Gotowa bibliografia na temat „Inflammation périphérique”
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Artykuły w czasopismach na temat "Inflammation périphérique"
De Campos, Charly. "Mettre en évidence une inflammation au chevet de l’animal". Le Nouveau Praticien Vétérinaire élevages & santé 14 (listopad 2022): 22–33. http://dx.doi.org/10.1051/npvelsa/2023010.
Pełny tekst źródłaAuboire, L., M. Becquet i C. Le Hello. "Atteinte artérielle périphérique dans la maladie de Horton : comment différencier athérome et inflammation ?" Journal des Maladies Vasculaires 36, nr 4 (lipiec 2011): 280–84. http://dx.doi.org/10.1016/j.jmv.2011.06.003.
Pełny tekst źródłaTessier-Marteau, A., S. le Cruguel, F. Grand, P. Asfar, M. Zandecki i L. Macchi. "CIVD et gangrène périphérique dans un cas de paludisme sévère: le cycle coagulation-inflammation appliqué au Plasmodium falciparum". Annales de biologie clinique 67, nr 5 (wrzesień 2009): 569–72. http://dx.doi.org/10.1684/abc.2009.0367.
Pełny tekst źródłaPoisbeau, P. "CS08 - Conséquences fonctionnelles de la productionendogène des métabolites de la progestérone observéedans la moelle épinière de rat développantune inflammation périphérique". Douleurs : Evaluation - Diagnostic - Traitement 7 (listopad 2006): 16. http://dx.doi.org/10.1016/s1624-5687(06)77779-4.
Pełny tekst źródłaHounkponou, H., P. Tirelle, E. Salameh, C. L’Huillier, W. Bahlouli, C. Guérin, C. Bôle-Feysot i in. "Étude du métabolisme central et périphérique du tryptophane et de la kynurénine dans un modèle de dénutrition secondaire à une inflammation aiguë". Nutrition Clinique et Métabolisme 33, nr 1 (marzec 2019): 98. http://dx.doi.org/10.1016/j.nupar.2019.01.409.
Pełny tekst źródłaRemmel, Paul, i Valérie Freiche. "Entéropathies chroniques du chat, quelles spécificités ?" Le Nouveau Praticien Vétérinaire canine & féline 19 (grudzień 2022): 60–67. http://dx.doi.org/10.1051/npvcafe/2023010.
Pełny tekst źródłaCourtet, P. "La sensibilité aux stress sociaux chez les suicidants. Observation écologique". European Psychiatry 30, S2 (listopad 2015): S12. http://dx.doi.org/10.1016/j.eurpsy.2015.09.041.
Pełny tekst źródłaKjær, Inger. "L’ectoderme, le mésoderme et le neurectoderme sont des types tissulaires importants pour la compréhension et la prévention des résorptions radiculaires. Recommandations cliniques". L'Orthodontie Française 87, nr 3 (wrzesień 2016): 309–19. http://dx.doi.org/10.1051/orthodfr/2016028.
Pełny tekst źródłaDosso, Mamadou, Allali Eugène Koffi, Doudjo Soro, Ali Traore i Nafan Diarrassouba. "Activités analgésique, antiinflammatoire et antipyrétique d’un extrait aqueux des tourteaux de la pomme de cajou (Anacardium occidentale L.)". International Journal of Biological and Chemical Sciences 15, nr 5 (20.01.2022): 1842–52. http://dx.doi.org/10.4314/ijbcs.v15i5.12.
Pełny tekst źródłaRozprawy doktorskie na temat "Inflammation périphérique"
Lamy, Christophe. "Rôle du Corticotropin-Releasing Factor (CRF) périphérique dans les relations stress-inflammation digestive". Université Joseph Fourier (Grenoble), 2003. http://www.theses.fr/2003GRE19020.
Pełny tekst źródłaInflammatory Bowel Disease (IDB) are worsened by stress. The aim of this work was to characterize the role of Corticotropin-Releasing Factor (CRF), a key neuropeptide of the stress response, its analog urocortin and their receptors, CRF1 and CRF2, in the gastro-intestinal tract during colitis. Expression of CRF, urocortin, CRF1 and CRF2 were localized to the enteric nervous system by immunohistochemistry and further detected by quantitative RT-PCR. There was no alteration of the messengers' profile of expression during a trinitrobenzenesulfonique acid (TNBS)-induced colitis. Immobilization stress improved colitis after 10 days and reactivated it after 6 weeks. There was a tendency to an increase in expression of CRF1 and a decrease in expression of CRF2 by stress. In conclusion, digestive peripheral CRF system may account for the proinflammatory of stress effects during colitis
Gautron, Laurent. "Substrats neuroanatomiques et cellulaires de l'anorexie associée à une inflammation périphérique chez le rat". Bordeaux 1, 2003. http://www.theses.fr/2003BOR12734.
