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3. Introduction

Author

Bousquet, J., Bourret, R., Camuzat, T., Augé, P., Domy, P., Bringer, J., Best, N., Jonquet, O., de la Coussaye, J.-E., Noguès, M., Robine, J.-M., Avignon, A., Blain, H., Combe, B., Dray, G., Dufour, V., Fouletier, M., Giraudeau, N., Hève, D., Jeandel, C., Laffont, I., Larrey, D., Laune, D., Laurent, C., Mares, P., Marion, C., Pastor, E., Pélissier, J.-Y., Radier-Pontal, F., Reynes, J., Royère, E., Ychou, M., Bedbrook, A., Granier, S., Abecassis, F., Albert, S., Adnet, P.-A., Alomène, B., Amouyal, M., Arnavielhe, S., Asteriou, T., Attalin, V., Aubas, P., Azevedo, C., Badin, M., Bakhti, Baptista, G., Bardy, B., Battesti, M.-P., Bénézet, O., Bernard, P.-L., Berr, C., Berthe, J., Bobia, X., Bockaert, J., Boegner, C., Boichot, S., Bonnin, H.-Y., Boulet, P., Bouly, S., Boubakri, C., Bourdin, A., Bourrain, J.-L., Bourrel, G., Bouix, V., Breuker, C., Bruguière, V., Burille, J., Cade, S., Caimmi, D., Calmels, M.-V., Camu, W., Canovas, G., Carre, V., Cavalli, G., Cayla, G., Chiron, R., Claret, P.-G., Coignard, P., Coroian, F., Costa, D.-J., Costa, P., Cottalorda, Coulet, B., Coupet, A.-L., Courrouy-Michel, M.-C., Courtet, P., Cristol, J.-P., Cros, V., Cuisinier, F., Daien, C., Danko, M., Dauenhauer, P., Dauzat, M., David, M., Davy, J.-M., Delignières, D., Demoly, P., Desplan, J., Dhivert-Donnadieu, H., Dujols, P., Dupeyron, A., Dupeyron, G., Engberink, O., Enjalbert, M., Fattal, C., Fernandes, J., Fesler, P., Fraisse, P., Froger, J., Gabrion, P., Galano, E., Gellerat-Rogier, M., Gellis, A., Goucham, A.-Y., Gouzi, F., Gressard, F., Gris, J.-C., Guillot, B., Guiraud, D., Handweiler, V., Hantkié, H., Hayot, M., Hérisson, C., Heroum, C., Hoa, D., Jacquemin, S., Jaber, S., Jakovenko, D., Jorgensen, C., Journot, L., Kaczorek, M., Kouyoudjian, P., Labauge, P., Landreau, L., Lapierre, M., Leblond, C., Léglise, M.-S., Lemaitre, J.-M., Le Moing, V., Le Quellec, A., Leclercq, F., Lehmann, S., Lognos, B., Lussert, J.-M., Makinson, A., Mandrick, K., Marmelat, V., Martin-Gousset, P., Matheron, A., Mathieu, G., Meissonnier, M., Mercier, G., Messner, P., Meunier, C., Mondain, M., Morales, R., Morel, J., Morquin, D., Mottet, D., Nérin, P., Nicolas, P., Ninot, G., Nouvel, F., Ortiz, J.-P., Paccard, D., Pandraud, G., Pasdelou, M.-P., Pasquié, J.-L., Patte, K., Perrey, S., Pers, Y.-M., Picot, M.-C., Pin, J.-P., Pinto, N., Porte, E., Portejoie, F., Pujol, J.-L., Quantin, X., Quéré, I., Raffort, N., Ramdani, S., Ribstein, J., Rédini-Martinez, I., Richard, S., Ritchie, K., Riso, J.-P., Rivier, F., Rolland, C., Roubille, F., Sablot, D., Savy, J.-L., Schifano, L., Senesse, P., Sicard, R., Soua, B., Stephan, Y., Strubel, D., Sultan, A., Taddei-Ologeanu, Tallon, G., Tanfin, M., Tassery, H., Tavares, I., Torre, K., Touchon, J., Tribout, V., Uziel, A., Van de Perre, P., Vasquez, X., Verdier, J.-M., Vergne-Richard, C., Vergotte, G., Vian, L., Viarouge-Reunier, C., Vialla, F., Viart, F., Villain, M., Villiet, M., Viollet, E., Wojtusciszyn, A., Aoustin, M., Bourquin, C., and Mercier, J.

