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Biomedical subjects

M Boisseau

Publications and source records attributed to M Boisseau.

At least 37 records · Page 2Linked to original sources
PubMed1995

Pyrido[2,3-d]pyrimidin-4(3H)-one derivatives and 1,2,3,4-tetrahydro- pyrido[2,3-d]pyrimidine derivatives: synthesis and in vitro study of their activity against platelet aggregation.

Some new derivatives of pyrido[2,3-d]pyrimidin-4(3H)-one A and 1,2,3,4-tetrahydro-pyrido[2,3-d]pyrimidines B were prepared. The study of their in vitro antiaggregating activity showed that the compounds A possessed an inhibitory potency when aggregation was induced with ADP. Their reduction to derivatives of 1,2,3,4-tetrahydro-pyrido[2,3-d]pyrimidine B led to a new series of molecules possessing a greater antiaggregating power. When compared to that of acetylsalicylic acid under the same conditions, this activity was weaker with collagen, the same with arachidonic acid-induced aggregation, but greater when aggregation was induced by ADP. However, they inhibited serotonin release only slightly. Compared to ginkgolide they remained weaker with PAF-induced aggregation.

Arachidonic Acid↗
PubMed1995

[Rheologic and biophysical aspects of cellular adhesion and aggregation: importance in hemorheology].

Interactions between blood cells in the form of cellular aggregates or adhesion are observed in a variety of normal and pathological conditions. Aggregation of erythrocytes or platelets, adhesion of platelets and leucocytes and immune agglutination of RBC are examples of interactions involving blood cells. Cell adhesion and aggregation are modulated by specific interactions (antigen-antibodies reactions, adhesive macromolecules interactions...) or non-specific (van der Waals forces, electrostatic interactions, molecular bridgings...). These interactions may result in morphological and structural changes, or polarization phenomena. At the dynamic level, cellular adhesion (or aggregation) can divided in 4 main steps: transport, cellular activation (endogenous or exogenous), morphological, physical or steric rearrangements, contact (intercellular or on an artificial surfaces). It will be the nature of the interactions involved in these steps that will determine the binding cohesion and kinetic. In this paper, different types of interactions and the regulation mechanisms of adhesion and aggregation phenomena involved in blood hemodynamics will be summarized and some examples (RBC or platelets aggregation; platelets or leucocytes adhesion) will illustrate the importance of these phenomena in clinical hemorheology.

Biophysical Phenomena↗
PubMed1994

[Quality control in clinical hemorheology: preliminary study by three centers].

Clinical or pharmacological trials require reproducible laboratory tests. The aim of this work was to investigate the conditions of quality control of two laboratory tests, blood viscosity and red cell aggregation used for hemorheology trials in three centers. The results showed that viscosity measurements require 2 standards. For red cell aggregation, the control suspension standardized media (normal an pathological aggregation) showed a good intercentre reproducibility of the dissociation thresholds but a wide variability of aggregation times. Complementary studies in 5 or 6 centres are planned in order to define national standards of quality control.

Blood Viscosity↗
PubMed1993

Interlaboratory evaluation of methods for the assay of Protein C in purified concentrates.

Determination of the quantity and activity of the Protein C molecule is of the utmost importance in highly purified concentrates prepared for replacement therapy. A multicenter study was undertaken to evaluate the comparability and accuracy of Protein C assays from commercial sources. Significant between-assay and interlaboratory differences were found for both functional and immunological assays. The interlaboratory variability is explained in part by the use of different control plasmas. The results also indicate the importance of the diluent used. This study emphasizes the need for standardized methods for determining the characteristics of Protein C concentrates.

Enzyme-Linked Immunosorbent Assay↗
PubMed1993

Plasma thrombomodulin: new approach of endothelium damage.

Endothelium damage is associated with thrombotic risk in a variety of diseases including atherosclerosis, gram negative sepsis, viral infections and neoplastic disease. Therefore, it appears necessary to find a mean for the clinical investigation for such a damage. Among the markers of these cells, thrombomodulin which is a membrane glycoprotein, seems to be of great interest for this purpose. Actually, thrombomodulin is also found in plasma, following an endothelial lesion. Plasma levels of thrombomodulin are increased in a certain number of pathologies associated with endothelium lesion: atheromatous arterial disease, disseminated intravascular coagulation syndrome and also in systemic lupus erythematosus where the levels of plasma thrombomodulin are related to the severity of the pathology. Moreover, previous in vitro studies confirm the fact that the release of thrombomodulin from the endothelial cell membrane occurs during the course of injury by activated leukocytes or hydrogen peroxide. So, one can suppose a prospective interest in the measurement of plasma thrombomodulin as a diagnostic tool for the approach of endothelium damage.

