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Biomedical subjects

M Dechavanne

Publications and source records attributed to M Dechavanne.

At least 127 records · Page 7Linked to original sources
PubMed1980

Studies on platelet glycoproteins in Glanzmann's thrombasthenia using 125I-labelled lectins.

Glycoproteins (GP) of Glanzmann's thrombasthenia (GT) and normal platelets were separated on sodium dodecyl sulphate (SDS) polyacrylamide slab gels and identified by their binding of 125I-labelled lectins having different sugar specificities. This highly sensitive technique showed that in thrombasthenic platelets, glycoproteins in the positions of IIb and III (IIIa) were greatly reduced when compared to normal platelets. After incubation with neuraminidase, IIb became undectable. GT platelet glycoproteins I, IV (IIIb), and high molecular weight GPs bound 125I-lectins more strongly than those in normal platelets, showing that there are drastic changes in the carbohydrate moieties of these major GPs.

Blood Platelets↗
PubMed1979

Effects of ticlopidine on platelet prostaglandin metabolism. Possible consequences for prostacyclin production.

Ticlopidine, known to inhibit the primary wave of ADP-induced platelet aggregation and to increase the bleeding time, can modify platelet prostaglandin metabolism. The basal level of platelet PGE1 is enhanced by the drug. Ticlopidine does not decrease biosynthesis of prostaglandin endoperoxides from arachidonic acid but increases production of primary prostaglandins, cheifly prostaglandin D2, and causes a slight diminution of thromboxane B2 formation. The excess of prostaglandin endoperoxides not converted to primary prostglandins may escape from platelets and produce more prostacyclin if endothelial cell microsomes are present in the incubate.

Adenosine Diphosphate↗
PubMed1979

Basal level of human platelet prostaglandins: PGE1 is more elevated than PGE2.

Radioimmunoassays of platelet prostaglandins E1 and F1 alpha in platelet rich plasma or platelet suspension, demonstrate that both PGE1 and PGF1 alpha are present at higher concentrations than prostaglandins E2 and F2 alpha. Gas chromatography--mass spectrometry determinations of prostaglandins E1 and E2 in resting washed platelets confirm this difference. Lastly, there is a greater incorporation of [1--14C] acetate into prostaglandins E1 and F1 alpha compared to that into prostaglandins E2 and F2 alpha.

Blood Platelets↗
PubMed1979

Immunofluorescence study of mucosal B lymphocytes in bile reflux gastritis.

Intracelluar immunofluorescence staining was used to identify lymphoid cells from human gastric mucosa. Staining of serial sections for each of the five classes of immunoglobulin-containing cells revealed the presence of all classes. Their relative frequencies in the antral mucosae of 30 patients with bile reflux gastritis were 51% IgA, 16% IgM, 18.5% IgG, 2.5% IgD and 12% IgE. The mucosae of 15 control subjects showed 75% IgA, 8% IgM, 15% IgG, 1% IgD and 1% IgE and the mucosae of 30 patients with inflammatory gastritis without bile reflux revealed 67% IgA, 6.5% IgM, 22.5% IgG, 1.5% IgD and 2.5% IgE. These features suggest that allergy participates in the physiopathology of bile reflux gastritis.

Adult↗
PubMed1979

[Antiplatelet drugs (author's transl)].

Acetyl salicylic acid, sulfinpyrazone, dipyridamole, hydroxychloroquine, ticlopidine, clofibrate, nicergoline are the most used antiplatelet drugs. A. S. A. and sulfinpyrazone have been tested in several large scale clinical trials. A. S. A. seems beneficial in the prevention of cerebral ischemia for patients, specially men who have previously had a transient cerebral ischemic attack. Sulfinpyrazone appears to be effective in reducing cardiac deaths during the first year after myocardial infarction.

Aspirin↗
PubMed1978

[Sterologic evaluation on in vitro thrombin-induced platelet degranulation and contraction (author's transl)].

