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127 results on '"Boyer-Neumann C"'

9. Endothelial cell dysfunction in HIV infection

Author

Lafeuillade, Alain, Alessi, M.C., Poizot-Martin, I., Boyer-Neumann, C., Zandotti, C., Quilichini, R., Aubert, L., Tamalet, C., Juhan-Vague, I., and Gastaut, J.A.

Subjects
Endothelium -- Physiological aspects, HIV infection -- Complications, Thrombosis -- Risk factors, Blood clotting disorders -- Physiological aspects, Fibrinolysis -- Physiological aspects, Health
Published
1992

13. The mutation in fibrinogen Bicêtre II (gamma Asn308-->Lys) does not affect the binding of t-PA and plasminogen to fibrin

Author

Grailhe, P., Boyer-Neumann, C., Haverkate, F., Grimbergen, J., Larrieu, M.J., Anglés-Cano, E., and Gaubius instituut Instituut voor verouderings- en vaatziekten onderzoek TNO

Subjects
Biology
Abstract

The aim of this study was to investigate the interactions of t-PA and plasminogen with fibrin derived from an abnormal fibrinogen detected in a 40-year-old male patient who had had an episode of thrombophlebitis with pulmonary embolism. An abnormal fibrinogen was diagnosed on the basis of prolonged thrombin and reptilase times also detected in two other family members. Fibrinogen purified from plasma, in the presence of protease inhibitors, by glycine precipitations, gel filtration and affinity chromatography, was devoid of plasminogen, fibronectin, and vWf. SDS-PAGE analysis according to Laemmli under reducing conditions, showed an abnormal gamma chain (approximately 50% of the total) migrating in a more anodic position (M(r) 48 kDa). By PCR amplification and DNA sequencing, the abnormality was identified as an Asn308-->Lys mutation of the gamma chain. Since such a mutation constitutes a new plasmin cleavage site as first reported for fibrinogen Kyoto I, it may modify interactions of plasminogen and t-PA with carboxy-terminal lysine residues. Ligand-binding studies were therefore performed using intact and plasmin-degraded fibrin surfaces obtained from the abnormal fibrinogen. The plasminogen and t-PA binding isotherms obtained with the abnormal fibrinogen were similar to the control. Moreover, the stimulation by fibrin of plasminogen activation by t-PA was not different from the control. These results suggest (i) that the lysine 308 residue may not be exposed to plasmin cleavage in fibrin, and (ii) that the thrombotic accident of the propositus cannot be explained by an abnormality of the plasminogen/t-PA binding to fibrin.

Published
1993

39. [Pulmonary arterial hypertension of chronic thrombo-embolic origin. 70 patients]

Author

Azarian R, Brenot F, Olivier SITBON, Musset D, Grimon G, Boyer-Neumann C, Rain B, Dartevelle P, and Simonneau G

Subjects
Adult, Aged, 80 and over, Male, Hypertension, Pulmonary, Angiography, Hemodynamics, Endarterectomy, Middle Aged, Thromboembolism, Chronic Disease, Humans, Female, Radionuclide Imaging, Aged, Lung Transplantation
Abstract

Chronic thrombo-embolic pulmonary hypertension is a rare and aberrant outcome of acute pulmonary embolism. Because it has become a potentially curable form of pulmonary hypertension, the frequency of recognized cases has increased. We report a case series of 70 patients with chronic thromboembolic pulmonary hypertension evaluated in our institution between 1984 and 1993, and discuss diagnostic clues and therapeutic approaches.All patients complained of dyspnoea on exertion. A history of acute thrombo-embolic events and lung murmurs were found in 60% and 17% of patients respectively. Coagulation disorders were found in 30% of the patients tested; the most common abnormality was lupus anticoagulant. The key non-invasive study for diagnosis was the lung perfusion scan which showed at least one segmental or wider perfusion defects in all patients. Pulmonary angiography confirmed the diagnosis in all cases and, sometimes associated with intravascular ultrasound imaging, established the feasibility of thromboendarterectomy. Medical therapy included the use of long-term oral anticoagulant, and in case of lower limb venous thrombosis, inferior vena cava filtration. Finally two surgical procedures were discussed in selected patients: thromboendarterectomy and lung transplantation. Since 1988, eight patients have benefited from lung transplantation (six patients are still alive) and 11 patients underwent thromboendarterectomy which was successful in 9 patients leading to dramatic functional and haemodynamic improvement.Chronic thrombo-embolic pulmonary hypertension is a severe, sometimes fatal, disease which can be successfully treated by pulmonary thromboendartectomy and lung transplantation.