Published
2015
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8. Morbidity and mortality in the antiphospholipid syndrome during a 10-year period: a multicentre prospective study of 1000 patients

Author

Cervera, R, Serrano, R, Pons-Estel, G J, Ceberio-Hualde, L, Shoenfeld, Y, de Ramón, E, Buonaiuto, V, Jacobsen, S, Zeher, M M, Tarr, T, Tincani, A, Taglietti, M, Theodossiades, G, Nomikou, E, Galeazzi, M, Bellisai, F, Meroni, P L, Derksen, R H W M, de Groot, P G D, Baleva, M, Mosca, M, Bombardieri, S, Houssiau, F, Gris, J-C, Quéré, I, Hachulla, E, Vasconcelos, C, Fernández-Nebro, A, Haro, M, Amoura, Z, Miyara, M, Tektonidou, M, Espinosa, G, Bertolaccini, M L, and Khamashta, M A

Published
2015
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13. Thrombotic microangiopathy, DIC-syndrome and COVID-19: link with pregnancy prothrombotic state.

Author

Makatsariya, A. D., Slukhanchuk, E. V., Bitsadze, V. O., Khizroeva, J. K. H., Tretyakova, M. V., Tsibizova, V. I., Elalamy, I., Gris, J.-C., Grandone, E., Makatsariya, N. A., and Mashkova, T.

Abstract

For last months, humanity has faced a formidable unknown enemy, which is presented as a new coronavirus infection. Despite the fact that the causative agents of new diseases appear at a certain frequency and that the virus SARS-CoV-2 has certain common properties with its predecessors, at the moment we are dealing with a new unknown pathogenesis of the development of severe complications in patients with risk factors. A final understanding of pathological process mechanisms is the goal of the scientific community. Summarizing research data from different countries, it became obvious that in severe cases of viral infection, we are dealing with a combination of the systemic inflammatory response syndrome, disseminated intravascular coagulation and thrombotic microangiopathy (TMA). Thrombotic microangiopathy is represented by a group of different conditions in which thrombocytopenia, hemolytic anemia, and multiple organ failure occur. The article reflects the main types of TMA, pathogenesis and principles of therapy. The main participants in the process are described in detail, including the von Willebrand factor and ADAMTS-13. Based on the knowledge available, as well as new data obtained from patients with COVID-19, we proposed possible models for the implementation of conditions such as sepsis, TMA, and DIC in patients with severe new coronavirus infection. Through a deeper understanding of pathogenesis, it will be possible to develop more effective diagnosis and therapy. [ABSTRACT FROM AUTHOR]

Published
2022
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17. Morbidity and mortality in the antiphospholipid syndrome during a 5-year period: a multicentre prospective study of 1000 patients

Author

Cervera, R, Khamashta, M A, Shoenfeld, Y, Camps, M T, Jacobsen, S, Kiss, E, Zeher, M M, Tincani, A, Kontopoulou-Griva, I, Galeazzi, M, Bellisai, F, Meroni, P L, Derksen, R H W M, de Groot, P G, Gromnica-Ihle, E, Baleva, M, Mosca, M, Bombardieri, S, Houssiau, F, Gris, J-C, Quéré, I, Hachulla, E, Vasconcelos, C, Roch, B, Fernández-Nebro, A, Piette, J-C, Espinosa, G, Bucciarelli, S, Pisoni, C N, Bertolaccini, M L, Boffa, M-C, and Hughes, G R V

Published
2009
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25. Role of allelic variants Gly972Arg of IRS-1 and Gly1057Asp of IRS-2 in moderate-to-severe insulin resistance of women with polycystic ovary syndrome.