Stereologic study of the in vitro release reaction from unstirred washed platelets provided quantitative information on the contractile wave induced by thrombin. Contraction was estimated from the reduction in the volume of both the granular compartment and the vacuoles of the surface connected canalicular system. Dibutyryl cyclic-AMP (10(-4) M) and dipyridamole (10(-3) M) inhibited degranulation, but they had no effect on the contraction produced by thrombin at high concentrations (0.1 UI/ml). Aspirin (10(-4) M) inhibited contraction induced by thrombin at concentration of 0.1 and 0.02 UI/ml (p less than 0.01 at each concentration). In two patients with hereditary cyclo-oxygenase deficiency, contraction produced by thrombin at low concentration (0.02 UI/ml) failed to induce contraction.

Aspirin↗
PubMed1978

Platelet phospholipid in stroke.

A study of platelet phospholipids in patients with stroke has been undertaken comparatively with patients without predisposition to thrombosis. An increase in the phospholipid/protein ratio in platelets was observed in patients with acute cerebrovascular accident. A significant increase of palmitoleic acid is observed in platelet phospholipids of these patients; it is accompanied by a decrease of linoleic acid. These modifications are reflected in plasma where linoleic acid is greatly diminished but where an important increase of palmitic acid is noted besides palmitoleic acid. A possible relation between higher clotting activity of platelets and those modifications in their phospholipids is discussed.

Aged↗
PubMed1978

Impairment of platelet thromboxane A2 generation and of the platelet release reaction in two patients with congenital deficiency of platelet cyclo-oxygenase.

Two cases of thrombocytopathia with congenital deficiency of platelet cyclo-oxygenase were investigated. The platelet release reaction was impaired. There was a marked decrease of aggregation with collagen and with adrenalin and a total absence of aggregation with sodium arachidonate. The platelet response to labile aggregation stimulating substance (LASS, mostly thromboxane A2) was normal. There was no biosynthesis of prostaglandin cyclic endoperoxides or of thromboxane A2 from arachidonic acid. Basal levels of platelet PGE1 were lowered although plasma levels were normal. Thrombin decreased the cyclic AMP content of patients' platelets and also that of control platelets pretreated with aspirin. The patients platelets showed no ultrastructural difference when compared with control platelets, except for a slight decrease of granule volume, but, in contrast to control platelets, thrombin (0.02 U/ml) did not provoke contraction of the patients' platelets.

Adult↗
PubMed1977

[The radioimmunological assay of fibrinogen breakdown products with E antigen during postoperative venous thromboses. Study in 46 cases of arthroplasty for osteoarthrosis of the hip (author's transl)].

Twenty six patients (without thrombosis) had a normal 125I-fibrinogen test, among whom 15 had a normal phlebography; 18 patients (with thrombosis) had a positive 125I-fibrinogen test among whom 11 had a positive phlebography. There was a discrepancy between phlebography and 125I-fibrinogen test in 2 patients. In patients with thrombosis, there is a significantly increase of FgE levels for several days after the intervention. However the measurement of FgE is not a reliable test (4% of false positive and 38% of false negative); but it is always elevated in femoral and popliteal thrombosis.

Adult↗
PubMed1977

A simple radiochemical assay of thromboxane B2, 12-hydroxyeicosatetraenoic acid (HETE) and 12-hydroxyheptadecatrienoic acid (HHT) synthetized by human platelets.

A simple radiochemical assay of thromboxane B2, 12-hydroxyeicosatetraenoic acid (HETE) and 12-hydroxyheptadecatrienoic acid (HHT) produced by platelets from arachidonic acid has been described. Moreover, this assay is suitable for measuring thromboxane A2 trapped as 11-mono-O-methylthromboxane B2 and minor products such as prostaglandins E2, F2alpha and D2. The advantage of this technique is discussed as to its ease and specificity.

Arachidonic Acids↗