Auswahl der wissenschaftlichen Literatur zum Thema „Régénération pulmonaire“
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Zeitschriftenartikel zum Thema "Régénération pulmonaire"
Ribeiro Baptista, B., J. Grégoire, M. Toigo, M. Zysman, F. Coulpier, C. Thiebaut De Menonville, R. Belgacemi et al. „La délétion de p16INK4a dans les cellules épithéliales alvéolaires favorise la régénération pulmonaire“. Revue des Maladies Respiratoires Actualités 15, Nr. 1 (Januar 2023): 14. http://dx.doi.org/10.1016/j.rmra.2022.11.022.
Der volle Inhalt der QuelleZysman, M., B. Ribeiro Baptista, L. A. Essari, C. Giffard, F. Chabot, R. Epaud, S. Lanone, J. Boczkowski und L. Boyer. „Déterminants précoces de la bronchopneumopathie chronique obstructive : la régénération pulmonaire, une nouvelle piste thérapeutique ?“ Revue des Maladies Respiratoires 36, Nr. 4 (April 2019): 447–50. http://dx.doi.org/10.1016/j.rmr.2019.03.006.
Der volle Inhalt der QuelleCoraux, C., T. Jolly, J. Roux, S. Lingee, V. Laplace und P. Birembaut. „016 Modèle d’étude de la régénération de l’épithélium respiratoire bronchiolaire humain“. Revue des Maladies Respiratoires 24, Nr. 9 (November 2007): 1196. http://dx.doi.org/10.1016/s0761-8425(07)74307-3.
Der volle Inhalt der QuelleHajj, R., P. Lesimple, V. Laplace, E. Puchelle und C. Coraux. „008 La régénération de l’épithélium de surface respiratoire est anormale dans la mucoviscidose“. Revue des Maladies Respiratoires 22, Nr. 5 (November 2005): 847. http://dx.doi.org/10.1016/s0761-8425(05)92420-0.
Der volle Inhalt der QuelleMaouche, K., B. Nawrocki-Raby, M. Polette, I. Cloëz-Tayarani, P. Birembaut und J. M. Tournier. „022 Rôle du récepteur nicotinique α7 dans la régénération de l’épithélium respiratoire humain“. Revue des Maladies Respiratoires 24, Nr. 9 (November 2007): 1199. http://dx.doi.org/10.1016/s0761-8425(07)74313-9.
Der volle Inhalt der QuelleRibeiro Baptista, B., M. Zysman, C. Thibault de Menonville, F. Chabot, S. Lanone, G. Derumeaux, J. Boczkowski und L. Boyer. „Cibler p16INK4a-/− et les pneumocytes de type 2 pour induire une régénération alvéolaire endogène“. Revue des Maladies Respiratoires 38, Nr. 6 (Juni 2021): 575–76. http://dx.doi.org/10.1016/j.rmr.2021.02.015.
Der volle Inhalt der QuelleMaouche, K., M. Polette, J. M. Zahm, T. Jolly, C. Coraux, I. Cloez-Tayarani, P. Birembaut und J. M. Tournier. „Implication du récepteur nicotinique à l’acétylcholine α7 dans la régénération de l’épithélium respiratoire humain“. Revue des Maladies Respiratoires 25, Nr. 9 (November 2008): 1188. http://dx.doi.org/10.1016/s0761-8425(08)75054-x.
Der volle Inhalt der QuelleRoux, J., T. Jolly, S. Lingee, P. Birembaut und C. Coraux. „Étude des facteurs épithéliaux intervenant dans la régénération et le remodelage de l’épithélium respiratoire humain“. Revue des Maladies Respiratoires 25, Nr. 9 (November 2008): 1187. http://dx.doi.org/10.1016/s0761-8425(08)75053-8.
