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Artykuły w czasopismach na temat "Balb/cJRj mice"
Barbier, E., J. Carpentier, O. Simonin, A. Chaumy, W. Laine, S. Anthérieu, P. Marchetti, J. M. Lo Guidice, J. Kluza i G. Garçon. "OS01-09 Mitochondrial dysfunction trigerred by air pollution-derived ultrafine particles chronic exposure in the lungs of Balb/cJRj mice". Toxicology Letters 384 (wrzesień 2023): S61—S62. http://dx.doi.org/10.1016/s0378-4274(23)00419-8.
Pełny tekst źródłaRiedl, Rebecca, Annika Kühn, Yvonne Hupfer, Betty Hebecker, Lukas K. Peltner, Paul M. Jordan, Oliver Werz, Stefan Lorkowski, Cornelia Wiegand i Maria Wallert. "Characterization of Different Inflammatory Skin Conditions in a Mouse Model of DNCB-Induced Atopic Dermatitis". Inflammation, 27.12.2023. http://dx.doi.org/10.1007/s10753-023-01943-x.
Pełny tekst źródłaSelle, Amandine, Carole Brosseau, Wieneke Dijk, Angéline Duval, Grégory Bouchaud, Anais Rousseaux, Aurélia Bruneau i in. "Prebiotic Supplementation During Gestation Induces a Tolerogenic Environment and a Protective Microbiota in Offspring Mitigating Food Allergy". Frontiers in Immunology 12 (5.01.2022). http://dx.doi.org/10.3389/fimmu.2021.745535.
Pełny tekst źródłaKasetty, Gopinath, Ravi K. V. Bhongir, Praveen Papareddy, Heiko Herwald i Arne Egesten. "The Nonantibiotic Macrolide EM703 Improves Survival in a Model of Quinolone-Treated Pseudomonas aeruginosa Airway Infection". Antimicrobial Agents and Chemotherapy 61, nr 9 (26.06.2017). http://dx.doi.org/10.1128/aac.02761-16.
Pełny tekst źródłaBrosseau, Carole, Amandine Selle, Angeline Duval, Barbara Misme-Aucouturier, Melanie Chesneau, Sophie Brouard, Claire Cherbuy i in. "Prebiotic Supplementation During Pregnancy Modifies the Gut Microbiota and Increases Metabolites in Amniotic Fluid, Driving a Tolerogenic Environment In Utero". Frontiers in Immunology 12 (14.07.2021). http://dx.doi.org/10.3389/fimmu.2021.712614.
Pełny tekst źródłaRozprawy doktorskie na temat "Balb/cJRj mice"
Barbier, Emeline. "Étude des mécanismes physiopathologiques impliqués dans la toxicité des particules ultrafines chez un modèle murin : une approche multi-organes". Electronic Thesis or Diss., Université de Lille (2022-....), 2023. http://www.theses.fr/2023ULILS063.
Pełny tekst źródłaAlthough there has been a significant reduction in air pollution since the 1990s, it remains a major public health problem, responsible for over 4.2 million premature deaths worldwide every year. At present, experts' attention is focused on ultrafine particles (PM0.1 or UFP) because of their ability to translocate into the systemic circulation and reach peripheral organs, where they are likely to have a harmful impact. Nevertheless, the knowledge of the cellular and molecular mechanisms involved in the toxicity of these particles is still very patchy, and most often remains focused on their main target, the lung. Thus, the main objectives of this thesis project were to provide innovative insights into the toxicokinetics (i.e., distribution/persistence) and toxicodynamics (i.e., pathophysiological mechanisms, associated cell signaling pathways) of UFP collected in urban environments, on the one hand, and the organospecific effects of UFP and the use of circulating miRNA as indicators of chronic and/or cumulative exposure to UFP in a mouse model, on the other hand. To answer these questions, Balb/cJRj mice were exposed for 3 months to various doses of UFP collected in the urban area of Lille, then analyzed in various target organs richly vascularized, and therefore directly exposed to UFP during their translocation and systemic distribution phase. The results showed that, in all target organs, the intrinsic oxidative potential of UFP undeniably induced the production of oxidative oxygen species and the activation of antioxidant defenses in sufficient quantities to restore a state of redox homeostasis, but were unable to prevent the onset of an inflammatory response in the lungs, heart and brain. Transcriptomic approaches carried out in the lungs, the target organ with the most marked deleterious effects, have suggested the deregulation of numerous signaling pathways in relation to oxidative and inflammatory responses, which constitute the central mechanisms of UFP toxicity, but also with more original toxicity mechanisms such as mitochondrial dysfunction, epithelial-mesenchymal transition and tissue remodeling, whose modulation has also been validated from a functional point of view. These promising data could ultimately contribute to better decision-making on the reduction of UFP emissions, as well as to the updating of current regulatory standards