Academic literature on the topic 'Système assimilé au complément'
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Journal articles on the topic "Système assimilé au complément"
Larcher, Pierre. "Le fāʾ al-sababiyya vu par Raḍī l-Dīn al-Astarābāḏī : logique et pragmatique." Arabica 67, no. 5-6 (December 23, 2020): 593–610. http://dx.doi.org/10.1163/15700585-12341571.
Full textDaugan, Marie, Remi Noe, Wolf Herman Fridman, Catherine Sautes-Fridman, and Lubka T. Roumenina. "Le système du complément." médecine/sciences 33, no. 10 (October 2017): 871–77. http://dx.doi.org/10.1051/medsci/20173310019.
Full textJouvin, M. H., and M. Kazatchkine. "Le système du complément." La Revue de Médecine Interne 8, no. 1 (January 1987): 47–61. http://dx.doi.org/10.1016/s0248-8663(87)80106-6.
Full textChouaki Benmansour, Nassima, Julien Carvelli, and Éric Vivier. "Implication de la cascade du complément dans les formes sévères de COVID-19." médecine/sciences 37, no. 4 (April 2021): 333–41. http://dx.doi.org/10.1051/medsci/2021021.
Full textRipoche, J., MJ Demares, N. Julen, C. Lemercier, H. Dauchel, C. Davrinche, M. Daveau, and M. Fontaine. "Les protéines régulatrices du système du complément." médecine/sciences 5, no. 4 (1989): 234. http://dx.doi.org/10.4267/10608/3955.
Full textEmile, Carole. "Pathologies du système du complément : cas cliniques." Option/Bio 31, no. 623-624 (October 2020): 28–29. http://dx.doi.org/10.1016/s0992-5945(20)30238-5.
Full textPerron, Jacques, Jean-Claude Coallier, and Maikke Van Herwijnen. "Les événements de vie à l’adolescence : un système multidimensionnel d’analyse qualitative." L’Orientation scolaire et professionnelle 24, no. 3 (1995): 233–49. http://dx.doi.org/10.3406/binop.1995.1109.
Full textZongo, Bétéo, Abdoulaye Diarra, Bruno Barbier, Malicki Zorom, Harouna Karambiri, Souleymane Ouédraogo, Patrice Toé, Yacouba Hamma, and Thomas Dogot. "Évaluation ex ante de l’irrigation de complément dans un contexte sahélien : couplage d’un modèle biophysique à un modèle économique d’exploitation agricole." BASE, no. 3 (2019): 174–87. http://dx.doi.org/10.25518/1780-4507.18056.
Full textAnnabi, Mohamed, Abderrahmane Mokhtari, and Toubet-Allah Hafrad. "Estimation des performances énergétiques du bâtiment dans le contexte maghrébin." Journal of Renewable Energies 9, no. 2 (June 30, 2006): 99–106. http://dx.doi.org/10.54966/jreen.v9i2.819.
Full textBilener, Tolga. "La Turquie et ses options eurasiennes : substitut ou complément ?" Recherches Internationales 127, no. 1 (2023): 149–66. http://dx.doi.org/10.3406/rint.2023.3416.
Full textDissertations / Theses on the topic "Système assimilé au complément"
Zmarlak, Natalia Marta. "Regulation of immune signalling in the malaria mosquito vector, Anopheles : the secreted mosquito leucine-rich repeat protein APL1C is a pathogen binding factor essential for immunity to Plasmodium ookinetes and sporozoites." Electronic Thesis or Diss., Sorbonne université, 2021. http://www.theses.fr/2021SORUS053.
