References of "DAVID, Jean-Louis"
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See detailNew developments on thromboxane and prostacyclin modulators. Part II: prostacyclin modulators
De Leval, X.; Hanson, Julien ULg; David, Jean-Louis ULg et al

in Current Medicinal Chemistry (2004), 11

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See detailProgress in the field of GPIIb/IIIa antagonists
Hanson, Julien ULg; De Leval, X.; David, Jean-Louis ULg et al

in Current Medicinal Chemistry - Cardiovascular and Hematological Agents (2004), 2

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See detailPharmacological evaluation of BM-573, a dual thromboxane A(2) receptor antagonist and thromboxane synthase inhibitor, as potential anti-metastatic agent
de Leval, X. J.; Dassesse, T.; Benoit, V. et al

in Blood (2003, November 16), 102(11, Part 2), 72

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See detailPharmacological evaluation of the novel thromboxane modulator BM-567 (I/II). Effects of BM-567 on platelet function
Dogne, J. M.; de Leval, X.; Kolh, Philippe ULg et al

in Prostaglandins, Leukotrienes, and Essential Fatty Acids (2003), 68(1), 49-54

The aim of this work was to evaluate the effects of BM-567 ( N-pentyl-N'-[(2-cyclohexylamino-5-nitrobenzene)sulfonyl]urea), a torasemide derivative. on both thromboxane A(2) (TXA(2)) receptors (TP) and ... [more ▼]

The aim of this work was to evaluate the effects of BM-567 ( N-pentyl-N'-[(2-cyclohexylamino-5-nitrobenzene)sulfonyl]urea), a torasemide derivative. on both thromboxane A(2) (TXA(2)) receptors (TP) and thromboxane synthase of human platelets. The drug affinity for TP receptors of human washed platelets has been determined. In this test BM-567 showed a high affinity (IC50: 1.1+/-0.1 nM) for the TP receptors in comparison with BM-531 (IC50: 7.8+/-0.7 nM) and sulotroban (IC50: 931+/-85 nM), two TXA(2) antagonists. We also demonstrated that BM-567 prevented platelet aggregation induced by arachidonic acid (AA) (600 muM) (ED100: 0.20+/-0.10muM), U-46619, a stable TXA(2) agonist (1 muM) (ED50: 0.30+/-0.04 muM) and collagen (1 mug ml(-1)) (% of inhibition: 44.3+/-4.3% at 10 muM) and inhibited the second wave of ADP (2 muM). Moreover, when BM-567 was incubated in whole blood from healthy donors, the closure time measured by the Platelet Function analyzer (PFA-100) was significantly prolonged (closure time: 215+/-21 s) by using collagen/epinephrine cartridges. Finally, at the concentration of 1 muM, BM-567 completely reduced the TXB2 production from human platelets stimulated with AA (600 muM). These results indicate that BM-567 is a novel combined TXA(2) receptor antagonist and thromboxane synthase inhibitor characterized by a powerful antiplatelet potency. (C) 2002 Elsevier Science Ltd. All rights reserved. [less ▲]

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See detailPharmacological evaluation of the novel thromboxane modulator BM-567 (I/II). Effects of BM-567 on platelet function
Dogné, Jean-Michel ULg; De Leval, X.; Kolh, Philippe ULg et al

in Prostaglandins, Leukotrienes, and Essential Fatty Acids (2003)

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See detailIncreased TGFβ1 plasma level in patients with lung cancer: potential mechanisms
Barthelemy, Nicole ULg; David, Jean-Louis ULg; Bosquee, Léon ULg et al

in European Journal of Clinical Investigation (2002), 32(3), 193-198

Background Plasma transforming growth factor β1 (TGFβ1) levels are elevated in patients with lung cancer. As TGFβ1 is mainly found in platelets and as nonmalignant pulmonary diseases (NMPD) are frequently ... [more ▼]

Background Plasma transforming growth factor β1 (TGFβ1) levels are elevated in patients with lung cancer. As TGFβ1 is mainly found in platelets and as nonmalignant pulmonary diseases (NMPD) are frequently associated with lung cancer, we investigated the potential contribution of platelet degranulation and/or of a concomitant NMPD to the increased plasma levels of TGFβ1 reported in patients with lung cancer. Materials and Methods Blood samples were collected in duplicate from 30 healthy subjects, 14 patients suffering from NMPD and 37 patients with lung cancer. The platelet count was determined and the samples were processed to obtain plasma. One sample was collected in EDTA (EDTA plasma) and the other in a mixture inhibiting platelet degranulation (PIM plasma). TGFβ1 concentrations and β-thromboglobulin (βTG) levels, an index of platelet degranulation, were measured in both plasma samples. Results TGFβ1 and βTG plasma levels measured in PIM plasma were lower than those obtained in EDTA plasma. With respect to PIM plasma, both TGFβ1 and βTG levels were higher in patients with lung cancer than those with NMPD and in healthy individuals. In patients with NMPD, only TGFβ1 levels were increased as compared to healthy controls, βTG levels being similar. Conclusion Methods for collecting and processing blood samples are critical in determining reliable circulating TGFβ1 levels. Increased TGFβ1 plasma levels observed in patients with lung cancer are related, at least partly, to concomitant NMPD and also to platelet degranulation as proved by increased βTG levels. [less ▲]

