Biomedical subjects

J P Caen

Publications and source records attributed to J P Caen.

At least 19 recordsLinked to original sources
PubMed1979

[Platelet functions in diabetes with angiopathy (author's transl)].

Platelet functions studied in 163 unselected diabetics compared with 163 controls had the following characteristics: hyperagregation induced by ADP (1.2 muM and 0.6 muM), delayed platelet disagregation (ADP: 0.6 muM), normal agregation in the presence of collagen and thrombin. Platelet hyperagregation induced by ADP was marked in both sexes in cases of retinopathy and in women after the age of 50. By contrast, no correlation was demonstrated between the degree of hyperagregation and age, weight, the duration of diabetes, blood glucose control, lipid profile, vascular complications other than retinopathy and the nature of treatment.

Adenosine Diphosphate↗
PubMed1979

Relationship between mepacrine-labelled dense body number, platelet capacity to accumulate 14C-5-HT and platelet density in the Bernard-Soulier and Hermansky-Pudlak syndromes.

We have used the mepacrine-labelling procedure to measure the dense body (serotonin storage organelle) content of the platelets of 2 hereditary disorders where abnormalities in dense body number were suspected. The platelets were incubated with mepacrine and examined by fluorescence microscopy. A mean number of 5.4 +/- 0.8 (SD) dense bodies per platelet was calculated from the data obtained using platelets isolated from 40 normal human subjects. In contrast the platelets of 2 patients with the Bernard-Soulier syndrome contained an average of 14 and 17 labelled granules. This increase was associated with a much greater capacity of the platelets to accumulate 14C-5-HT. The opposite result was obtained using the platelets from 2 patients with the Hermansky-Pudlak syndrome which contained few granules labelled by mepacrine and took up less 14C-5-HT than normal human platelets. Centrifugation of the patients' platelets on discontinuous sucrose gradients showed that the platelets of the 2 Bernard-Soulier patients were much denser than normal whereas a high proportion of low density platelets was observed in the Hermansky-Pudlak syndrome. These results further define the platelet abnormalities in the two syndromes and suggest that dense body number may be one of the factors governing platelet density.

Adolescent↗
PubMed1979

[Immunochemical study of protein anomalies in platelets of patients with Glanzmann's thrombasthenia and Bernard-Soulier syndrome].

Crossed immunoelectrophoresis of "Triton X-100" solubilized proteins from (125I) iodinated normal and abnormal (Bernard-Soulier and thrombasthenic) platelets was performed using rabbit antibodies raised against whole, normal platelets. In Bernard-Soulier platelets neither of the two surface oriented forms of GP I, glycocalicin and glycoprotein Ib (band 13) were detected. In two patients with type I thrombasthenia, the most prominent precipitate (No. 16) and platelet fibrinogen (No 24) were not detected whereas in one patient with type II thromblasthenia, fibrinogen was normally detected and the amount of protein 16 was around 15% of the normal level. The alloantibody IgG L..., able to induce a "thrombasthenic-like" reactivity in normal human platelets, has been shown to be directed against protein 16.

Animals↗
PubMed1979

[Transfusion of platelets loaded with periwinkle alkaloids as a treatment for chronic idiopathic thrombocytopenic purpura (author's transl)].

In a 70 year-old woman with a chronic idiopathic thrombocytopenic purpura refractory to all the therapeutic used, the absence of antiplatelet antibodies and the action of patient mononuclear cells on normal platelet 14C serotonin release was observed. The injection of vincristine loaded platelets was followed by a remission and a normalisation of the cellular immunological tests.

Adrenal Cortex Hormones↗
PubMed1979

Further studies on a specific platelet antibody found in Bernard-Soulier syndrome and its effects on normal platelet function.

An IgG antiplatelet antibody found in a multitransfused patient with Bernard-Soulier syndrome (BSS), reacted with a normal platelet surface antigen of 150 000 daltons which was similar to the glycoprotein missing from BSS platelets. The BSS platelet antibody (BSS-Pab) aggregated all control platelets which then released ADP and 5-HT and synthesized thromboxane. When mixed with the antibody, BSS platelets did not aggregate, did not release ADP and 5-HT and failed to synthesize thromboxane. The BSS-Pab was not inactivated by incubation with BSS platelet stroma. While the antibody did not aggregate thrombasthenic platelets, its aggregating activity was lost after incubation with their stroma. The BSS-Pab did not provoke ADP or 5-HT release or thromboxane synthesis in thrombasthenic platelets or in the platelets of a patient with platelet cyclooxygenase deficiency or in normal platelets treated with indomethacin. The aggregating, release and synthetic responses of platelets after binding of BSS-Pab to its membrane antigen (probably glycoprotein I) requires the presence of glycoprotein IIb and/or IIa and the normal metabolism of arachidonic acid.

Antibodies↗
PubMed1979

A platelet defect in a patient with eosinophilic leukaemia: absent ristocetin-induced platelet aggregation associated with a reduced platelet sialic acid content.

Platelets from a patient with eosinophilic leukaemia were not aggregated by ristocetin. The defect was not corrected by normal human plasma and was due to a platelet abnormality. The patient's platelets also showed a diminished sensitivity to aggregation by bovine factor VIIIVWF. The defect was not associated with a prolonged bleeding time. No abnormalities were detected in ADP, collagen or thrombin-induced platelet aggregation. Biochemical studies showed that the platelets were deficient in sialic acid. This deficiency was associated with a reduced staining for glycoprotein I following SDS-polyacrylamide gel electrophoresis. The results suggest an acquired platelet surface abnormality.

Adenosine Diphosphate↗
PubMed1979

Increased interaction of vascular endothelium and leucocytes after administration of antiplatelet serum: role in the developing vascular defect.

Antiplatelet serum (APS) induced an increase in the stickiness of white cells which manifests itself in the increase in number of granulocytes rolling along or sticking to the venous endothelium. Lidocaine treatment prevented the increased stickiness of white cells and, at the same time, the microvascular haemorrhage developing after APS. It can be assumed that increased stickiness of white cells after APS may contribute to endothelial damage.

Animals↗
PubMed1979

Specific and quantitative method for estimation of platelet adhesion to fibrillar collagen.

A quantitative method (Sepharose test) was devised to measure the adhesion of blood platelets to fibrillar collagen. [14C]5HT-labeled platelets were isolated from plasma, resuspended in EDTA buffer, and incubated with buffer (control) or with fibrillar collagen for 150 sec at 33 degrees C. The mixtures were then filtered through Sepharose 2B columns. In controls the platelets were rapidly eluted, and this was confirmed after 51Cr labeling. [C]5HT was recovered in two stages: 60% with the platelets and 40% retarded, as free 5HT. After incubation with fibrillar collagen (50 micrograms), platelets were retained with the fibrils on the top of the column, and only free [14C]5HT (released from the platelets) was eluted. The percentage of adhesion depended on the number of platelets, the amount of collagen, its degree of polymerization, and the time of incubation at 33 degrees C. [14C]5HT release was markedly diminished when both incubation and filtration were performed at low temperature. ASA, used either in vitro or in vivo in rabbits, did not change the percentage of adhesion but significantly diminished the total amount of [14C]5HT eluted. This method offers a quantitative and reproducible system for the differentiation of adhesion and release, independent of platelet aggregation.

Animals↗