Full textAnopheles mosquito is a vector of Plasmodium parasite, the causative agent of malaria. The Anopheles leucine-rich repeat (LRR) proteins were described as key antagonists of Plasmodium parasites in Anopheles mosquito midgut. APL1C (Anopheles Plasmodium-responsive factor) is a representative of LRR members which specifically protects against rodent malaria parasites by stabilizing the complement-like protein TEP1. By combining cell biology with functional genomic approaches, this study shows that mosquito bloodmeal induce the presence of an extracellular layer of APL1C protein surrounding the midgut beneath of the basal lamina. Consistently with the formation of this layer, APL1C binds to the ookinetes that emerged on the basal side of the midgut. This presence occurs independently from TEP1 function, requires the contribution of the phagocytic cells and nitration pathway. In addition, APL1C defence function is not restricted to the ookinete in the midgut but it also acts against the latest Plasmodium stage, the sporozoites. APL1C inhibits salivary glands infection prevalence, and consistently, it also binds to the surface of the sporozoites in the hemocoel. However, unlike to the midgut stages, anti-sporozoites APL1C-dependent mechanism involves different partners. Moreover, RNAseq study revealed APL1C gene targets, including genes with immune-like function. These results generate novel biological insight for the function of APL1C, and probably other LRR family members, as a pathogen recognition receptor inducing immune response against pathogens that come in contact with mosquito hemolymph compartment
Chatagner, Alexandra. "Complément et neuroprotection." Rouen, 2005. http://www.theses.fr/2005ROUES037.
Full textFor a long time, the classical dogma has considered complement activation in brain pathology deleterious for surrounding cells since it promotes inflammation processes and triggers membran attack complexe formation resulting in cell lysis. A growing body of evidence implicates complement in neuoroprotection processes. My PhD work consisted in exploring the different mecanisms set up by complement activation to protect cells, neurons essentially. The up-regulation of neuronal CD55 or NGF secretion by astrocytes following a simultaneous anaphylatoxins and IL-1b stimulation may contibute to neuronal protection. On the other hand, phagocytosis of apoptotic cells, which is an important process to prevent inflammatory reaction is not regulated by C3a
Toufik, Jamila. "Interactions de copolymères fonctionnels dérivés du Sephadex avec le système du complément et les monocytes humains." Paris 13, 1994. http://www.theses.fr/1994PA132010.
Full textThomas, Anne. "Expression du complément dans le système nerveux central : un marqueur des processus inflammatoires." Rouen, 1999. http://www.theses.fr/1999ROUES018.
Full textMontdargent, Béatrice. "Interactions du système du complément avec les surfaces artificielles : dérives fonctionnalisés du polystyrene." Paris 13, 1991. http://www.theses.fr/1991PA132021.
Full textJauneau, Anne-Christine. "Complément et système nerveux central, rôles des anaphylatoxines C3a et C5a au niveau de l'astrocyte." Rouen, 2002. http://www.theses.fr/2002ROUES063.
Full textInflammatory reactions could occur in the brain during numerous pathological disorders when an increase of complement synthesis, actor of natural immunity, has been observed. In the absence of cellular infiltration, an intrathecal inflammatory reaction could be realized by glial cells. The activation of these cells, which synthesize the totality of the complement cascade components, leads to the release of C3a and C5a anaphylatoxins, two potent inflammatory mediators, and to the formation of the membrane attack complex. The presence of anaphylatoxin receptors on brain cells and the increase of their expression during some pathologies led us to determine their roles in the brain, in particular on astrocytes, immunocompetent glial cells. Our studies show that C3a and C5a activate several transduction pathways leading to an increase of chemokine mRNA expression, including IL-8. However an increase of IL-8 secretion could be detected only in the presence of IL-1ß. Thus, at least in part, anaphylatoxins may participate to leukocyte recruitment into the brain. C3a and C5a also increase neurotrophin mRNA expression and lead to a weak secretion of NGF, and so, participate to neuroprotection and post-lesioned repairing. Finally, we show an unexpected role for C3a in the clearance of apoptotic cells via the increase of phosphatidylserine receptor expression by astrocytes. Our data allocate new roles to anaphylatoxins on astrocytes and suggest that they could have a dual effect in the brain
Tissot, Bérangère. "Rôle des interactions protéine-sucre dans le mécanisme d'inhibition du système du complément par le fucoi͏̈dane." Nantes, 2003. http://www.theses.fr/2003NANT19VS.