Pełny tekst źródłaProinflammatory cytokines, the soluble mediators of immunity, play a key role in triggering disease-associated anorexia. The anorectic effect of cytokines results from a regulated brain response in sick animals. However, the mechanisms of action of cytokines in the brain remain unclear. The first goal of this thesis was to determine the anatomical and cellular targets for cytokines with an emphasis on interleukin-6 (IL-6), one of the major mediator of brain response to inflammation. By using immunohistochemistry, we lirst looked at the expression of STAT1 et STAT3, two major transcription factors associated with IL-6 signaling. Our findings show that both STAT1 and STAT3 are abundantly expressed in the rat brain. Moreover, the intraperitoneal injection of lipopolysaccharide (LPS) in rat,that mimics a peripheral inflammation, actives STAT3 with a specific spatio-temporal distribution in pituitary and brain. The second goal of this thesis was to clarify if feeding-related neuronal circuitry is involved in inflammatory anorexia. Our work demonstrates that the brain response to LPS implies glutamate sensitive neurons in the brainstem which are important in feeding. We also report that fasting attenuates LPS-induced anorexia and wasting. This effect is correlated with a modified response of feeding-related structures in the hypothalamus. By way of conclusion, this thesis favors the idea that cytokines act directly on the pituitary gland and the brain by recruiting various cell types and that disease-associate anorexia involves feeding-related neuronal pathways
Launay, Pierre-Serge. "Etudes de la neuro-inflammation périphérique et centrale dans un modèle pré-clinique de douleur oculaire". Thesis, Paris 6, 2015. http://www.theses.fr/2015PA066429/document.
Pełny tekst źródłaAcute and chronic eye pain are among the most debilitating and difficult to treat. They particularly affect the cornea, the most innervated and most sensitive tissue of the human body. Corneal innervation comes from primary sensory neurons localized in the trigeminal ganglion (TG) that directly transmit pain information to the trigeminal sensory complex (TSC). However, pathophysiological mechanisms of ocular pain with neurogenic and /or inflammatory type remain poorly understood. Deeper fundamental knowledge about the anatomy of the corneal nociceptive system and the cellular and molecular mechanisms involved in the initiation and chronicity of eye pain, are essential to improving current therapies. Therefore, the work of this thesis are focused on two main topic: 1) expand our current knowledge about the neuroanatomy of the corneal nociceptive system by establishing the first three-dimensional mapping of corneal neurons within the TG; 2) study the neuro-inflammatory consequences in the corneal trigeminal pathways (cornea, TG and TSC) in a murine model of ocular pain induced by chronic instillations of benzalkonium chloride (neurotoxic preservative). Overall, our experimental work reveals that a corneal lesion in mice induces neuroinflammation that spreads from the periphery to the central nervous system, and offer new therapeutic opportunities for patients with acute or chronic eye pain
Juaneda, Christian. "Etude de la plasticité sécrétoire des neurones à CRH hypophysiotropes en réponse à une inflammation périphérique induite par le lipopolysaccharide". Bordeaux 1, 1999. http://www.theses.fr/1999BOR10537.
Pełny tekst źródłaLayé, Sophie. "Régulation des cytokines et de leurs récepteurs dans le système nerveux central sous l'effet d'une inflammation périphérique induite par le lipopolysaccharide". Bordeaux 2, 1995. http://www.theses.fr/1995BOR28395.
Pełny tekst źródłaBegon-Pescia, Christina. "Etude in vitro de l'impact de la drogue ABX sur les macrophages primaires humains issus de monocytes du sang périphérique dans un contexte inflammatoire : Implication du micro-ARN 124". Thesis, Montpellier, 2020. http://www.theses.fr/2020MONTT020.
