Literatura científica selecionada sobre o tema "Facteur de nécrose tumorale (TNF)"
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Artigos de revistas sobre o assunto "Facteur de nécrose tumorale (TNF)"
Gueydan, C., e E. Coessens. "Avancées et perspectives de la recherche sur le facteur de nécrose tumorale (TNF)". médecine/sciences 13, n.º 1 (1997): 83. http://dx.doi.org/10.4267/10608/309.
Texto completo da fonteHamaï, Ahmed, Jane Muret, Andrea Cavalcanti, Sylvie Bonvalot e Salem Chouaïb. "Le facteur de nécrose tumorale: de la biologie à la thérapie oncologique". Hématologie 15, n.º 4 (julho de 2009): 291–304. http://dx.doi.org/10.1684/hma.2009.0366.
Texto completo da fonteConstans, J., JL Pellegrin, I. Pellegrin, E. Peuchant, MF Dumon, C. Sergeant, M. Simonoff et al. "Interféron et facteur de nécrose tumorale sériques chez 95 patients infectés par le VIH". La Revue de Médecine Interne 14, n.º 10 (janeiro de 1993): 1004. http://dx.doi.org/10.1016/s0248-8663(05)80122-5.
Texto completo da fonteFautrel, Bruno, Manon Belhassen, Christophe Hudry, Marie-Christine Woronoff-Lemsi, Laurie Levy-Bachelot, Eric Van Ganse e Florence Tubach. "Facteurs prédictifs du maintien sous traitement par inhibiteurs du facteur de nécrose tumorale dans la polyarthrite rhumatoïde : étude observationnelle sur 8052 patients". Revue du Rhumatisme 87, n.º 5 (outubro de 2020): 412–14. http://dx.doi.org/10.1016/j.rhum.2020.07.011.
Texto completo da fonteBeldi-Ferchiou, A., S. Oro, V. Molinier-Frenkel, F. Lemonnier, A. Thiolat, C. Pilon, J. Giustiniani et al. "Le récepteur type 2 du facteur de nécrose tumorale pourrait représenter une cible thérapeutique alternative au cours du syndrome de Sézary et du mycosis fongoïde". Annales de Dermatologie et de Vénéréologie - FMC 3, n.º 8 (dezembro de 2023): A37. http://dx.doi.org/10.1016/j.fander.2023.09.004.
Texto completo da fonteDreyfus, J. C. "De nouveaux mutants du facteur nécrosant des tumeurs (TNF), capables de dissocier les activités anti-tumorale et cytotoxique générale". médecine/sciences 9, n.º 3 (1993): 335. http://dx.doi.org/10.4267/10608/2921.
Texto completo da fonteOliveira, D., A. Martins, F. Martins, M. Rato, F. Pinheiro, D. Fonseca, S. Garcia et al. "L’association entre les niveaux d’auto-anticorps et les résultats du traitement anti-facteur de nécrose tumorale alpha dans la polyarthrite rhumatoïde – une étude de cohorte rétrospective avec un suivi de deux ans". Revue du Rhumatisme 89 (dezembro de 2022): A164. http://dx.doi.org/10.1016/j.rhum.2022.10.243.
Texto completo da fonteKurtulus, Idris, Serdar Basim e Yasar Ozdenkaya. "Le facteur de nécrose tumorale alpha (TNF-α) peut-il prédire la présence d’adhérences avant une chirurgie laparoscopique ?" Journal de Chirurgie Viscérale, junho de 2023. http://dx.doi.org/10.1016/j.jchirv.2022.11.003.
Texto completo da fonteDie Redaktion. "Existe-t-il une association? / Viagra / Malaria / Facteur de nécrose tumorale / la dermatite atopique / falsification de médicaments". Forum Médical Suisse ‒ Swiss Medical Forum, 26 de junho de 2002. http://dx.doi.org/10.4414/fms.2002.04566.
Texto completo da fonteTeses / dissertações sobre o assunto "Facteur de nécrose tumorale (TNF)"
Ameyar-Zazoua, Maya. "Etude des mécanismes de résistance à la lyse tumorale induite par le facteur de nécrose tumorale-α (TNF)". Paris 11, 2001. http://www.theses.fr/2001PA11T008.
Texto completo da fonteRayhane, Naima. "Démonstration à l'aide de 2 modèles expérimentaux du rôle protecteur du TNF au cours d'une infection fongique". Paris 5, 2000. http://www.theses.fr/2000PA05N018.
Texto completo da fonteMiron, Pierre-Olivier. "Effets du TNF-a sur les propriétés biologiques des cellules souches de la papille apicale". Master's thesis, Université Laval, 2020. http://hdl.handle.net/20.500.11794/66341.
