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Добірка наукової літератури з теми "Réparation de lésion pulmonaire"
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Статті в журналах з теми "Réparation de lésion pulmonaire"
Noël-Savina, É., and R. Descourt. "Une lésion pulmonaire." La Revue de Médecine Interne 33, no. 2 (February 2012): 109–10. http://dx.doi.org/10.1016/j.revmed.2011.02.010.
Повний текст джерелаLe Chevalier, B., D. Lyonnet, F. Bejui, J. M. Pasquier, E. Boniface, and J. C. Guérin. "Ponction transthoracique et lésion pulmonaire excavée." La Revue de Médecine Interne 10, no. 1 (January 1989): 31–35. http://dx.doi.org/10.1016/s0248-8663(89)80110-9.
Повний текст джерелаDjian, P. "Lésion méniscale latérale sur genou stable : réparation ou méniscectomie." Revue de Chirurgie Orthopédique et Réparatrice de l'Appareil Moteur 92, no. 5 (September 2006): 175–77. http://dx.doi.org/10.1016/s0035-1040(06)75889-5.
Повний текст джерелаLebras, L., D. Arpin, S. Collardeau-Frachon, S. Isaac, J. C. Guerin, and M. Perol. "L’hyperplasie neuroendocrine pulmonaire idiopathique : une lésion prénéoplasique méconnue." Revue des Maladies Respiratoires 25, no. 9 (November 2008): 1131–35. http://dx.doi.org/10.1016/s0761-8425(08)74985-4.
Повний текст джерелаLeroy-Terquem, E., and J. Bellamy. "Traitement chirurgical exclusif d’une lésion pulmonaire cavitaire infectée par Mycobacterium xenopi." Revue de Pneumologie Clinique 61, no. 4 (September 2005): 261–63. http://dx.doi.org/10.1016/s0761-8417(05)84822-9.
Повний текст джерелаGrimberg, J., A. Diop, R. Bou Ghosn, L. D. Duranthon, G. Nourissat, and N. Maurel. "Le remplissage améliore-t-il la stabilité de l’épaule ? Étude biomécanique comparative randomisée entre réparation isolée d’une lésion de Bankart et réparation d’une lésion de Bankart associée à un remplissage." Revue de Chirurgie Orthopédique et Traumatologique 98, no. 8 (December 2012): S451. http://dx.doi.org/10.1016/j.rcot.2012.10.037.
Повний текст джерелаLaflamme, Anne-Marie. "Le droit de retour au travail et l’obligation d’accommodement : le régime de réparation des lésions professionnelles peut-il résister à l’envahisseur ?" Les Cahiers de droit 48, no. 1-2 (April 12, 2005): 215–47. http://dx.doi.org/10.7202/043929ar.
Повний текст джерелаTournier, Louis, Dominique Berrebi, Michel Peuchmaur, Arnaud Bonnard, Nadia Belarbi, Olivier Sibony, and Guillaume Morcrette. "Hétérotopie gliale pulmonaire : une lésion exceptionnelle chez un nourrisson avec un jumeau anencéphale." Annales de Pathologie 39, no. 1 (February 2019): 24–28. http://dx.doi.org/10.1016/j.annpat.2018.08.006.
Повний текст джерелаKodama, Y., T. Furumatsu, M. Fujii, T. Tanaka, S. Miyazawa, and T. Ozaki. "Lésion de la racine postérieure du ménisque médial : réparation transtibiale par le système FasT-Fix®." Revue de Chirurgie Orthopédique et Traumatologique 102, no. 7 (November 2016): 675. http://dx.doi.org/10.1016/j.rcot.2016.07.020.
Повний текст джерелаRakotoson, J. L., H. M. D. Vololontiana, R. E. Raherison, R. L. Andrianasolo, J. R. Rakotomizao, H. Rakotoharivelo, J. Rajaoarifetra, et al. "Volumineux aspergillome développé au sein d’une lésion de fibrose pulmonaire secondaire à une sclérodermie." Revue de Pneumologie Clinique 68, no. 1 (February 2012): 31–35. http://dx.doi.org/10.1016/j.pneumo.2011.03.001.
Повний текст джерелаДисертації з теми "Réparation de lésion pulmonaire"
Terrien, Xavier. "Implication de l'Insulin-like Growth Factor Binding Protein-2 dans les processus de lésion/réparation de l'alvéole pulmonaire." Paris 12, 2005. https://athena.u-pec.fr/primo-explore/search?query=any,exact,990003941690204611&vid=upec.
