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Biomedical subjects

M Boisseau

Publications and source records attributed to M Boisseau.

At least 19 recordsLinked to original sources
PubMed1999

Three months supplementation of hyperhomocysteinaemic patients with folic acid and vitamin B6 improves biological markers of endothelial dysfunction.

Hyperhomocysteinaemia is a risk factor for premature atherosclerosis and venous thromboembolic disease. Supplementation with folic acid and vitamin B6 has been shown to decrease plasma homocysteine but data fail to assess an effect on the progression of vascular disease. We measured plasma homocysteine and two markers of endothelial injury (plasma soluble thrombomodulin and von Willebrand factor) at baseline and after 3 months of treatment with folic acid and vitamin B6. After this treatment there was a significant decrease in fasting soluble thrombomodulin (-15 ng/ml, 95%CI 5-22.2). Von Willebrand factor was significantly raised after methionine load at baseline but did not significantly rise after supplementation.

Adult↗
PubMed1999

[Hemorheology and vascular endothelial cells].

The vascular endothelium is a biologically active monolayer of cells providing an interface between the blood flow and tissues. Vascular Endothelial Cells (VEC) have two functional states. The endothelium is normally anti-thrombotic and anti-adhesive to ensure blood fluidity. During aggressions, such as atherosclerosis, inflammation states, metabolic diseases (through chemical or mechanical stimuli), VEC can reverse its functions by expressing stored material or by slower involvement of previously are repressed genes. Endothelial cells have three types of anti-thrombotic properties: vaso regulating properties: VEC release vasomotor components, such as endothelin (vasoconstriction), prostacyclin and nitric oxide, (vasodilatation). Endothelial cells also have antithrombotic and hemostatic properties. They express proteoglycans on their surface, including some negative-charge, plasminogen, sulfate glycosaminoglycans (heparan-sulfate), and secrete plasminogen tissular activator (t-PA) and tissular factor inhibitor. One fundamental action of the endothelium in that area is the production and expression of thrombomodulin, a thrombin receptor. This function has a major anticoagulation effect, controlling continual thrombin generation at the sub-endothelium and blood cell interface. Moreover, endothelial cells show anti-adhesion properties. During cardio-vascular diseases, all of these properties may be reversed. Thus the VEC have a determinant role in hemodynamic control through these various metabolic activities, such as control of homeostasis, vascular tone, blood fluidity, coagulating properties, cellular adhesion. Otherwise, many studies have demonstrated that local blood flow conditions have a crucial role on the VEC properties (mechanoactivation and mechanotransduction concept). In conclusion, knowledge of all the properties of the endothelial cells and control of the phenomena which define their functions is a key element in understanding cardiovascular diseases.

Animals↗
PubMed1999

Hemorheology and vascular endothelial cells.

The vascular endothelium is a biologically active monolayer of cells provided an interface between blood and tissues. Vascular endothelial cells (ECs) have two functional states, which are allowed by their different properties: (i) vaso regulating properties: ECs releases vasomotor components, as endothelin (vaso constriction), prostacyclin and nitrite oxide (vaso dilatation); (ii) antithrombotic and hemostatic properties; and (iii) anti-adhesion properties. The endothelium is normally antithrombotic and anti-adhesive to ensure blood fluidity. During many cardio-vascular diseases, these properties may be reversed. Thus, the ECs have a determinant role in hemodynamic control through these various metabolic activities. Otherwise, many studies have demonstrated that local blood flow conditions have a crucial role on the EC properties (mechanotransduction concept). The knowledge of the properties of ECs and the control of the phenomena which define their functions is a key element in the cardiovascular diseases understanding.

Animals↗
PubMed1998

Erythrocyte hyperaggregation and thrombogenic dysfibrinogenemia.

Erythrocyte aggregation was measured in 12 patients with congenital dysfibrinogenemia. The results showed hyperaggregation in four patients who had presented a thrombotic disorder, while aggregation was entirely normal in patients with asymptomatic dysfibrinogenemia. None of the four symptomatic patients had any other anomaly of hemostasis, in particular no coagulation inhibitor deficit or anti-phospholipid antibodies. The possible involvement of erythrocyte hyperaggregation in the thrombotic process is discussed.

Adult↗
PubMed1997

[Assay of plasma thrombomodulin in systemic diseases].