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See detailEffects of thromboxane A2 receptor antagonists and thromboxane synthase inhibitors on osteogenic sarcoma cell-induced platelet aggregation
De Leval, X.; Benoit, V.; Neven, P. et al

in Fundamental & Clinical Pharmacology (2002), 16

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See detailEffects of BM-573, a dual thromboxane A(2) receptor antagonist and thromboxane synthase inhibitor, on osteogenic sarcoma cell-induced platelet aggregation
de Leval, X.; David, Jean-Louis ULg; Neven, P. et al

in Blood (2001, November 16), 98(11, Part 2), 43

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See detailLe cas clinique du mois. A propos d'un cas de syndrome des antiphospholipides
Fumal, Arnaud ULg; Belachew, Shibeshih ULg; Moonen, Gustave ULg et al

in Revue Médicale de Liège (2001), 56(7), 480-3

This article reports a case of Anton-Babinski syndrome, due to right middle cerebral artery thrombosis and attributed to a likely primary antiphospholipid syndrome. It is always difficult to diagnose the ... [more ▼]

This article reports a case of Anton-Babinski syndrome, due to right middle cerebral artery thrombosis and attributed to a likely primary antiphospholipid syndrome. It is always difficult to diagnose the latter, especially in the case of our patient who had a past history of multiple venous thromboses but also a heterozygosity for the mutation of the factor V of Leyden. We reviewed the literature dedicated to the prothrombotic events linked to the presence of these antiphospholipid antibodies: the lupus anticoagulant and the anticardiolipin antibodies. [less ▲]

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See detailPharmacology of the Thromboxane Receptor Antagonist and Thromboxane Synthase Inhibitor Bm-531
Dogné, J. M.; Rolin, S.; de Leval, X. et al

in Cardiovascular Drug Reviews (2001), 19(2, Summer), 87-96

BM-531 (N-tert-butyl-N'-[(2-cyclohexylamino-5-nitrobenzene)sulfonyl]urea), a torasemide derivative, is a novel noncarboxylic thromboxane receptor antagonist and thromboxane synthase inhibitor. Indeed, its ... [more ▼]

BM-531 (N-tert-butyl-N'-[(2-cyclohexylamino-5-nitrobenzene)sulfonyl]urea), a torasemide derivative, is a novel noncarboxylic thromboxane receptor antagonist and thromboxane synthase inhibitor. Indeed, its affinity for human washed platelet TXA2 receptors labeled with [3H]SQ-29548 (IC50 = 0.0078 microM) is higher than sulotroban (IC50 = 0.93 microM) and SQ-29548 (IC50 = 0.021 microM). Moreover, BM-531 is characterized by a potent antiaggregatory property. Indeed, on one hand, in human citrated platelet-rich plasma BM-531 prevents platelet aggregation induced by arachidonic acid (600 microM) (ED100 = 0.125 microM), U-46619, a stable TXA2 agonist (1 microM) (ED50 = 0.482 microM) or collagen (1 microgram/mL) (percentage of inhibition: 42.9% at 10 microM) and inhibits the second wave of ADP (2 microM)-induced aggregation. On the other hand, when BM-531 is incubated in whole blood from healthy donors, the closure time measured by the recently developed platelet function analyser (PFA-100) is significantly prolonged. In addition, at the concentrations of 10 and 1 microM, BM-531 totally prevents the production of TXB2 by human platelets activated by arachidonic acid. Finally, at 10 microM, BM-531 significantly prevents rat fundus contractions induced by U-46619 but not by prostacyclin. These results suggest that BM-531, which is devoid of the diuretic property of torasemide, can be regarded as a promising antiplatelet agent. [less ▲]