Full textComplement System (C) is an important part of the innate humoral immunity and comprises about thirty plasmatic proteins. In the case of several pathologies, this System supports and worsens inflammation. These phenomena occur in several neurodegenerative diseases in which the inhibition of the Complement System may lead to a substantial therapeutic benefit. However, such anticomplementary drugs are not yet available. Glycans represent a huge source of bioactives molecules, although not thoroughly explored. Among those molecules, fucoidan is a polysaccharide extracted from brown seaweed (like Ascophyllum nodosum) and composed of sulfated-fucose units. This polymer is a potent Complement inhibitor. We evidenced that fucoidan inhibits both alternative and classical activation pathways. The classical one is blocked at the Cl-complex activation step and at the C3 convertase formation level. Experiments based on single-molecule observations enable us to show that fucoidan interacts with specifie domains of Clq that leads to the inhibition of the association of the enzymatic sub-unit of the Cl complex. Protein C4 is another target of fucoidan:the analysis by affinity capillary electrophoresis demonstrate for the first time the formation of a complex between the polysaccharide and C4 and also C4b, a fragment of C4. Concerning the alternative pathway, our study shows that fucoidan potentiates the Factor I-mediated inactivation of C3b, in the presence of Factor H. Zonal capillary electrophoresis experiments suggest that H induces a conformational change of C3b, rendering it sensitive to the proteolytic activity of I. We assume that fucoidan interferes with the activation of alternative pathway by potentiating the H-mediated conformational change of C3b. Concerning the structure-activity relationships, structural studies demonstrated that branchings, 2-sulfated units and disulfated units are essential to the anticomplementary activity of fucoidan
Van, Beek Johan. "La réaction inflammatoire dans le système nerveux central : rôle de la synthèse locale du complément dans la physiopathologie de l'ischémie cérébrale." Rouen, 2000. http://www.theses.fr/2000ROUES075.
Full textGasque, Philippe. "Expression du complément par des cellules du système nerveux central : analyse in vitro de la biosynthèse des protéines du complément par un modèle de lignées d'astrocytes humains." Rouen, 1993. http://www.theses.fr/1993ROUES038.
Full textJeandel, Jérémy. "Effets de stress associés aux vols spatiaux sur le système du complément et les cellules dendritiques." Thesis, Université de Lorraine, 2019. http://docnum.univ-lorraine.fr/ulprive/DDOC_T_2019_0198_JEANDEL.pdf.
Full textDuring spaceflights, astronauts encounter numerous stresses leading to immune system impairment. Given the scarcity of space missions, simulation models are used on Earth to study the effects of spaceflight-associated stresses on the immune system. The aim of this thesis was to study the effects of spaceflight-associated stresses on the complement system and on dendritic cells (DC). First, we studied the effects of individual or combined spaceflight-associated stresses on the C3 molecule expression in amphibians and mice. We showed that some of these stresses such as microgravity increased the C3 complement expression in P. waltl larvae but no variation were found in mice subjected to simulated microgravity (hindlimb unloading model). We also studied the effects of simulated microgravity by RPM on murine DC phenotype and function. We showed that RPM exposure impaired both DC actin cytoskeleton and survival. Moreover, DC exposed to simulated microgravity showed an immature phenotype characterized by a decrease of co-stimulation molecule expression and pro-inflammatory cytokines secretion, which are essentials for DC functions. However, these numerous alterations did not affect antigen presentation to T cells. Taken together, these results highlight the significant effects of spaceflight-associated stresses on the immune system. Studying microgravity will allow to better understand its effects on health and to develop adapted countermeasures
Book chapters on the topic "Système assimilé au complément"
Owen, Judy A., Jenni Punt, and Sharon A. Stranford. "6. Le système du complément." In Immunologie, 187–223. Dunod, 2014. http://dx.doi.org/10.3917/dunod.owen.2014.01.0187.
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