Membrane thrombomodulin (TM) is a very efficient natural anti-thrombin glycoprotein with anticoagulant properties expressed on endothelial cell surface. Circulating plasmatic thrombomodulin (TMp) detected by enzyme immunoassay in plasma is considered as a cell marker of endothelial injury. The TMp levels are increased in many conditions (diabetes mellitus, atheromatous disease...). In cases of collagen vascular diseases, where vascular endothelium damage is suspected, TMp is increased particularly in systemic lupus erythematosus (SLE) and systemic sclerosis (SSc). It is noteworthy that the TMp level is correlated with disease activity. Since TMp is a non specific marker of endothelial damage, it may be of interest as a useful marker for the supervision of these diseases. Further studies are needed on larger series. TMp level change during spontaneous evolution or under treatment will help determine wether TMp is a predictor and prognostic marker of these systemic diseases.

Acute Disease↗
PubMed1997

Acute stroke in a young female with anti-human beta2-glycoprotein I antibodies.

We report the case of a woman who, at the age of 27, developed a cerebral arterial occlusion. The laboratory investigations showed an anti-human beta2-glycoprotein I antibody, but no other biological sign of antiphospholipid antibody syndrome or autoimmune disorders. The patient otherwise presented with diabetes and moderate obesity. The species specificity of anti-beta2-glycoprotein I antibodies probably explains the discrepancy between false negative results for antiphospholipid antibodies assayed by clotting and ELISA studies and positivity for anti-human beta2-glycoprotein I. Further studies will be important to evaluate the frequency of such antibodies, as well as their value as a risk factor for venous and arterial thrombosis, and their signification within the antiphospholipid antibody syndrome.

Adult↗
PubMed1997

Soluble adhesion molecules and endothelial cell damage in HIV infected patients.

Endothelial damage is present in HIV infection but our understanding of markers and mechanisms is incomplete. We found increased levels of markers of endothelial cell damage such as von Willebrand factor (vWf), soluble thrombomodulin (sTM) and adhesion molecule E-selectin in 90 subjects seropositive for HIV relative to healthy controls. sTM was strongly raised in those patients with the lowest CD4+ cell count (p < 0.001), but levels of vWf increased at each incremental fall in CD4+ cell count and the two indices correlated significantly (r = -0.485, p < 0.001). vWf correlated strongly with levels of the inflammatory cytokines tumor necrosis factor (TNF-alpha) and alpha interferon (IFN-alpha) but sTM correlated only weakly with IFN-alpha. We suggest that increased vWf is largely the result of inflammatory stimulus of the endothelium but that sTM is found only in those patients with more severe disease, and so truly represents endothelial damage.

Adolescent↗
PubMed1996

Influence of rhGM-CSF on Ara-C sensitivity of patients with acute myeloid leukemia in relapse: a flow cytometry study.

Twenty-three patients with acute myelogenous leukemia (AML) in first relapse were treated with high-dose cytosine-arabinoside (Ara-C) and amsacrine or idarubicin. To prime the cells, the patients were given rhGM-CSF. We studied the influence of 48-h infusion of rhGM-CSF on proliferation and Ara-C sensitivity of leukemic cells both ex vivo and in vitro. We found that a 48-h infusion of rhGM-CSF increased both white blood cell counts and peripheral blood blast cell percentages. Using a Bromodeoxyuridine/DNA (BrdUrd/DNA) staining in flow cytometry, we found an non-constant increase in cells in the S-phase. Ex vivo 48-h culture of leukemic cells with or without rhGM-CSF, with or without other hematopoietic growth factors (HGFs), showed a greater increase of the cells in the S-phase with GF but no correlation with the ex vivo results. We used a method of quantitation of the DNA synthesis previously described (Lacombe F., et al. (1992) Cytometry 13, 730) to monitor the Ara-C sensitivity of the cells in S-phase before and after 48-h infusion with rhGM-CSF. We observed a great variation in the Ara-C sensitivity of the leukemic cells before and after infusion with rhGM-CSF from one patient to another. The BrdUrd/DNA method seems a convenient method to study the influence of HGFs on Ara-C sensitivity of the patients.

Acute Disease↗
PubMed1996

Vascular endothelial lesion in patients undergoing bone marrow transplantation.