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See detailSma Circuits Reduce Platelet Consumption and Platelet Factor Release During Cardiac Surgery
Defraigne, Jean-Olivier ULg; Pincemail, Joël ULg; Dekoster, Guy ULg et al

in Annals of Thoracic Surgery (2000), 70(6), 2075-81

BACKGROUND: Platelet count and function are particularly damaged by cardiopulmonary bypass (CPB). This study evaluated the effects of a novel CPB circuit in terms of platelet count and activation, and ... [more ▼]

BACKGROUND: Platelet count and function are particularly damaged by cardiopulmonary bypass (CPB). This study evaluated the effects of a novel CPB circuit in terms of platelet count and activation, and postoperative need for blood products. METHODS: One hundred patients undergoing coronary grafting were randomized in two groups: control group (n = 50) and test group (n = 50, surface modifying additives circuit, SMA group). Blood samples were taken before, during, and after CPB. Postoperative blood loss, number of transfused blood products, and postoperative variables were recorded. RESULTS: The platelet count decreased less in the SMA group compared to the control group (end of CPB: respectively, 165 +/- 9 x 10(3)/mm3 vs 137 +/- 8 x 10(3)/mm3; p < 0.01). This was paralleled by a reduction in beta-thromboglobulin plasma levels in the SMA group. There was a trend to decreased blood loss in the SMA group, but the difference was significant only in patients taking aspirin preoperatively (p < 0.05). In the SMA group nearly 50% less fresh frozen plasma and platelet units were administered (p < 0.01). No operative deaths were observed. CONCLUSIONS: The use of circuits with surface additives is clinically safe, preserves platelet levels, and attenuates platelet activation. This may lead to a reduced need for blood products. [less ▲]

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See detailAntiplatelet Activity of Clopidogrel in Coronary Artery Bypass Graft Surgery Patients
David, Jean-Louis ULg; Limet, Raymond ULg

in Thrombosis and Haemostasis (1999), 82(5), 1417-21

Clopidogrel is a recently introduced platelet ADP receptor antagonist, belonging to the thienopyridine derivatives, like its analogue ticlopidine. Its potential advantage is to be safer than ticlopidine ... [more ▼]

Clopidogrel is a recently introduced platelet ADP receptor antagonist, belonging to the thienopyridine derivatives, like its analogue ticlopidine. Its potential advantage is to be safer than ticlopidine. At 75 mg/od clopidogrel significantly inhibits platelet aggregation in ambulatory patients with symptomatic atherosclerotic disease and it prevents the recurrence of ischemic events more efficiently than aspirin. Its adequate dose in more acute situations remained to be determined. Therefore, sixty two patients with coronary artery disease were randomly assigned in four groups treated, within 24 h after coronary artery bypass graft, by clopidogrel 50 mg/od, 75 mg/od or 100 mg/od or by ticlopidine 250 mg/bid which was considered as the reference. The tolerance of clopidogrel was fairly good during the whole period of the study. Bleeding time and ex-vivo platelet aggregation induced by ADP 2 microM and 5 microM were performed at day -1, +9 and +28 after surgery. Like ticlopidine, the three dose levels of clopidogrel significantly inhibited ex-vivo platelet activity and prolonged the bleeding time at day 28. However, unlike ticlopidine, the inhibitory effects of clopidogrel were not significant at day 9, especially with 75 mg/od, a dose which was found to significantly protect patients in a chronic situation. Hence, although the clinical outcome for patients included in this limited study was the same in the four groups, these results suggest that the dose regime of clopidogrel should be more extensively investigated during the early period following coronary artery bypass graft, facing an overproduction of young and hyperreactive platelets. By analogy, the dose regime should be also investigated in other situations with an acute risk of arterial thrombotic occlusion. [less ▲]

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See detailConcentrations plasmatiques de la vitamine K1 et de l'acenocoumarol en fonction du temps de quick (I.N.R.)
Gougnard, Thierry; Charlier, Corinne ULg; David, Jean-Louis ULg et al

in Acta Clinica Belgica. Supplementum (1999), S1

Reduced vitamins K are acting as cofactors of glutamic carboxylation of procoagulant factors (II, VII, IX and X). The reduction of these vitamins is inhibited by oral anticoagulants. The response to ... [more ▼]

Reduced vitamins K are acting as cofactors of glutamic carboxylation of procoagulant factors (II, VII, IX and X). The reduction of these vitamins is inhibited by oral anticoagulants. The response to antivitamins K is individual and may change during the treatment of a patient. The determinations of plasmatic vitamin K and acenocoumarol may help to explain the mechanism of a resistance to the anticoagulant therapy. Quantifications of vitamin K1 are realized after liquid-liquid extraction with liquid chromatography and fluorescence detection after post-column reduction. For acenocoumarol, plasma concentration is measured, after liquid-liquid extraction, by liquid chromatograph, with ion trap mass spectrometer detector. [less ▲]