Endothelium, Vascular↗
PubMed1992

Thieno[2,3-d]pyrimidin-4(3H)-one derivatives and 1,2-dihydrogenated homologues: synthesis, enhanced in vitro antiaggregant activity for reduced compounds.

Some derivatives of thieno[2,3-d]pyrimidin-4(3 H)-one A and their 1,2-dihydrogenated homologues B were synthesized. The study of their in vitro antiaggregating activity showed that the first compounds exhibited significant inhibiting power when aggregation was induced with ADP. Their reduction to derivatives of 1,2-dihydrothieno[2,3-d]pyrimidin-4(3 H)-one led to a new series of molecules possessing a large antiaggregant activity. When compared to that of acetylsalicylic acid under the same conditions, this activity was the same with collagen or arachidonic acid-induced aggregation, but greater when aggregation was induced by ADP. Serotonin release was also inhibited.

Adenosine Diphosphate↗
PubMed1992

Synthesis and in vitro study of platelet antiaggregant activity of some 4-quinazolinone derivatives.

Some new 4-quinazolinones were prepared. Their antiplatelet activity was evaluated in vitro with respect to aggregation induced by ADP, collagen, arachidonic acid and the platelet serotonin release reaction. Most molecules showed an inhibiting power similar to that of acetylsalicylic acid under the same conditions, and even greater when aggregation was induced by ADP. Reduction of the 4-quinazolinone derivatives to their 1,2,3,4-tetrahydroquinazoline homologues produced an increase in platelet inhibitory action except when ADP is the inductor.

Blood Platelets↗
PubMed1991

Action of some salicylate derivatives on in vitro platelet aggregation. Inhibitory and inhibition antagonistic effects.

Twenty salicylate derivatives were tested for their antagonistic activity on the inhibitory effect of aspirin on platelet aggregation. The blocking effect was not limited to the salicylate but also characterised some of its substituted compounds. The substituant influence did not seem to be related to electronic or size parameters. This antagonistic activity of these derivatives decreased as concentrations increased, owing to the emergence of their own inhibitory activity: several salicylate derivatives showed dual inhibitory and inhibition antagonistic activity, with both properties present at the same concentration. A mechanism involving dissociated activities on the two enzymatic sites of cyclooxygenase is proposed.

Arachidonic Acid↗
PubMed1991

An open trial of enoxaparin in the treatment of deep vein thrombosis of the leg.

An open and prospective phase II trial assessing the action of a fixed dose of a low molecular weight heparin (enoxaparin), determined by the patient's weight, in the treatment of established deep vein thrombosis of the leg is hereby described. A series of 51 patients received a regimen of 1 mg.kg-1 or 105 anti-Xa IU.kg-1 s.c. every 12 h for a period of 12 days. Thromboses were categorized as postsurgical (28 cases) or medical (23 cases). There was a significant improvement in clinical signs (pain and edema) and phlebographic indices (Marder and Arnesen scores). The extent of vascular clearing was a 30% reduction in phlebographic scores between day 0 and day 12. Only 5 patients had an absence of improvement. Two of the 51 patients stopped the drug in the first week of treatment because of bleeding. There were no occurrences of thrombocytopenia, and the agent was well tolerated.

Aged↗
PubMed1991

[Multicenter study on purified protein C concentrates and defined plasma levels].

A variety of protein C assays are available as commercial kits. A collaborative study was undertaken to evaluate the performance of protein C assays. Various samples including calibrated plasmas and high purity concentrates destined to therapy were distributed among five laboratories. This comparison of protein C assays indicates that protein C levels measured by different functional or immunological assays and by five laboratories are very close for calibrated plasmas but not for high purity concentrates. The selection of the standard and the dilution buffer for protein C concentrates have important implications for the interpretation of the results. Dilution of purified protein C concentrates in protein C deficient plasma which restaure a total protein level similar to that of normal plasma improve the accuracy of functional protein C assays.