Author

El Mkadem, Samira Ait, Lautier, Corinne, Macari, Francoise, Molinari, Nicolas, Lefebvre, Patrick, Renard, Eric, Gris, Jean Christophe, Cros, Gerard, Daures, Jean Pierre, Bringer, Jacques, White, Morris F., Grigorescu, Florin, El Mkadem, S A, Lautier, C, Macari, F, Molinari, N, Lefèbvre, P, Renard, E, Gris, J C, and Cros, G

Subjects
ALLELES, INSULIN, OVARIAN cysts
Abstract

To assess the role of insulin receptor, insulin receptor substrate (IRS)-1, and IRS-2 genes in insulin resistance, we explored the genomic DNA in women with polycystic ovary syndrome (PCOS) and a variable degree (mean +/- SE) of insulin resistance (homeostasis model assessment index for insulin resistance [HOMA(IR)] 3.2 +/- 0.6, n = 53; control subjects 1.56 +/- 0.34, n = 102) using direct sequencing. Whereas no novel mutations were found in these genes, gene-dosage effects were found on fasting insulin for the Gly972Arg IRS-1 variant and on 2-h plasma glucose for the Gly1057Asp IRS-2 variant. The Gly972Arg IRS-1 variant was more prevalent in insulin-resistant patients compared with non-insulin-resistant individuals or control subjects (39.3 vs. 4.0 and 16.6%, P < 0.0031, respectively). A multivariate model that included BMI as a variable revealed significant effects of the Gly1057Asp IRS-2 variant on insulin resistance (P < 0.016, odds ratio [OR] 7.2, 95% CI 1.29-43.3). HOMA(IR) was higher in carriers of both IRS variants than in those with IRS-2 mutations only or those with wild-type variants (6.2 +/- 2.3, 2.8 +/- 0.5, and 1.8 +/- 0.2, respectively; P < 0.01), and it was significantly associated with this genotype (P < 0.0085, OR 1.7, 95% CI 1.09-2.99). We conclude that polymorphic alleles of both IRS-1 and IRS-2, alone or in combination, may have a functional impact on the insulin-resistant component of PCOS. [ABSTRACT FROM AUTHOR]

Published
2001
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26. APC resistance and third-generation oral contraceptives: Acquired resistance to activated protein C, oral contraceptives and the risk of thromboembolic disease.

Author

Gris, Jean-Christophe, Jamin, Christian, Benifla, Jean-Louis, Quere, Isabelle, Madelenat, Patrick, Mares, Pierre, Gris, J C, Jamin, C, Benifla, J L, Quere, I, Madelenat, P, and Mares, P

Subjects
BLOOD diseases, BLOOD coagulation factors, BLOOD coagulation tests, GENETIC mutation, ORAL contraceptives, THROMBOEMBOLISM, IN vitro studies, DISEASE complications
Abstract

Using a newly-developed technique, a severe acquired plasma resistance to activated protein C has been described in women using third-generation (rather than second-generation) oral contraceptives. The following items are discussed: (i) the technical parameters used to appreciate the effect of activated protein C induce a bias of interpretation, the mean intrinsic effect of activated protein C, in plasmas from women on second or third-generation oral contraceptives being strictly identical; (ii) there are no data available to show that this assay can indicate a thromboembolic risk in asymptomatic women on oral contraceptives; and (iii) this assay is a global and non-specific test, basically sensitive to the plasma concentrations of many coagulation factors which are increased or decreased by oestrogens and progestogens. For instance protein S, in which oral contraceptive-induced modifications account for the differential effect of oral contraceptives on Rosing's assay, but which modifications are not related to the thromboembolic risk of oral contraceptives. The androgenic potential of the progestogen may counteract the effect of oestrogens in the test. More generally, in such a complex situation in which there is a 'modification of the modification', there is no haemostasis-related test which provides a risk indicator for thrombosis. Based on testing of the plasma response to activated protein C, it is impossible to state that third-generation oral contraceptives induce a more important thromboembolic risk than oral contraceptives containing a more androgenic progestogen. [ABSTRACT FROM AUTHOR]

Published
2001
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28. Comparison of the protein and DNA approaches for the characterization of a beta-globin chain variant, hemoglobin Cocody [beta 21 (B3) Asp--->Asn], in a Caucasian patient.