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See detailLes agents antiplaquettaires en chirurgie vasculaire périphérique
VAN DAMME, Hendrik ULg; DAVID, Jean-Louis ULg; Limet, Raymond ULg

in Revue Médicale de Liège (1999), 54(2), 109-17

Prescription of platelet inhibitors after arterial surgery is common use. The major concern of the vascular surgeon is to maintain patency of arterial reconstructions. Major causes of graft failure or ... [more ▼]

Prescription of platelet inhibitors after arterial surgery is common use. The major concern of the vascular surgeon is to maintain patency of arterial reconstructions. Major causes of graft failure or arterial thrombosis are the non-thromboresistant nature of the grafts and of the endarterectomised or balloon-dilated surfaces, restenosis due to intimal hyperplasia and progression of atherosclerotic disease in in- or outflow vessels. Platelet adhesion and intimal injury are the primary causes in both processes of graft thrombosis and intimal hyperplasia. To understand how antiplatelet drugs can interfere with these processes, a brief review of platelet function, and of the main platelet inhibitors (aspirin, dypiridamole, ticlopidine) is given. The pathophysiology of intimal hyperplasia is discussed. From clinical trials of peripheral vascular surgery or percutaneous transluminal angioplasty with or without periprocedural antiplatelet therapy, it appears that platelet inhibitors reduce early failure rate by 50% (thrombosis rate at one year reduced from 40 to 20%). There is also evidence that antiplatelet drugs allow to slow down the progression of the atherosclerotic degenerative process in the outflow vessels and in other vascular territories. For the polyvascular patients with charged passed history, platelet inhibitors reduce the risk of myocardial or cerebral infarction by 30% (secondary prevention). Today, there is a general consensus that antiplatelet drugs, started the day before the procedure, are beneficial for early and late patency of peripheral vascular reconstructions (carotid endarterectomy, infrainguinal bypass grafts or endovascular procedures). [less ▲]

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See detailEffect of Ketoprofen on Paf-Induced Bovine Platelet Aggregation
Bastos da Silva, Miriam; Gustin, Pascal ULg; Herion, Francine ULg et al

in Veterinary Journal (1998), 155(2), 201-203

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See detailProtective Effects of Web 2086 (Paf Antagonist) and Ketoprofen (Nsaid) on Paf-Induced Changes in the Morphological Ultrastructure of Blood Platelets in Calves
Bastos da Silva, Miriam; Doizé, Cécile ULg; Coghe, Joost et al

in Veterinary Research Communications (1998), 22(4), 273-291

The ultrastructure of bovine platelets was examined by transmission electron microscopy without any pretreatment (control), and after WEB 2086 (a triazolodiazepine) or ketoprofen (NSAID) pretreatment ... [more ▼]

The ultrastructure of bovine platelets was examined by transmission electron microscopy without any pretreatment (control), and after WEB 2086 (a triazolodiazepine) or ketoprofen (NSAID) pretreatment, followed by PAF infusion. The blood platelet count was also investigated. The group of calves that received WEB 2086 pretreatment before platelet-activating factor (PAF) infusion did not show a decreased number of platelets. However, in the other group, with ketoprofen pretreatment before PAF infusion, there was a rapid decrease from 1 to 3 min, while from 5 min the number of platelets recovered to the normal value. Electron microscopy revealed that pretreatment with WEB 2086 followed by PAF infusion did not alter the morphological ultrastructure of bovine platelets, except that the microtubules were briefly modified from 1 until 3 min after PAF challenge. After ketoprofen pretreatment, bovine platelets kept their regular shape, the number of dense bodies was not significantly altered, the number of mitochondria was maintained from 5 min after PAF infusion, giant platelets were not observed and the Golgi apparatus was rarely visible. Thus pretreatment with WEB 2086 and ketoprofen before PAF infusion had a protective activity on the ultrastructure of bovine platelets and, in cattle, pretreatment with WEB 2086 and ketoprofen before PAF challenge prevented the thrombocytopenia induced by PAF. [less ▲]

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See detailMorphological alterations of blood platelets induced by Platelet Activating Factor (PAF) and partial inhibition by Ketoprofen in calves
Bastos da Silva, Miriam; Doizé, Cécile ULg; David, Jean-Louis ULg et al

in Veterinary Research (1997), 28(5 Sep-Oct), 489-502

The influence of platelet activating factor (PAF) was investigated in vivo on the ultrastructure of bovine platelets, and on the platelet count. The effect of an intravenous administration of ketoprofen ... [more ▼]