47. Safety of therapeutic doses of tinzaparin during pregnancy.

Author

Parent F, Deruelle P, Sanchez O, Meyer G, Girard P, Jilwan F, Boyer-Neumann C, Wolf M, and Simonneau G

Subjects
Adult, Female, Fibrinolytic Agents administration & dosage, Heparin, Low-Molecular-Weight administration & dosage, Humans, Pregnancy, Tinzaparin, Fibrinolytic Agents adverse effects, Heparin, Low-Molecular-Weight adverse effects, Pregnancy Complications, Cardiovascular drug therapy, Pregnancy Outcome, Venous Thromboembolism drug therapy
Abstract

Background/aims: Low molecular weight heparin is recommended for the treatment of venous thromboembolism (VTE) during pregnancy. However, there are few reliable data regarding the safety of therapeutic doses of tinzaparin in this setting. The objective of this study was to assess the safety of once-daily therapeutic doses of tinzaparin for the treatment of VTE during pregnancy., Methods: A retrospective study was carried out in 3 tertiary care centres in France, from 1998 to 2009, including consecutive pregnant women who received once-daily therapeutic doses of tinzaparin (175 IU/kg/day)., Results: We analyzed 87 pregnancies in 83 women, representing a total of 13,320 patient-days of treatment. Live-birth rate was 97.8%, with one case of miscarriage (<20 weeks of gestation) and one case of intrauterine foetal death (≥20 weeks). There was no antenatal major bleeding. Major bleeding occurred in 4 women during an emergency caesarean section. No case of heparin-induced thrombocytopenia and no maternal death were reported. There was no neonatal haemorrhage and no case of congenital abnormality. VTE recurred on treatment in one patient and after treatment interruption for several days in 2 other patients., Conclusions: These results support the safety of once-daily tinzaparin at therapeutic dose for the treatment of VTE during pregnancy., (© 2015 S. Karger AG, Basel.)

Published
2015
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48. Perioperative management of hemostasis for surgery of benign hepatic adenomas in patients with glycogen storage disease type ia.

Author

Mollet-Boudjemline A, Hubert-Buron A, Boyer-Neumann C, Aldea R, Franco D, Trioche-Eberschweiller P, Mas AE, Mabille M, Labrune P, and Gajdos V

Abstract

The development of hepatocellular adenomas in the liver of patients with glycogen storage disease type I is a well-known complication of the disease. Surgical procedures and perioperative managements described so far have reported persistent and important morbidity. We report here a series of six patients (three males and three females) who underwent hepatic resection, and we propose a new hemostatic management protocol comprising glucose infusion, corticosteroids, desmopressin, and antifibrinolytic drugs, used to prevent efficaciously hepatic hemorrhage due to glycogen storage disease (GSD) platelet dysfunction.

Published
2011
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49. Obstetrical Complications and Outcome in Two Families with Hereditary Angioedema due to Mutation in the F12 Gene.

Author

Picone O, Donnadieu AC, Brivet FG, Boyer-Neumann C, Frémeaux-Bacchi V, and Frydman R

Abstract

Backgroud. Hereditary angioedema (HAE) is characterized by recurrent swelling of the skin, the abdomen (causing severe acute pain), and the airways. A recently discovered type caused by mutations in the factor XII gene (designated as HAE type III) occurs mainly in women. Estrogens may play an important role, but few obstetrical complications have been reported. Case. We report the symptoms and obstetrical complications of women in two families with HAE attributable to the p. Thr328Lys mutation in the F12 gene. Clinical manifestations included acute and severe maternal abdominal pain, with transient ascites, laryngeal edema, and fetal and neonatal deaths. Patients had normal C4 levels and a normal C1 inhibitor gene. Administration of C1-inhibitor concentration twice monthly decreased the attack rate in one mother, and its predelivery administration (1000 U) led to the delivery of healthy girls. Conclusions. Obstetricians and anesthesiologists should be aware of this rare cause of unexplained maternal ascites and in utero or fetal death associated with edema.

Published
2010
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50. Functional characterization of fibrinogen Bicêtre II: a gamma 308 Asn-->Lys mutation located near the fibrin D:D interaction sites.

Author

Marchi RC, Carvajal Z, Boyer-Neumann C, Anglés-Cano E, and Weisel JW

Subjects
Adult, Asparagine genetics, Coagulation Protein Disorders etiology, Factor XIII metabolism, Fibrin chemistry, Fibrin genetics, Fibrin ultrastructure, Fibrinogens, Abnormal physiology, Fibrinolysis genetics, Humans, Lysine genetics, Male, Microscopy, Electron, Scanning, Models, Molecular, Reference Values, Blood Coagulation genetics, Coagulation Protein Disorders genetics, Fibrin Fibrinogen Degradation Products genetics, Fibrinogens, Abnormal genetics, Fibrinogens, Abnormal metabolism, Mutation, Missense genetics
Abstract

The effects of the gamma-308 Asn-->Lys substitution of fibrinogen Bicêtre II on clot formation, structure and properties were determined to elucidate the role of this part of the molecule in fibrin polymerization. This process was followed by measurement of turbidity, and the structure and biophysical characteristics of the clots were studied by permeation, scanning electron microscopy, and rheological techniques. Turbidity studies revealed an increased lag period and greater final turbidity for fibrin BII clots, indicating impaired oligomer formation. By permeation it was found that BII clots had greater network porosity, four times more than that of the control. The clot architecture visualized by scanning electron microscopy was similar to that of control clots with pore size and fiber diameter slightly increased. BII clots had a stiffness decreased by more than half, and an increased loss tangent, a measure of the inelastic deformation of the clot. All these results suggest a disruption of the proper alignment of fibrin monomers during oligomer formation. Consistent with these results, fibrin cross-linking by adding the physiological concentration of factor XIII to the purified protein showed that gamma and alpha chain cross-linking was impaired in BII clots. This amino acid substitution defines distinctive effects on the surface of the D:D interaction sites that are reflected in the clot structure and functional properties.

Published
2006
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