Academic literature on the topic 'Facteur de croissance placentaire'
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Journal articles on the topic "Facteur de croissance placentaire"
Behar cohen, F., L. Kowalczuk, E. Touchard, C. Goumeaux, L. Jonet, and P. Bigey. "676 La surexpression intraoculaire du facteur de croissance placentaire : un modèle de rétinopathie diabétique ?" Journal Français d'Ophtalmologie 32 (April 2009): 1S201. http://dx.doi.org/10.1016/s0181-5512(09)73800-8.
Full textAUROUSSEAU, B., D. DURAND, and D. GRUFFAT. "Contrôle des phénomènes oxydatifs pendant la gestation chez les monogastriques et les ruminants." INRAE Productions Animales 17, no. 5 (October 5, 2004): 339–54. http://dx.doi.org/10.20870/productions-animales.2004.17.5.3607.
Full textLotoy, Jésual Banza, Berthe Ilunga Zinga, Jean Pierre Ilango-Banga Lotoy, and Jules Mpoy Odimba. "Interest and Perspectives of Ultrasound Surveillance of Pregnancy in the third trimester in Urban Areas: A case series from the Kinshasa University Hospital, The Democratic Republic of Congo." Annales Africaines de Medecine 17, no. 1 (January 3, 2024): e5519-e5526. http://dx.doi.org/10.4314/aamed.v17i1.9.
Full textLaaouze, Mehdi, Sarah SeghrouchniIdrissi, Mohammed Karamsaoud, Mamouni Nisrine, Errarhaysanae a, Bouchikhi Shehrazad, and Abd Aziz Bananni. "CHORIOANGIOME PLACENTAIRE : A PROPOS DUN CAS ET REVUES DE LA LITTERATURE." International Journal of Advanced Research 9, no. 01 (January 31, 2021): 643–45. http://dx.doi.org/10.21474/ijar01/12339.
Full textHENNEN, G., F. FRANKENNE, Marie-Louise SCIPPO, A. IGOUT, J. CLOSSET, G. PIRENS, and Françoise GOMEZ. "Hormone de croissance placentaire. Signification par rapport aux hormones de croissance et lactogène." Reproduction Nutrition Développement 28, no. 6B (1988): 1699–706. http://dx.doi.org/10.1051/rnd:19881014.
Full textEyraud, J.-L., M. Fiorenza, C. Yardin, E. Decroisette, S. Gheck, A. Bedu, and Y. Aubard. "67 Retard de croissance intra-utérin et mosaïque placentaire." Journal de Gynécologie Obstétrique et Biologie de la Reproduction 33, no. 1 (January 2004): 86. http://dx.doi.org/10.1016/s0368-2315(04)96386-7.
Full textFève, B. "FGF21, un facteur de croissance prometteur." Annales d'Endocrinologie 82, no. 5 (October 2021): 225. http://dx.doi.org/10.1016/j.ando.2021.07.018.
Full textMayeux, Patrick. "L’érythropoïétine : un facteur de croissance neuronale." médecine/sciences 18, no. 6-7 (June 2002): 654–57. http://dx.doi.org/10.1051/medsci/20021867654.
Full textJacobs, Scott. "La codification, facteur de croissance économique." Revue française d'administration publique 82, no. 1 (1997): 291–97. http://dx.doi.org/10.3406/rfap.1997.3108.
Full textToutain, J., M. Prochazkova-Carlotti, F. Pelluard, E. Chevret, D. Cappellen, J. P. Merlio, J. Horovitz, and R. Saura. "Retard de croissance intra-utérin dysgravidique et longueur télomérique placentaire." Journal de Gynécologie Obstétrique et Biologie de la Reproduction 43, no. 6 (June 2014): 478–79. http://dx.doi.org/10.1016/j.jgyn.2014.01.009.
Full textDissertations / Theses on the topic "Facteur de croissance placentaire"
Peron, Marie-Christine. "Epidermal growth factor (EGF)et développement foeto-placentaire." Paris 5, 1993. http://www.theses.fr/1993PA05P097.
Full textKlein, Jean-Louis. "Inhibition de la prolifération de cellules cancéreuses : études comparatives entre un nouveau facteur placentaire et le TGF Beta." Lyon 1, 1992. http://www.theses.fr/1992LYO1T113.