Chromogenic Compounds↗
PubMed1989

[Low molecular weight heparin: an real alternative in thrombolysis in hemodialyzed patients. A trial of coronary thrombolysis].

Fibrinolytic treatments pose serious problems in subjects at high risk for hemorrhage, such as those requiring chronic dialysis. A 36-year-old patient requiring dialysis for the last 14 years due to chronic kidney failure was hospitalized for unstable angina combined with calcified mitral stricture. Prompt coronary arteriography revealed recent intracoronary thrombi. The failure of drug treatment and the surgical indication in light of unstable angina led the authors to use low-molecular-weight heparin b.i.d. for 12 days with monitoring of laboratory parameters (anti-Xa activity, APTT). No thrombotic or hemorrhagic episode was recorded. Control angiography indicating partial lysis of the left and right intracoronary thrombi led to exact evaluation of the residual underlying stenoses. A double aortocoronary bypass was subsequently performed combined with replacement of the mitral valve. This case gives a glimpse of the potential value of low-molecular-weight heparin as a valid alternative to conventional fibrinolysis in subjects requiring dialysis.

Adult↗
PubMed1989

Study of the effect of metformin on platelet aggregation in insulin-dependent diabetics.

The role of metformin on platelet aggregation was studied in subjects affected by relatively well controlled type 1 diabetes. 1700 mg of metformin were added to their usual daily treatment; nothing else was changed. Patients were trained to monitor their own glycaemia and presence of degenerative retinopathy was proved. Before the administration of metformin and on day 21, the platelet induced by 1.25, 2.5 and 5 mumol of ADP and by collagen was studied. Fibrinogen, cholesterol, triglycerides, glycosylated haemoglobin and mean blood glucose levels did not show any significant modification after treatment but the maximum aggregation induced by ADP was significantly decreased; the inhibition of aggregation was particularly sensitive for low doses of ADP. No significant correlation was found between the variations in metabolism data and the reduction of the amplitude of platelet aggregation. Metformin, added to the usual treatment undergone by a diabetic treated with insulin, seems to affect platelet aggregation independently of other metabolic factors.

Adult↗
PubMed1988

Decrease of lipid extractability of chloroform-methanol upon water addition to human erythrocytes.

The yield of lipids extractable by chloroform-methanol 2:1 from human erythrocytes decreases as a function of the relative amount of water added to--or present in--the erythrocyte pellet prior to the lipid extraction. Only slight modifications are observed as long as the volume of water does not exceed that of the red blood cell pellet. As the volume of added water increases, the phosphatidylserine recovery drops dramatically and tends to zero while the yield of the other phospholipids remains unchanged. This phenomenon is not observed when the lipids are extracted by a mixture of isopropanol-chloroform.

1-Propanol↗
PubMed1987

[CY 222, a very low molecular weight heparin, in the curative treatment of deep venous thrombosis. Apropos of 95 cases. Clinical and phlebographic results].

Efficacy of a very low molecular weight heparin, CY 222, in the treatment of deep venous thrombosis of lower limbs was evaluated in a prospective clinical trial instituted in November 1984. CY 222 was administered as subcutaneous injections of 0.03 ml.kg-1 daily (750 anti-Xa U.kg-1.d-1) as 3 divided doses over a minimum of 10 days. Efficacy was rated as a function of clinical and phlebographic criteria. The group of 95 patients treated was a heterogenious one: 38% medical, 62% surgical, and 48% of the total group had partial interruption of vena cava previous to study. The period between first clinical manifestations of the deep thrombosis and therapy varied between one day and 3 months (mean: 1 1/2 days). Clinical symptomatology significantly and globally regressed in 88% of the patients. Comparisons between phlebographic findings at start and end of treatment are expressed using Arnesen's score (cf. table).

Drug Evaluation↗
PubMed1987

[Familial protein C deficiency and venous thrombosis].

Constitutional deficiency in C-protein appears to be a very often underestimated or unrecognized cause of thromboembolic disease. C-protein deficiency in a family (father, son and daughter) was associated with clinical manifestations of thrombosis (post-embolic cor pulmonale, fatal pulmonary embolism, post-partum phlebitis), all appearing before 35 years of age. These three cases confirm the absolute need for routine exploration of physiologic inhibitors of coagulation in all young patients with venous thrombosis.

Adult↗