The influence of platelet activating factor (PAF) was investigated in vivo on the ultrastructure of bovine platelets, and on the platelet count. The effect of an intravenous administration of ketoprofen (a non-steroidal anti-inflammatory drug) pretreatment followed by PAF infusion was also observed in a group of six healthy male Friesian calves. PAF infusion alone caused a moderate thrombocytopenia, which peaked one minute post challenge and returned to levels not significantly different from control after 30 min. Electron microscopy revealed that after PAF infusion, platelets lost their lentiform shape and became irregular, with many pseudopods. Their microtubules became impossible to distinguish. The numbers of alpha granules and dense bodies were significantly decreased. Glycogen particles became rare or even disappeared. Giant platelets occasionally appeared. The Golgi apparatus was more often visible and the number of mitochondria was significantly increased. Ketoprofen pretreatment lowered PAF-induced thrombocytopenia and decrease in the number of dense bodies. Under these conditions, the Golgi apparatus was rarely visible and giant platelets were not observed. These results showed that the morphological ultrastructure of blood platelets in bovines were modified following PAF infusion and that ketoprofen pretreatment before PAF infusion provided partial protection, limiting the extent of the morphological alterations and maintaining a normal platelet count [less ▲]

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See detailThe Effect of Intravenous Administration of Web 2086 on Paf-Induced Platelet Aggregation in Healthy Friesian Calves
Bastos da Silva, Miriam; Gustin, Pascal ULg; Herion, Francine ULg et al

in Veterinary Research Communications (1997), 21(7), 521-531

The in vivo ability of the specific PAF-antagonist WEB 2086, a thienotriazolodiazepine, to inhibit platelet-activating factor (PAF) in cattle was investigated by in vitro determination of platelet ... [more ▼]

The in vivo ability of the specific PAF-antagonist WEB 2086, a thienotriazolodiazepine, to inhibit platelet-activating factor (PAF) in cattle was investigated by in vitro determination of platelet aggregation curves. WEB 2086 was infused intravenously into a group of 5 healthy male Friesian calves in a dose of 3 mg/kg over 1 min. The resultant inhibition peaked between 30 min and 1 h after administration of WEB 2086. The inhibition was significantly reduced after 3 h and became non-significant after 6 h, but maximal pre-treatment aggregation had not been restored by 24 h after the injection of WEB 2086. These results confirm previous results obtained in vitro and suggest that WEB 2086 is a potent antagonist of PAF activity in calves. They also suggest that further clinical studies with WEB 2086 in cattle are desirable. [less ▲]

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See detailCombined Effect of Web 2086 (Paf Antagonist) and Ketoprofen (Nsaid) on Paf-Induced Ex Vivo Platelet Aggregation in Bovine
Bastos da Silva, Miriam; Herion, Francine ULg; Raskinet, Renée ULg et al

in Journal of Veterinary Medicine. A, Physiology, Pathology, Clinical Medicine (1997), 44(2), 65-71

The effect of the specific PAF-antagonist WEB 2086, a thieno-triazolo-diazepine, and ketoprofen, a NSAID, was investigated on PAF-induced bovine platelet aggregation measured ex vivo in platelet-rich ... [more ▼]

The effect of the specific PAF-antagonist WEB 2086, a thieno-triazolo-diazepine, and ketoprofen, a NSAID, was investigated on PAF-induced bovine platelet aggregation measured ex vivo in platelet-rich plasma (PRP). WEB 2086 was infused intravenously over 1 min followed immediately by ketoprofen administration over 1 s (both drugs = 3 mg/kg), in a group of six healthy male Friesian calves. Depending on the PAF concentration, a reversible (10(-8)-10(-9) mol/l) and irreversible (10(-5)-10(-7) mol/l) platelet aggregation was observed. The reversible aggregation was completely blocked by pretreatment of the animal with WEB 2086 and ketoprofen. The inhibitory effects observed during the irreversible aggregation were 47.22%, 54.00% and 88.00% at 10(-5), 10(-6) and 10(-7) mol/l PAF, respectively. Moreover, the aggregation obtained in these condition became reversible. Maximal inhibitory effect of WEB 2086 and ketoprofen on PAF-induced platelet aggregation in calves was observed within 30 min after administration of both drugs. This inhibition persisted even after 24 h and was significantly different from control with P < 0.05. The combined effect of both drugs exceeded the sum of the individual effects (synergism). It was concluded that WEB 2086 and ketoprofen very effectively blocked PAF-induced bovine platelet aggregation in platelet-rich plasma. The study also suggested a synergism between both substances. [less ▲]

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