Full textGrissa, Oussama. "Défenses antioxydantes, inflammation et immunomodulation, au cours du diabète gestationnel, dans les compartiments maternel, foetal et placentaire." Thesis, Dijon, 2010. http://www.theses.fr/2010DIJOS099/document.
Full textGestational diabetes mellitus (GDM) is defined as ‘carbohydrate intolerance of variable severity with onset or first recognition during pregnancy’, irrespective to necessary treatment and its evolution in the post partum. GDM is associated with a number of complications/ pathologies both in mother and in their newborns, with short and long-term. In this study, we investigated the role of cytokines, adipokines and antioxidant status during GDM and macrosomia. Our study has demonstrated that these pathologies are associated with a perturbation in lipid metabolism, and antioxidant and immune status. GDM is linked to the down-regulation of adiponectin along with Th1 cytokines and upregulation of leptin and inflammatory cytokines whereas macrosomia was associated with the up-regulation of Th1 cytokines and the down-regulation of the obesity-related agents (IL-6, TNF-α, leptin and adiponectin). Several alterations observed at birth in carbohydrates and lipids metabolism in the children born to diabetic mothers, still persist at the adulthood. It seems that in utero programming during diabetic pregnancy creates a ‘‘metabolic memory’’ which is responsible for the development of obesity and physiological anomalies in macrosomic offspring. According to multiple linear regressions incremental that we established, it appears that growth factors that influence the increase of foetal weight are: PDGF in mother's side and FGF2 in maternal and foetal side
Hoffmann, Pascale. "Fonctions biologiques d'EG-VEGF (Endocrine gland-derived vascular endothelial growth factor) dans le développement placentaire." Grenoble 1, 2006. http://www.theses.fr/2006GRE10256.
Full textThe role of EG-VEGF was explored in human and murine placenta. Assumptions were made about its contribution in pathologies of pregnancy including pre-eclampsia and intrauterine growth restriction
Cronier, Laurent. "Evolution de la communication jonctionnelle et des perméabilités membranaires du trophoblaste humain lors de sa différenciation : influence de facteurs autocrines et paracrines : hormone gonadotrope chorionique humaine (hCG), facteur de croissance transformant bêta 1 (TGFbêta 1) et glucocorticoïde." Poitiers, 1995. http://www.theses.fr/1995POIT2345.
Full textBarjat, Tiphaine. "Vers une meilleure connaissance des pathologies vasculaires placentaires." Thesis, Lyon, 2017. http://www.theses.fr/2017LYSES026/document.
Full textPlacenta-mediated adverse pregnancy outcomes are frequent and severe pathologies whose predominant maternal form is preeclampsia and fetal form, intrauterine growth retardation. The questions asked about this subject concern first of all the prediction of the occurrence of its pathologies in a sufficiently early way to allow for close monitoring, administration of corticosteroids, and management in an appropriate level of maternity. The prevention of the occurrence and recurrence and the treatment of its pathologies in the constituted phase are also unresolved problems. Our objective was therefore to work on its various questions through three studies: the ANGIOPREI study, the VOLUPLA study and the GROWTH study. The results of his work and of the literature show that the factors of haemostasis anc angiogenic factors are disturbed in preeclampsia and in growth retardation. The association of maternal, ultrasound, angiogenic and serum factors constitutes a predictive model that is effective mainly by an excellent negative predictive value. The placental volume is correlated with the D-dimer level and is interesting for placenta-mediated adverse pregnancy outcomes prediction. New studies will have to continue the exploration of the prediction, prevention and treatment of this pathologies related to the placenta. The treatment is notably the object of the study Growth which aims to evaluate the effectiveness of the Enoxaparin for the treatment of constituted vascular growt retardation
Mayeur, Sylvain. "Retard de croissance intra-utérin et vulnérabilité au syndrome métabolique : recherche de marqueurs placentaires dans un modèle de dénutrition maternelle prénatale et chez l'Homme." Phd thesis, Université du Droit et de la Santé - Lille II, 2011. http://tel.archives-ouvertes.fr/tel-00829097.
