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294 results on '"Ambroise, J"'

52. P6066AMPK-ACC signaling modulates platelet phospholipids content and potentiate platelet function and thrombus formation

Author

Lepropre, S, primary, Kautbally, S, additional, Octave, M, additional, Onselaer, M.-B, additional, Steinberg, G R, additional, Kemp, B E, additional, Wera, O, additional, Darley-Usmar, V M, additional, Ambroise, J, additional, Guigas, B, additional, Heemskerk, J, additional, Bertrand, L, additional, Oury, C, additional, Beauloye, C, additional, and Horman, S, additional

Published
2018
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71. Genetic Risk Factors of Venous Thromboembolism in the East Algerian Population.

Author

Moussaoui, S., Saussoy, P., Ambroise, J., Defour, J. P., Zouitene, R., Sifi, K., and Abadi, N.

Abstract

Many genetic risk factors have been identified for causing venous thromboembolism (VTE). Most of them affect the function of natural anticoagulant pathways, particularly the protein C system, although recent studies suggest a role of components of the hematopoietic pathway in the etiology of venous thrombosis. In this case-control study, we aimed to determine the frequency of prothrombin G20210A and factor V Leiden (FVL) G1691A polymorphisms and protein C, protein S, and antithrombin III deficiencies in the East Algerian population and to investigate whether these genetic factors are associated with VTE. On the other hand, our study tends to evaluate the status of JAK2V617F and calreticulin (CALR) mutations among these cases. The participants consisted of 121 cases with VTE and 146 healthy controls. Polymorphisms of FVL G1691A and prothrombin G20210A were genotyped by polymerase chain reaction (PCR) restriction fragment length polymorphism. JAK2-V617F and calreticulin mutations were analyzed by quantitative PCR and PCR followed by capillary electrophoresis sequencing, respectively. Protein C, protein S, and antithrombin levels were determined and then hereditary deficiencies were identified. Of all cases and controls, none was a carrier of the antithrombin III deficiency, prothrombin gene G20210A, and CALR mutations. Only 1 case reported having a positive JAK2 mutation (mutant allele burden was 15%). The FVL mutation (GA/AA) was found in 14 (11.6%) cases and 2 (1.4%) controls and it was significantly different between both the groups (P = .001). Deficiencies of protein S and protein C were detected in 17 (18.8%) cases. The univariate analysis resulted in a significant impact of FVL (odds ratio [OR] = 9.4, 95% confidence interval [CI] = 2.1-42.3; P = .003) and of protein S deficiency (OR = 16.9, 95% CI =2.1-132.8, P = .007) on the VTE status. Both factors stayed significant after adjustment for sex and age. The OR of the protein C deficiency was slightly elevated (OR = 6.4, 95% CI = 0.7-55.5), but it did not reach the level of statistical significance (P = .091), and it was therefore not considered as a risk factor. In conclusion, coagulant factor V gene G1691A mutation and protein S deficiency constitute important genetic risk factors in patients with VTE in Eastern Algeria. The somatic mutation of JAK2 V617F and CALR mutations are less frequent causes of VTE, thus routine testing for these mutations is not recommended. [ABSTRACT FROM AUTHOR]

Published
2017
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73. A novel splice-site mutation in angiotensin I-converting enzyme (ACE) gene, c.3691+1G>A (IVS25+1G>A), causes a dramatic increase in circulating ace through deletion of the transmembrane anchor

Author

Persu, A., Lambert, M., Deinum, J., Cossu, M., Visscher, N. de, Irenge, L., Ambroise, J., Minon, J.M., Nesterovitch, A.B., Churbanov, A., Popova, I.A., Danilov, S.M., Danser, A.H., Gala, J.L., Persu, A., Lambert, M., Deinum, J., Cossu, M., Visscher, N. de, Irenge, L., Ambroise, J., Minon, J.M., Nesterovitch, A.B., Churbanov, A., Popova, I.A., Danilov, S.M., Danser, A.H., and Gala, J.L.

Abstract

Contains fulltext : 116540.pdf (publisher's version ) (Open Access), BACKGROUND: Angiotensin-converting enzyme (ACE) (EC 4.15.1) metabolizes many biologically active peptides and plays a key role in blood pressure regulation and vascular remodeling. Elevated ACE levels are associated with different cardiovascular and respiratory diseases. METHODS AND RESULTS: Two Belgian families with a 8-16-fold increase in blood ACE level were incidentally identified. A novel heterozygous splice site mutation of intron 25 - IVS25+1G>A (c.3691+1G>A) - cosegregating with elevated plasma ACE was identified in both pedigrees. Messenger RNA analysis revealed that the mutation led to the retention of intron 25 and Premature Termination Codon generation. Subjects harboring the mutation were mostly normotensive, had no left ventricular hypertrophy or cardiovascular disease. The levels of renin-angiotensin-aldosterone system components in the mutated cases and wild-type controls were similar, both at baseline and after 50 mg captopril. Compared with non-affected members, quantification of ACE surface expression and shedding using flow cytometry assay of dendritic cells derived from peripheral blood monocytes of affected members, demonstrated a 50% decrease and 3-fold increase, respectively. Together with a dramatic increase in circulating ACE levels, these findings argue in favor of deletion of transmembrane anchor, leading to direct secretion of ACE out of cells. CONCLUSIONS: We describe a novel mutation of the ACE gene associated with a major familial elevation of circulating ACE, without evidence of activation of the renin-angiotensin system, target organ damage or cardiovascular complications. These data are consistent with the hypothesis that membrane-bound ACE, rather than circulating ACE, is responsible for Angiotensin II generation and its cardiovascular consequences.