Der volle Inhalt der QuelleLesimple, P., C. Coraux, C. Catusse, M. P. Buisine, M. C. Copin, I. Van Seuningen, N. Porchet und E. Puchelle. „014 Expression différentielle des mucines et des peptides trifoliés (TFF) durant la régénération de l’épithélium respiratoire humain“. Revue des Maladies Respiratoires 22, Nr. 5 (November 2005): 850. http://dx.doi.org/10.1016/s0761-8425(05)92426-1.
Der volle Inhalt der QuelleJusteau, G., M. Toigo, T. Castro de Freitas, B. Ribeiro Baptista, E. Zana-Taieb und L. Boyer. „Lipofibroblastes pulmonaires chez l’adulte et régénération alvéolaire au cours de l’emphysème“. Revue des Maladies Respiratoires, März 2024. http://dx.doi.org/10.1016/j.rmr.2024.02.015.
Der volle Inhalt der QuelleDissertationen zum Thema "Régénération pulmonaire"
Thériault, Marie-Eve. „Altération de la régénération musculaire dans la maladie pulmonaire obstructive chronique“. Doctoral thesis, Université Laval, 2016. http://hdl.handle.net/20.500.11794/27055.
Der volle Inhalt der QuelleSkeletal muscle regeneration is altered in skeletal muscles of patients with Chronic Obstructive Pulmonary Disease. Chronic Obstructive Pulmonary Disease is associated with an irreversible and a progressive airflow obstruction. In COPD, the loss of muscle mass has a significant impact on quality of life and is associated with premature death. Many biochemical factors have been proposed to trigger and perpetuate the skeletal muscle atrophy in COPD. The maintenance of peripheral muscle mass may be compromised in patients with COPD due to premature cellular senescence and exhaustion of the regenerative potential of the muscles. Shortening of telomeres in patients with COPD is consistent with an increased number of senescent satellite cells and an exhausted muscle regenerative capacity, compromising the maintenance of muscle mass in these individuals. Muscle mass maintenance relies on the delicate regulation between protein degradation, synthesis and the addition of new myonuclei from satellite cells. Comparing the signalisation involved in the skeletal muscle regeneration between two muscles with different levels of activation within the same subjects is an interesting strategy to evaluate the impact of local versus systemic factors in the regulation of skeletal muscle regeneration. Impaired satellite cell activation, proliferation and differentiation affecting skeletal muscle regeneration could contribute to the progression of muscle dysfunction in patients with COPD. Resistance training, as provided in pulmonary rehabilitation, is an essential tool to promote muscle hypertrophy and increase muscle strength. However, hypertrophic response to resistance training is heterogeneous in patients with COPD. Failure in satellite cell function can lead to delayed, impaired or failed recovery after muscle injury, and such failures become increasingly prominent in cases of progressive muscle disease. Although the inflammatory response has been linked to the initiation and development of muscle atrophy, discrepancies exist in the literature concerning the presence and the nature of systemic and/or local inflammatory response in patients with COPD. This inflammation could be linked to the skeletal muscle protein imbalance and ultimately atrophy. The quest to identify a key inflammatory factor that could orchestrate the signaling cascade involved in contractile protein synthesis/degradation or even tissue renewal in peripheral muscles of patients with COPD is of major importance for future direction in this research field. This thesis demonstrates for the first time the role played by satellite cells in muscle atrophy associated with COPD. Better knowledge of the regenerative capacity in the context of COPD will enhance the understanding of the atrophying process and deepen the reasoning on training interventions in this population.
Thériault, Marie-Eve. „Caractérisation des cellules satellites chez des personnes ayant une maladie pulmonaire obstructive chronique“. Thesis, Université Laval, 2010. http://www.theses.ulaval.ca/2010/27196/27196.pdf.
Der volle Inhalt der QuelleTruchi, Marin. „Le séquençage de transcrits sur cellule unique appliqué à l'étude des mécanismes de formation et de résolution de la fibrose pulmonaire“. Electronic Thesis or Diss., Université Côte d'Azur, 2023. http://www.theses.fr/2023COAZ6016.