Texto completo da fonteHaddy, Nadia. "Inflammation, athérosclérose et leurs indicateurs de risque : interleukine-6, facteur de nécrose tumorale-alpha et apolipoprotéine-E". Nancy 1, 2003. http://www.theses.fr/2003NAN12510.
Texto completo da fonteDagenais, Pierre. "Modulation de l'expression génique du récepteur du facteur activateur des plaquettes (PAF-R) par le facteur de nécrose tumorale alpha (TNF[lettre grecque alpha]) chez les monocytes humains". Thèse, Université de Sherbrooke, 1998. http://savoirs.usherbrooke.ca/handle/11143/4109.
Texto completo da fonteCordova, Jaime Gonzalo. "Role of CTGF and TNF on fibrosis in muscular dystrophy". Thesis, Paris 6, 2014. http://www.theses.fr/2014PA066546/document.
Texto completo da fonteThe Duchenne Muscular Dystrophy (DMD) is an X-linked disease characterized by progressive damage in the muscle due to the absence of the dystrophin protein. Fibrosis, the excessive accumulation of extracellular matrix (ECM) proteins, is also present in the muscle of DMD patients and several animal models (such as the mdx mice). Among the factors that induce fibrosis are Transforming Growth Factor type β (TGF-β) and Connective Tissue Growth Factor (CTGF), the latter being a target of the TGF-β/SMAD signaling pathway and is the responsible for the profibrotic effects of TGF-β and are augmented in fibrosis tissues. Little is known about the regulation of the expression of CTGF mediated by TGF-β in muscle cells. In here, we described a novel SMAD Binding Element (SBE) located in the 5’ UTR region of the CTGF gene important for the TGF-β mediated expression of CTGF in myoblasts. In addition, our results suggest that additional transcription factor binding sites present in the 5’ UTR of the CTGF gene are important for this expression. On the other hand, the Tumor Necrosis Factor (TNF) is an inflammatory cytokine that is present in DMD muscles and is responsible for muscle necrosis and inflammatory cell infiltration. In this study, we show that the increased expression of the soluble TNF Receptor I by electrotransfer (ET) in the tibialis anterior muscle attenuates inflammation, damage and fibrosis in the skeletal muscle of the mdx mice. In addition, we found increased muscle strength in the mdx mice. Therefore, we propose that ET could be used as an efficient anti-TNF therapy for treating muscle dystrophies
Mulleman, Denis. "Variabilité de réponse aux anti TNF-alpha dans les rhumatismes inflammatoires : apport des marqueurs biologiques et d'imagerie". Thesis, Tours, 2009. http://www.theses.fr/2009TOUR3113/document.
Texto completo da fonteThere is an interindividual variability of the dose - response relationship in patients with inflammatory rheumatic diseases treated by Tumor Necrosis Factor-alpha (TNF-a) inhibitors. In the first part of this thesis, the pathophysiology of TNF-a in inflammatory processes is presented. Then, the work focuses on the concentration-effect relationship using pharmacokinetic-pharmacodynamic (PK-PD) models. At the end, after discussion on imaging biomarkers, the thesis discusses the usefulness of a new technique to detect the early response to treatment, namely the positron emission tomography (PET). In summary, this work describes the PK-PD relationship in rheumatic inflammatory diseases treated by monoclonal antibodies using clinical and biological markers and demonstrates also the influence of high concentrations of monoclonal antibodies on maintenance to treatment. PET is a promising technique to identify early response to TNF-a antagonists
Afonso, Valéry. "Etude de la régulation de l'expression du gène codant la superoxyde dismutase 1 (SOD1) par le TNF alpha et l'hormone thyroïdienne T3 dans la lignée monocytaire humaine U937". Paris 7, 2009. http://www.theses.fr/2009PA077161.