Published
2013

74. A Novel Splice-Site Mutation in Angiotensin I-Converting Enzyme (ACE) Gene, c.3691+1G>A (IVS25+1G>A), Causes a Dramatic Increase in Circulating ACE through Deletion of the Transmembrane Anchor

Author

Persu, A. (Alexandre), Lambert, M. (Michael), Deinum, J. (Jacob), Cossu, M. (Marta), Visscher, N. (Nathalie) de, Irenge, L. (Leonid), Ambroise, J. (Jerôme), Minon, J.M. (Jean-Marc), Nesterovitch, A.B. (Andrew), Churbanov, A. (Alexander), Popova, I.A. (Isolda), Danilov, S.M. (Sergei), Danser, A.H.J. (Jan), Gala, J.L. (Jean-Luc), Persu, A. (Alexandre), Lambert, M. (Michael), Deinum, J. (Jacob), Cossu, M. (Marta), Visscher, N. (Nathalie) de, Irenge, L. (Leonid), Ambroise, J. (Jerôme), Minon, J.M. (Jean-Marc), Nesterovitch, A.B. (Andrew), Churbanov, A. (Alexander), Popova, I.A. (Isolda), Danilov, S.M. (Sergei), Danser, A.H.J. (Jan), and Gala, J.L. (Jean-Luc)

Abstract

Background: Angiotensin-converting enzyme (ACE) (EC 4.15.1) metabolizes many biologically active peptides and plays a key role in blood pressure regulation and vascular remodeling. Elevated ACE levels are associated with different cardiovascular and respiratory diseases. Methods and Results: Two Belgian families with a 8-16-fold increase in blood ACE level were incidentally identified. A novel heterozygous splice site mutation of intron 25 - IVS25+1G>A (c.3691+1G>A) - cosegregating with elevated plasma ACE was identified in both pedigrees. Messenger RNA analysis revealed that the mutation led to the retention of intron 25 and Premature Termination Codon generation. Subjects harboring the mutation were mostly normotensive, had no left ventricular hypertrophy or cardiovascular disease. The levels of renin-angiotensin-aldosterone system components in the mutated cases and wild-type controls were similar, both at baseline and after 50 mg captopril. Compared with non-affected members, quantification of ACE surface expression and shedding using flow cytometry assay of dendritic cells derived from peripheral blood monocytes of affected members, demonstrated a 50% decrease and 3-fold increase, respectively. Together with a dramatic increase in circulating ACE levels, these findings argue in favor of deletion of transmembrane anchor, leading to direct secretion of ACE out of cells. Conclusions: We describe a novel mutation of the ACE gene associated with a major familial elevation of circulating ACE, without evidence of activation of the renin-angiotensin system, target organ damage or cardiovascular complications. These data are consistent with the hypothesis that membrane-bound ACE, rather than circulating ACE, is responsible for Angiotensin II generation and its cardiovascular consequences.

Published
2013
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75. A Novel Splice-Site Mutation in Angiotensin I-Converting Enzyme (ACE) Gene, c.3691+1G > A (IVS25+1G > A), Causes a Dramatic Increase in Circulating ACE through Deletion of the Transmembrane Anchor

Author

Persu, A, Lambert, M, Deinum, J (Jacob), Cossu, M, Irenge, L, Ambroise, J, Minon, JM, Nesterovitch, AB, Churbanov, A, Popova, IA, Danilov, SM, Danser, Jan, Gala, JL, Visscher, N, Persu, A, Lambert, M, Deinum, J (Jacob), Cossu, M, Irenge, L, Ambroise, J, Minon, JM, Nesterovitch, AB, Churbanov, A, Popova, IA, Danilov, SM, Danser, Jan, Gala, JL, and Visscher, N

Abstract

Background: Angiotensin-converting enzyme (ACE) (EC 4.15.1) metabolizes many biologically active peptides and plays a key role in blood pressure regulation and vascular remodeling. Elevated ACE levels are associated with different cardiovascular and respiratory diseases. Methods and Results: Two Belgian families with a 8-16-fold increase in blood ACE level were incidentally identified. A novel heterozygous splice site mutation of intron 25 - IVS25+1G>A (c.3691+1G>A) - cosegregating with elevated plasma ACE was identified in both pedigrees. Messenger RNA analysis revealed that the mutation led to the retention of intron 25 and Premature Termination Codon generation. Subjects harboring the mutation were mostly normotensive, had no left ventricular hypertrophy or c Conclusions: We describe a novel mutation of the ACE gene associated with a major familial elevation of circulating ACE, without evidence of activation of the renin-angiotensin system, target organ damage or cardiovascular complications. These data are consistent with the hypothesis that membrane-bound ACE, rather than circulating ACE, is responsible for Angiotensin II generation and its cardiovascular consequences.

Published
2013

76. le fan-club des Beatles : une communauté imaginaire ?

Author

Le-Bart, Christian, Ambroise, J. C., Centre de Recherches sur l'Action Politique en Europe (ARENES), Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Institut d'Études Politiques [IEP] - Rennes-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Centre National de la Recherche Scientifique (CNRS), and Université de Rennes (UR)-Institut d'Études Politiques [IEP] - Rennes-École des Hautes Études en Santé Publique [EHESP] (EHESP)-Centre National de la Recherche Scientifique (CNRS)

Subjects
fan-club des Beatles, communauté imaginaire, ComputingMilieux_MISCELLANEOUS, [SHS.SCIPO]Humanities and Social Sciences/Political science
Abstract

National audience

Published
2002

100. Dynamics in a Nonfragile Glass-Forming Liquid

Author

Rufflé, B., primary, Beaufils, S., additional, Etrillard, J., additional, Gallier, J., additional, Toudic, B., additional, Ecolivet, C., additional, Coddens, G., additional, Ambroise, J. P., additional, Guéguen, E., additional, and Marchand, R., additional

Published
1996
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