Full textRobert, Fabien. "Étude du BMP-9 et du PlGF dans la physiopathologie du syndrome hépatopulmonaire : À la recherche de cibles thérapeutiques." Electronic Thesis or Diss., université Paris-Saclay, 2024. http://www.theses.fr/2024UPASQ054.
Full textHepatopulmonary syndrome (HPS) is a severe pulmonary complication caused by liver diseases. It is characterized by abnormal proliferation and dilation of the small blood vessels in the lungs, leading to reduced blood oxygenation. Currently, liver transplantation is the only available treatment for this condition. Understanding the mechanisms involved in both the development and progression of HPS is crucial for developing more effective treatments. During this PhD, we explored two promising therapeutic targets. The first is BMP-9, a protein whose loss is necessary for the development of the disease. The second is PlGF, a protein that increases specifically in the context of cirrhosis and can worsen blood oxygenation issues. These new avenues could lead to the development of more targeted treatments for HPS
Deloison, Benjamin. "Imagerie fonctionnelle placentaire par résonance magnétique : étude de la perfusion placentaire." Thesis, Paris 11, 2014. http://www.theses.fr/2014PA112256.
Full textPlacental insufficiency is a serious medical condition with a diagnosis made usually too late to prevent introduction of effective therapies. The aim of this thesis is to develop, in pregnant rats and translate to humans, functional MRI (fMRI) tools allowing quantification of placental perfusion in clinical practice.Materials and Methods: Three studies using fMRI are part of this thesis. The first two were performed on a murine model. A dynamic sequence with injection of a contrast agent (DCE) has been developed with an iron oxide particle (SPIO) in a surgical model of chronic placental hypoperfusion with placental perfusion measurement (f) in ml / min / 100 ml and placental fractionnal volume (Vb) in %. Another technique of fMRI was developed with Arterial Spin Labeling (ASL) to estimate placental perfusion in ml / min / 100g without injection of contrast media.The latest study was a translational research. It consisted in the development of a dynamic sequence with injection of gadolinium chelate, in order to obtain perfusion (f) in ml / min / 100 ml and placental fractionnal volume (Vb) in %. We also studied maternal and fetal pharmacokinetics of gadolinium chelate.Results: In animals with SPIO DCE, our study allowed us to show that it is possible to use the T1 effect of SPIO to characterize the placental microcirculation by f = 159.4 ml / min / 100ml (+ / - 54.6) and Vb = 39.2% (11.9 +/-) for 31 « normal » placentas. In case of IUGR, f decreases significantly for the 23 examined placentas (f = 108.1 ml / min / 100ml +/- 41, p = 0.004), whereas the volume fraction placenta is not modified (Vb = 42 +/- 16.7 8 %, p = 0.24). ASL has allowed us to estimate placental perfusion for 47 placentas under physiological conditions, with an estimated perfusion of 146.8 ml / min / 100 g (70.1 +/-).In humans, 14 placentas were studied with an estimated perfusion of 183 ml / min / 100ml (+/- 144) and we also identified two types of placental kinetic enhancement (early and intense and later and less intense). Pharmacokinetics have allowed us to study quantitatively the transfer of gadolinium chelate in the fetus. This transfer is low compared to the initial concentration of Dotarem® : fetal blood concentration is 18.1x10-6%, concentration in amniotic fluid is 242.8 x10-6 % and 0.3% of the Dotarem® initial dose is present in the placenta approximately 70 hours after injection.Conclusion: This study illustrates the variety of functional MRI techniques available for placental study. Placental perfusion can be quantified by DCE with an iron oxide particle (SPIO) or without injection of contrast in ASL, in a rat model. The study of placental perfusion in humans is also possible in DCE with gadolinium chelates
Perimenis, Pierrette. "Prolactine placentaire et anomalies de croissance au cours du diabète maternel." Thesis, Lille 2, 2014. http://www.theses.fr/2014LIL2S047/document.