Texto completo da fonteOxidative stress is involved m the development of several diseases (cancer, cataract, speeded up ageing). It results from an unbalance between the antioxidant Systems of defense and production of free radicals. To face the situation the organism has antioxidizing enzymes like superoxide dismutase (SOD) and NAD (P) H. Numerous experiments allowed to determine the protective fonction of SODl gene against oxidative damages in various pathological conditions. It is well known that TNF-a leads to the production of RLO in ail cell types. On the other hand, oxidative stress is a factor of amplification of TNF-α synthesis and one of the mechanisms of action of this cytokine. Weak concentration of RLO acts as second messengers to induce transduction pathways activated by TNF-α. Few things are known on the manner how TNF-a and the thyroid hormone T3 regulate SODl gene transcription. That's why the purpose of this thesis was to study the effects of these two factors on the regulation of human SODl promoter in the human monocytic cell line U937, and to determine the cellular and molecular mechanisms implicated. We show, m the first part this work that, the treatment of the U937 cell line by TNF-a regulates negatively SOD1 transcription, and as this reduction of mRNA is associated with a fall of the protein. These effects are not linked to a production of RLO in our culture conditions. Furthermore, the synthesis of a new protein is not necessary for the inhibition of SOD1 gene transcription by TNF-α and suggests post translational modifications of the transcription factors involved in this regulation. The analysis of SOD1 promoter, allowed to show that Egr-1 is the key protein for the formation of the transcriptional complex necessary for the initiation of transcription, and that this complex I is involved in the basal activity of SOD1. Finally, AP-1 protein plays a negative role (co-repressor) in the regulation of transcription by interfering with the binding of activating factors. It would seem therefore that TNF-α would act at two levels, first of ail by increasing the binding of AP-1 protein (activation of the inhibitory pathway) and by diminishing that of Spl (inhibition of the activating pathway) to suppress SOD1 gene. Finally, the intracellular JNK signaling pathway located upstream of AP-1 is involved in the suppression of SOD1 promoter by TNF-α. In second part of this work, we show that TRpl, in dose dependant manner activates SOD1 promoter and that in the presence of T3 this effect is diminished. We located the T3 responsible element (TRE) between nucléotides-157 and -t-17 of SOD1 promoter. The DBD is essential to suppress the activity of SOD1 promoter in the presence of T3 but does not intervene in the activation of the promoter. Contrary to the classical skim schema of gene regulation, these results let think that TRpl, activates SOD1 promoter by linking preferentially co-repressor proteins. This work allowed to show in vitro, that SOD1 promoter is sensitive to the action of TNF-a and to that of thyroid hormone, and that this effect is not mediated by an increase of free radicals. It also shows that TNF-α suppresses SOD1 through AP-1 and not NF-kB, via JNK transduction pathway. We also show that SOD1 is a target gene of T3 and that this effect, involved the DNA binding domain (DBD). Finally SOD1 could be a therapeutic target in the inflammatory situations linked to an increase of TNF-α or thyroid hormone (T3)
Dagenais, Pierre. "Modulation de l'expression génique du récepteur du facteur activateur des plaquettes (PAF-R) par le facteur de nécrose tumorale alpha (TNFÃ) chez les monocytes humains". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0002/NQ40519.pdf.
Texto completo da fonteAzria, David. "Association du facteur de nécrose tumorale (TNFα) et de la radiothérapie dans les cancers digestifs exprimant l'antigène carcinoembryonnaire (ACE) : intérêts d'un anticorps bispécifique anti-ACE/anti-TNFα". Montpellier 1, 2004. http://www.theses.fr/2004MON1T005.
Texto completo da fonteLivros sobre o assunto "Facteur de nécrose tumorale (TNF)"
Marialuisa, Melli, e Parente Luca, eds. Cytokines and lipocortins in inflammation and differentiation: Proceedings of the International Conference on Molecular and Cellular Biology of IL-1, TNF, and Lipocortins in Inflammation and Differentiation, held in Siena, Italy, October 22-25, 1989. New York, NY: Wiley-Liss, 1990.
Encontre o texto completo da fonteT, Osawa, e Bonavida Benjamin, eds. Tumor necrosis factor: Structure-function relationship and clinical application. Basel: Karger, 1992.
Encontre o texto completo da fonteInternational Conference on Tumor Necrosis Factor and Related Cytokines (4th 1992 Veldhoven, Netherlands). Tumor necrosis factor: Molecular and cellular biology and clinical relevance. Editado por Fiers Walter e Buurman Wim A. Basel: Karger, 1993.
Encontre o texto completo da fonteL, Moses Harold, Lengyel Peter 1929-, Stiles Charles D e 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.
Encontre o texto completo da fonteFiers, Walter, e Wim A. Buurman. Tumor Necrosis Factor: Molecular and Cellular Biology and Clinical Relevance. S Karger Pub, 1993.
Encontre o texto completo da fonteGrowth inhibitory and cytotoxic polypeptides ; proceedings of a Genentech-Smith, Kline & French-Triton Biosciences-UCLA Symposium held in Keystone, Colorado, ... symposia on molecular and cellular biology). A.R. Liss, 1989.
Encontre o texto completo da fonte(Editor), Marialuisa Melli, e Luca Parente (Editor), eds. Cytokines and Lipocortins in Inflammation and Differentiation: Proceedings of the International Conference on Molecular and Cellular Biology of Il-1, (Progress in Clinical & Biological Research). Wiley-Liss, 1990.
Encontre o texto completo da fonte