Changes in endothelial cell activity are likely to play a role in the thrombotic complications of bone marrow transplantation (BMT) such as the development of veno-occlusive disease. Accordingly, we measured established plasma endothelial cell markers von Willebrand factor (vWf), soluble thrombomodulin (sTM), soluble ICAM-1 (sICAM-1), and possible inducers of these molecules, TNF alpha and elastase, in the plasma of 25 patients, 1 week before as well as 1 and 3 weeks after BMT. Compared to healthy age and sex-matched controls, patients exhibited increased vWf and sTM. One week after transplantation, there were significant increases in vWf and sICAM-1, with a significant fall in elastases. Three weeks after the transplantation, sICAM-1 and, to a lesser extent, vWf increased still further, whereas elastases were unchanged. There were no significant changes in sTM and in TNF alpha through the serial study. Our data suggest that before conditioning, vascular endothelium is damaged by both injury and activation, as seen by the variations of vWf and sTM. After transplantation, the enhancement of this damage seems to be more specifically related to activation, since we observed a strong subsequent increase in vWf and markedly in sICAM-1.

Adolescent↗
PubMed1995

Correction of post-renal transplant erythrocytosis by enalapril.

We studied whether post-renal transplant erythrocytosis (PRTE) could be corrected by enalapril with minimal side-effects, thus avoiding iterative phlebotomies or bilateral nephrectomy of native kidneys. From our renal transplant patients, 12 presented a true PRTE as defined by a 51-Cr red blood cell mass (RBCM) above 32 ml/kg for women and above 36 ml/kg for men. Secondary polycythemia was ruled out: all the patients had a normal renal artery pulsed ultrasonography; in all cases the blood arterial 02 saturation was above 96%. Bone marrow aspiration and histology were performed for each patient: none of them showed evidence of Vaquez disease. All of them had stable renal function i.e. the mean serum creatinine was 112.8 +/- 26.3 mumol/l. They all received the same immunosuppression: azathioprine; ciclosporine A; methylprednisolone. PRTE occurred within the first year post transplant (median 7.5 months; range: 2-34). Their mean RBCM was 37.38 +/- 2.7 ml/kg. Their mean serum value of Epo was 17.41 +/- 13.5 mU/ml (range: 9.1-54). After informed consent, all patients received enalapril starting with 5 mg/day, progressively increased to 20 mg/day, if necessary, in order to maintain the hematocrit below 45%. The mean daily dosage of enalapril was 13.75 +/- 6.1 mg (range: 5-20). The mean follow-up was 14.8 months (range: 3.5-29.5). There was no change in renal function (mean serum creatinine: 126.3 +/- 35 mumol/l). A successful response to enalapril was obtained with a median of 40 days (range: 20-120). 11 patients out of 12 responded to enalapril with a decrease of Hb (14 +/- 2 g/dl vs 16.8 +/- 1.04 g/dl; p = 0.0006) and Ht (41.9 +/- 6.17% vs 51.14 +/- 2%; p = 0.0002) without a significant decrease of Epo (8.1 +/- 3.87; p = 0.1). One patient did not respond to enalapril nor to captopril, but did respond to a combined treatment of enalapril and theophilline. Moreover, all PRTE patients but two did not have Epo levels, before enalapril, above the normal range, suggesting mechanisms other than Epo overproduction by native kidneys i.e. erythropoiesis dysregulation. In conclusion, all patients but one were successfully treated by enalapril without side effects. The treatment was effective as early as 3 weeks from the start and avoided the need for iterative phlebotomies and nephrectomy of native kidneys.

Adult↗
PubMed1995

Circulating endothelial markers and ischemic status in peripheral occlusive arterial disease.

In 34 patients with peripheral occlusive arterial disease, circulating levels of endothelial cell markers were compared with the ischemic status. Unlike tissue plasminogen activator and plasminogen activator inhibitor, plasma levels of thrombomodulin were closely related to both transcutaneous oxygen pressure (p = 0.01) and the graded clinical stages of disease (p = 0.02). Levels of von Willebrand factor were correlated only with the transcutaneous oxygen pressure (p = 0.04). Since thrombomodulin and von Willebrand factor constitute markers of endothelial cell damage, the extent of endothelial injury would appear to be determined by the ischemic status.

Aged↗
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↗