Pełny tekst źródłaMacrophages are heterogeneous cell mediators, which play a crucial role in inflammation. A chemical molecule ABX has been developed by the private company ABIVAX and is currently undergoing phase II clinical trials (ulcerative colitis, rheumatoid arthritis). In collaboration with the CNRS, it has been observed that drug ABX is a potent anti-inflammatory drug able to specifically induce the overexpression of the miR-124, described for its anti-inflammatory properties. The aim of my PhD project was to characterize in vitro the phenotypic modulations and molecular mechanisms involved by drug ABX, on Human Monocyte-Derived Macrophages (Hu MDM) of healthy donors in an inflammatory context, and pretreated with drug ABX versus control. The data obtained on six Hu MDM show on the one hand, a significant decrease in the membrane receptors of the M1 phenotype (CD86, CD274) and on the other hand, a significant decrease in the factors involved in the TLR4 signaling pathway (p65/RelA, IkBζ/NFKBIZ, TRAF6). In addition, the secretory profile shows a significant decrease of a set of pro-inflammatory proteins such as cytokines (IL-6, TNFα, IL-1β), proteins involved in cell adhesion and leukocyte recruitment (ICAM-1, CXCL1), as well as the chemokine responsible for the infiltration of macrophages (MCP-1/ CCL2). Remarkably, the data obtained with 14 Hu MDM, show a significant overexpression of micro-RNA 124 of 3.4 times that of the DMSO control. All of these data suggest that drug ABX limits excessive inflammation and could play a role in the control of cellular homeostasis. The overexpression of miR-124 is consistent with in vitro data obtained with T CD4 lymphocyte and human PBMC data, as well as clinical data from ulcerative colitis patients. For the first time, the laboratory identifies the immunomodulatory potential of drug ABX in inflammation. By inducing specific overexpression of miR-124, drug ABX attenuates the pro-inflammatory profile of macrophages by a negative feedback loop of the TLR4/NF-kB signaling. MiR-124 potentiates the homeostatic effect of drug ABX. This new chemical molecule ABX could represent a new therapeutic perspective, in order to rebalance some mediators involved in innate and adaptive immunity
Chiot, Aude. "Implication des macrophages périphériques dans la Sclérose latérale Amyotrophique". Thesis, Sorbonne université, 2018. http://www.theses.fr/2018SORUS595.
Pełny tekst źródłaMicroglial cells and peripheral macrophages participate to motor neuron degeneration in ALS. However, the precise role of the peripheral macrophages surrounding motor neuron axons had not been discriminated from the role of CNS microglia. Although microglia and peripheral macrophages share common characteristics both populations have different developmental origins and are located in different cellular environments, which could lead to specific implications in the disease. In this study, we aimed to characterize the implication and the site of action of peripheral macrophages in ALS. We first confirmed the activation of peripheral macrophages in the sciatic nerve of two different mouse lines (expressing mutant SOD1) with different disease progression. We also showed for the first time the presence of macrophages surrounding motor neuron axons in the ventral root of a human ALS case. We showed that infiltration of macrophages in the spinal cord was minimal during the disease and was dependent on disease progression. Our transcriptional analyses showed major differences between microglia and peripheral macrophages even though both populations displayed a complex inflammatory profile. Finally, replacement of mutated macrophages by cells more neurotrophic or less neurotoxic led to an improvement of several pathophysiological markers and delayed symptomatic stage of the disease in ALS mice. In conclusion, we provide new evidence suggesting an active role of peripheral macrophages in ALS, supporting future therapeutic strategies by targeting peripheral macrophages
Fabre, Thierry. "Contribution à l'élaboration de biomatériaux hybrides dans le cadre de la réparation de pertes de substance nerveuse périphérique". Bordeaux 2, 1999. http://www.theses.fr/1999BOR28702.
Pełny tekst źródłaGuillou, Clément. "Étude des effets de l'alpha-énolase sur les cellules mononucléées du sang périphérique de sujets sains et de patients atteints de polyarthrite rhumatoïde, et dans le modèle murin d'arthrite induite au collagène". Rouen, 2015. http://www.theses.fr/2015ROUENR07.
Pełny tekst źródłaSalim, Cláudio. "Expression de la protéine géante AHNAK après lésion de la moelle épinière et dans le système nerveux périphérique : études fonctionnelles sur les cellules de Schwann in vitro". Paris 6, 2007. http://www.theses.fr/2007PA066507.
Pełny tekst źródłaAhnak gene in rat has been first identified by a differential screening that aimed in identifying proteins overexpressed in a spinal cord injury. After a spinal injury in rat, AHNAK is expressed by different types of cells invading the lesion epicenter as soon as 48h after injury. Those cells constitute the fibrotic component of the glial scar, and produce ahank at least until 6 months after injury. AHNAK expressing cells delineate the inner border of cystic cavities in the lesion epicenter, suggesting that AHNAK may participate in the formation of a tissue-protective barrier. In the peripheral nervous system, AHNAK is constitutively expressed by sensory neurons of the dorsal root ganglia, satellite cells, and Schwann cells from the nerve. During myelination in rat, AHNAK is redistributed from a strictly perimyelinic compartment of the external cytoplasm, to a more diffuse distribution associated with the outer surface of vesicles, and with the abaxonal plasma membrane. In non confluent Schwann cells in vitro, AHNAK and the laminin-receptor dystroglycan are associated with filopodia-like cell extensions. Ahnak interference in Schwann cells induces retraction of cell processes and detachment from laminin coated surfaces, associated with a reduction of the Schwann cell content in beta-dystroglycan and a nuclear translocation of Schwann cell specific dystrophin Dp116 which normally binds beta dystroglycan with the actin cytoskeleton. . We suggest AHNAK to be implicated in targeting and/or scaffolding of the dystroglycan-associated complex to the abaxonal membrane. Thus, similarly to periaxin with which it shares certain features, AHNAK may contribute to SC-basal lamina interaction, and myelin formation and/or maintenance