Der volle Inhalt der QuelleRestoration of lung tissue integrity in response to injury depends in particular on the regenerative capacities of capillary endothelial cells (CEc), which may decline with ageing. Inadequate responses can lead to the development of chronic diseases such as idiopathic pulmonary fibrosis (IPF), which is characterised by the accumulation of extracellular matrix and remodelling of the alveolar environment, leading to progressive destruction of the parenchyma and culminating in respiratory failure. In mice, bleomycin-induced lung injury can be used to trigger a transient fibrotic response, which is resolved within a few weeks. However, preliminary data indicated a delay in fibrosis resolution in aged mice.To investigate the mechanisms of lung endothelial regeneration and the potential influence of ageing on resolution dynamics, we measured gene expression by single-cell RNA sequencing (scRNA-seq) in cells from whole lungs of young (7 weeks) and old (18 months) mice collected 14, 28 or 60 days after injection of bleomycin (2U.kg-1) or PBS. The count matrices from the 36 sequenced samples were integrated to obtain a single dataset of 44541 cells. Based on their transcriptomic profile, the cells were clustered and manually annotated on the basis of the expression of specific marker genes. In addition to the two subpopulations of CEc present in physiological conditions, called general capillaries (gCap) and aerocytes (aCap), three subpopulations almost exclusively present in bleomycin-treated mouse samples were identified. A first population of Col15a1-expressing cells, named SV EC, corresponds to systemic venous vessels normally restricted to the bronchi and which are described in IPF as invading the alveolar tissue. The other two populations, not described in the literature, are cells similar to gCap or aCap but expressing specific and angiogenesis-associated markers, such as Lrg1, a modulator of the TGF-β pathway. The transcriptomic signatures of these subpopulations suggested their involvement in the regenerative processes of the alveolar niche through intense signaling activity. Comparison of their observed dynamics during the evolution of fibrosis between young and old mice showed a shift in resolution in old mice, which at 28 days still showed a pathological signature in contrast to young mice. This delay was then confirmed by in situ hybridization approaches and by spatial transcriptomics data analysis. Furthermore, differential expression analyses between gCap from young and old mice revealed age-dependant signatures in both physiological and fibrotic conditions, with gCap from old control mice expressing genes of the bleomycin-induced signature. Finally, the similarities between the bleomycin-induced SV EC signature and that induced in human IPF suggest that the observed remodelling in the mouse model partially mimics that which characterizes the human pathology
Marinval, Nicolas. „Fucoïdanes extraits de l'algue brune ascophyllum nodosum : effets pro-angiogéniques in vitro et régénération de valves pulmonaires acellularisées“. Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCD014/document.
Der volle Inhalt der QuelleFucoidans are marine sulfated polysaccharides carrying various biological activities comparable to endogenous glycosaminoglycans (GAGs).Their use as therapeutic agents in cardiovascular diseases treatment is considered. The structural heterogeneity linked to their natural diversity and to the extraction and purification methods induce variation in their physico-chemical properties and biological activities. The aim of this study is first to etablish a structure-function study of fucoidans extracted from the seaweed Ascophyllum nodosum on their in vitro pro-angiogenic effects (cell migration and vascular network formation by human endothelial cells, HUVECs) and the role of the endogenous GAGs ; and the study of the regenerative potential of the application of a biofilm of fucoidan/VEGF on acellular porcine heart valves. In the first part, our results show the fractionated low molecular weight fucoidan (LMWF, 4900 g/mol) induces higher pro-angiogenic effects than medium molecular weight fucoidan (MMWF, 26700 g/mol) on HUVECs. LMWF kept a pro-angiogenic potential with GAG-free HUVECs and is mainly endocyted in a clathrin-dependant pathway in which GAGs could be partially involved. In our second study, our data demonstrated that the application of the biofilm fucoidan/VEGF on acellular porcine pulmonary valves induce antithrombotic potential and allow the adhesion and survival of HUVECs. This work suggest that this method allows re-endothelialization of acellular heart valve and could be used to develop self-regenerative valve bioprosthesis