Full textDespite the improvement of obstetrical and diabetological care, the pregnancy of the patient presenting a gestational or pregestational diabetes remains ourdays at a high risk for the mother and for its child. For the child, fetal growth disorders such as macrosomia but also intra-uterine growth restriction (IUGR) are still very frequent with short and long-term consequences. Fetal growth is a complex process involving the fetal genetic susceptibility but also the intra-uterine environment especially in its maternal and placental metabolic aspects. The link between the physiopathological mechanisms of these disorders and fetal growth in this context of maternal diabetes remains unclear and partially explained by maternal hyperglycemia only. At an interface between the mother and the fetus, the placenta employes multiples functions that influence maternal, fetal and placental metabolisms and consequently the fetoplacental unit development. The placenta, as crucial actor of fetal programming, must adapt to its environnment for the survival of the fetus.The objectives of this thesis were to study the placental compartment with an analysis of expression of genes involved in feto-placental growth to determine the predictive factors of these growth disorders during maternal diabetes. To bring a response to these objectives, we used initially a model of gestant rat diabetes induced by streptozotocin alone or in combination with nicotinamide and we validated some of our results in the placenta from type 1 diabetic mothers.The placental transcriptomic analysis pointed out the involvment of some genes of the prolactin (PRL) family, of the renine-angiotensin-aldosterone system and of metalloproteinase family. The principal phenotypical characteristic of the pups at birth was an IUGR with an histological aspect of a placental hypovascularization associated.We focused especially to the placental genes of the PRL familly, non described before in the litterature in diabetes, such as prl8a2 also known as Dprp (decidual prolactin related-protein). PRL in its native form of 23 kDa is proangiogenic but when processed by Bone morphogenetic protein 1 (BMP-1) or cathepsin D (CTSD) to vasoinhibins has antiangiogenic properties. In our 2 rat models, we demonstrated by qPCR an upregulation of Bmp-1 and Dprp with an increase amount of vasoinhibins when compared to controls.We could validate some of our results in the placenta from diabetic type 1 women with a characteristic of small birth weight of the newborns.Finally, we interested in the course of these disorders concerning PRL family in our animal models during their pregnancy. We could demonstrate that IUGR was present by 14th day of gestation. Bmp-1 or Dprp gene expression and the vasoinhibin amount were not different between groups at the 14th day of gestation but modified by 17th day of gestation.These studies highlighted a placental involvment of PRL and its vasoinhibins during maternal diabetes suggesting a role in placental hypovascularisation in animal and women.The perspectives will be in continuing these studies with a more functional approach. We have to bring more details about the involvment of BMP-1 in this PRL process with an in-depth analysis of the link between hyperglycemia and vasoinhibins among the degree and the time of exposition to hyperglycemia. Finally, it would be interesting to study the involvment of placental PRL not only in the cases of IUGR but also in that of macrosomia, that remains the most frequent fetal growth disorder during maternal diabetes
Books on the topic "Facteur de croissance placentaire"
Bascans, Jean-Marc. Le commerce international, accélérateur du progrès technique, facteur de croissance? Grenoble: A.N.R.T, Université Pierre Mendes France (Grenoble II), 2000.
Find full textMaya, Sieber-Blum, ed. Neurotrophins and the neural crest. Boca Raton, Fla: CRC Press, 1999.
Find full textFafeur, Veronique. Rôle des métabolites de l'acide arachidonique et en particulier de la prostaglandine E2 dans la sécrétion de l'hormone de croissance: Implication dans le mécanisme d'action du facteur hypothalamique de libération de l'hormone de croissance. Grenoble: A.N.R.T, Université Pierre Mendes France (Grenoble II), 1986.
Find full textL, Moses Harold, Lengyel Peter 1929-, Stiles Charles D, and Genentech Inc, eds. Growth inhibitory and cytotoxic polypeptides ; proceedings of a Genentech-Smith, Kline & French-Triton Biosciences-UCLA Symposium held in Keystone, Colorado, January 24-30, 1988. New York: A.R. Liss, 1989.
Find full textInternational Symposium on Molecular and Cellular Biology of Insulin and IGFs (3rd 1990 Gainesville, Fla.). Molecular biology and physiology of insulin and insulin-like growth factors. New York: Plenum Press, 1991.
Find full textA, Joyeaux, Sanofi Recherche, and Symposium "Quo Vadis?" (1985 : Toulouse-Labege), eds. Production d'agents thérapeutiques par génie génétique: Exemple de l'hormone de croissance et de son facteur de libération = Therapeutic agents produced by genetic engineering : the example of growth hormone and its releasing factor, 29-30 mai 1985, Toulouse-Labege. Montpellier: Sanofi Recherche, 1986.