Author

Aguilar-Martinez, P, Galacteros, F, Schved, J F, Blouquit, Y, Gris, J C, Demaille, J, and Claustres, M

Subjects
DNA analysis, ASPARAGINE, ASPARTIC acid, COMPARATIVE studies, DNA, DOCUMENTATION, ELECTROPHORESIS, GENEALOGY, GENETICS, GENETIC techniques, HEMOGLOBINS, HIGH performance liquid chromatography, RESEARCH methodology, MEDICAL cooperation, NUCLEOTIDES, POLYMERASE chain reaction, RESEARCH, EVALUATION research
Abstract

Over the past few years, the methodologies used for the identification of hemoglobin A variants have been greatly improved. Both the protein- and DNA-based strategies have their own advantages and limitations. In this report we illustrate the use of both assays for the characterization of a hemoglobin Cocody variant in a women of Spanish descent. After evaluating the mobility value matrix of the abnormal hemoglobin, the amino acid transition was determined by HPLC and micro-sequencing of the protein. The beta 21 Asp was shown to be substituted by an Asn. At the DNA level, the only nucleotide replacement responsible for this amino acid substitution is GAT--->AAT at codon 21. The analysis of the beta-globin gene by denaturing gradient gel electrophoresis (DGGE) method showed that the mutation was situated in a fragment including exon 1. The hemoglobin variant was then identified to be hemoglobin Cocody by DNA sequencing of this fragment. [ABSTRACT FROM AUTHOR]

Published
1993

30. Low–molecular-weight Heparin and Recurrent Placenta-mediated Pregnancy Complications: A Meta-Analysis of Individual Patient Data From Randomized Controlled Trials.

Author

Rodger, M. A., Gris, J. C., De Vries, J. I. P., Martinelli, I., Rey, É., Schleussner, E., Middeldorp, S., Kaaja, R., Langlois, N. J., Ramsay, T., Mallick, R., Bates, S. M., Abheiden, C. N. H., Perna, A., Petroff, D., De Jong, P., van Hoorn, M. E., Bezemer, P. D., and Mayhew, A. D.

Published
2017
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33. Rapid recovery of acquired purpura fulminans in a patient with familial C4bBP deficiency.

Author

Lemesle, F., Gris, J., Schwed, J., Arich, C., Lemesle, F G, Gris, J C, and Schwed, J F

Abstract

A 32-year-old pregnant woman developed meningococcemia associated purpura fulminans and quickly improved with therapy. After this disease C4b-Binding Protein (C4bBP) plasma levels remained very low while protein S activity was in the normal range. Familial investigation proved a hereditary C4bBP deficiency. This observation points out the role of the protein C-protein S system during acquired purpura fulminans. [ABSTRACT FROM AUTHOR]

Published
1993
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38. P-015: Association of FOXD1 variants with pregnancy failures in mice and humans.

Author

Laissue, P., Lakhal, B., Vatin, M., Batista, F., Burgio, G., Dos Santos, E., Buffat, C., Sierra-Diaz, A.C., Renault, G., Montagutelli, X., Salmon, J., Monget, P., Veitia, R.A., Méhats, C., Fellous, M., Cocquet, J., Vaiman, D., and Gris, J.-C.

Subjects
*PREGNANCY complications, *FORKHEAD transcription factors, *HUMAN genetic variation, *MEDICAL publishing, *LABORATORY mice
Published
2017
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39. P-060: OTTILIA and FIRST: two international registries of foeto-maternal prognosis in women with recurrent reproductive failures after spontaneous or assisted conception.

Author

Villani, M., Larciprete, G., Kovac, M., Martinelli, I., Tamborini Permunian, E., Cacciola, R., Lo Pinto, G., Bucherini, E., De Stefano, V., Lodigiani, C., Bartolotti, T., Totaro, P., Carone, D., Baldini, D., Gris, J.-C., Brenner, B., Monreal, M., and Grandone, E.

Subjects
*RECURRENT miscarriage, *MATERNAL health, *HUMAN reproductive technology, *THROMBOSIS, *MEDICAL registries
Published
2017
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