Find full text1924-, Guillemin Roger, and Centre de R & D en biotechnologie (Toulouse, France), eds. Production d'agents thérapeutiques par génie génétique: Exemple de l'hormone de croissance et de son facteur de libération : 29-30 mai 1985, Toulouse-Labège : symposium satellite des 28es journées internationales H.P. Klotz d'endocrinologie clinique, Paris, les 31 mai et ler juin 1985. Montpellier, France: SANOFI recherche, 1986.
Find full textGregory, Bock, and Goode Jamie, eds. The molecular basis of cellular defence mechanisms. Chichester: Wiley, 1997.
Find full textTakao, Kumazawa, Kruger Lawrence, and Mizumura Kazue, eds. The polymodal receptor: A gateway to pathological pain. Amsterdam: Elsevier, 1996.
Find full textDonald, Djatcho Siefu. Infrastructures de Transport Routier: Facteur de Croissance Economique et des Echanges en Zone Cemac. BAYSHOP (Generis Publishing), 2022.
Find full textBook chapters on the topic "Facteur de croissance placentaire"
Dupont, Jean-Claude. "Levi-Montalcini et la découverte du facteur de croissance du nerf." In De Diversis Artibus, 137–42. Turnhout: Brepols Publishers, 1999. http://dx.doi.org/10.1484/m.dda-eb.5.113560.
Full textJulien, Pierre-André, and Michel Périgny. "La participation comme premier facteur de performance." In Les PME à forte croissance, 189–98. Presses de l'Université du Québec, 2002. http://dx.doi.org/10.2307/j.ctv18pgqh2.22.
Full textUlmann, Philippe. "5. La santé, facteur de croissance économique." In Traité d'économie et de gestion de la santé, 53–61. Presses de Sciences Po, 2009. http://dx.doi.org/10.3917/scpo.bras.2009.01.053.
Full textMaurer, Jean-Luc. "1.2. Le rôle du facteur humain : croissance et répartition de la population." In Indonésie : l'envol mouvementé du Garuda. Graduate Institute Publications, 2021. http://dx.doi.org/10.4000/books.iheid.7941.
Full textSato, Shoichi. "Les implantations monastiques dans la Gaule du nord : un facteur de la croissance agricole au viie siècle ?" In La croissance agricole du Haut Moyen Âge, 169–77. Presses universitaires du Midi, 1990. http://dx.doi.org/10.4000/books.pumi.22742.
Full textMontmarquette, Claude. "Développer Un Système Éducatif Qui Assure L’Épanouissement Individuel Et Demeure Un Facteur Clé De La Croissance Économique." In Le Québec économique 7, 435–42. Les Presses de l’Université de Laval, 2017. http://dx.doi.org/10.1515/9782763737126-017.
Full textConference papers on the topic "Facteur de croissance placentaire"
Romanet, I., J. H. Catherine, P. Laurent, R. Lan, and E. Dubois. "Efficacité de l’ostéotomie interalvéolaire par piezocision : revue de la littérature." In 66ème Congrès de la SFCO. Les Ulis, France: EDP Sciences, 2020. http://dx.doi.org/10.1051/sfco/20206603010.
Full textReports on the topic "Facteur de croissance placentaire"
Fonseca, Raquel, and Markus Poschke. L’évolution et la composition de la richesse des ménages Québécois. CIRANO, September 2023. http://dx.doi.org/10.54932/hqtc4594.
Full textCampbell, Bryan, Michel Magnan, Benoit Perron, and Molivann Panot. Modélisation de règles budgétaires pour l’après-COVID. CIRANO, January 2022. http://dx.doi.org/10.54932/nesj4065.
Full textBusque, Marc-Antoine, Jaunathan Bilodeau, Martin Lebeau, and Daniel Côté. Portrait statistique des lésions professionnelles chez les immigrants au Québec. IRSST, September 2024. http://dx.doi.org/10.70010/zshi6028.
Full textDéfis poses par le RIS3: analyse l'espace transfrontalier Nouvelle-Aquitaine Euskadi-Navarre. Universidad de Deusto, 2020. http://dx.doi.org/10.18543/xvmk2716.
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