Повний текст джерелаAlveolar epithelial cells proliferation plays a major role in lung repair process. Our laboratory has previously reported the involvement of the Insulin-like Growth Factor Binding Protein-2 (IGFBP-2) in the control of type 2 alveolar epithelial cells proliferation. During this work, I have characterized the induction and the intracellular colocalization of IGFBP-2 and the cell cycle inhibitor p21CIP1 in growth-arrested lung epithelial cells. Moreover, I found the implication of IGFBP-2 in the stimulation of alveolar macrophages maturation. Taken together, these data suggest the importance of IGFBP-2 in alveolar repair process. In addition, the identification of a novel direct interaction between IGFBP-2 or -3 and p21CIP1 suggest a new mechanism of cell cycle control
Meloche, Jolyane. "Nouvelles avenues thérapeutiques dans l'hypertension artérielle pulmonaire : un regard sur la réparation des dommages à l'ADN et l'épigénétique." Doctoral thesis, Université Laval, 2018. http://hdl.handle.net/20.500.11794/31446.
Повний текст джерелаPulmonary arterial hypertension (PAH) is a rare clinical condition characterized by a progressive increase in pulmonary vascular resistance leading to right heart failure and death. Histologically, several processes coexist within the pulmonary arteries, including inflammation, vasoconstriction and vascular remodeling. Remodeling of the pulmonary vessel is due to abnormal and uncontrolled growth of resident pulmonary artery smooth muscle cells (PASMC). As such, PAH exhibits some cancer-like characteristics. In spite of recent progress in understanding the pathophysiological mechanisms involved in disease development and progression, as well as major improvements in symptomatic treatments, no substantial modification in the fatal course of this disease has been achieved. The mean survival rate is about 60% 5 years after diagnosis. Therefore, the identification of new targets has become mandatory. PAH is associated with sustained inflammation, oxidative stress, shear stress and pseudo-hypoxia, all known to promote DNA damage. Despite these unfavorable environmental conditions, PAH PASMC exhibit increased proliferation and resistance to apoptosis. Using a translational approach, we highlighted the role for DNA damage signaling and epigenetic mechanisms in the pathophysiology of PAH. Since PAH shares many hallmarks with cancer, we first studied Poly(ADP-ribose) polymerase-1 (PARP-1), a key enzyme in DNA repair mechanisms and in cell survival in the pathophysiology of PAH. In Chapter 2, we demonstrate that PAH is associated with sustained DNA damage leading to PARP-1 activation. Interestingly, we showed that PARP-1 overexpression triggers the expression and activation of transcription factors known to be implicated in PAH progression, such as HIF-1α (Hypoxia-inducible factor 1-alpha) and NFAT (Nuclear factor of activated T-cells). Overexpression of PARP-1 alsoresulted in decreased expression of microRNA miR-204, another key player in the disease. In animal studies, administration of a clinically available PARP-1 inhibitor decreased PAH in two experimental rat models. In addition, PARP-1 inhibitor was more effective than the first-line treatments offered to patients with PAH. In Chapter 3, we investigated the mechanisms by which PARP-1 was overexpressed in PAH. In silico analyses and studies in cancer demonstrated that miR-223 downregulation triggers PARP-1 overexpression. We provided evidence that miR-223 is downregulated in human PAH lungs, distal pulmonary arteries, and isolated PASMC. Furthermore, using a gain and loss of function approach, we showed that increased HIF-1α (hypoxia-inducible factor 1α), which is observed in PAH, triggers this decrease in miR-223 expression and subsequent overexpression of PARP-1 allowing PAH-PASMC proliferation and resistance to apoptosis. We also demonstrated that restoring the expression of miR-223, by using a mimic, allowed to improve pulmonary and cardiac hemodynamic parameters. In Chapter 4, we investigated epigenetic mechanisms downstream of PARP-1 and miR- 204. Interestingly, the epigenetic reader BRD4 (Bromodomain-containing protein 4) is a predicted target of miR-204 and has binding sites on NFAT’s promoter region. In our study, we showed that BRD4 is upregulated in lungs, distal pulmonary arteries and PASMC of PAH patients. Epigenetic readers bind to acetylated histone tails to promote gene transcription. In PAH, we demonstrated that BRD4 increases the expression of oncogenes involved in PAH pathogenesis, such as NFAT, Bcl-2, p21 and Survivin. BRD4 also regulates mitochondrial metabolism of PASMC. Blocking this oncogenic signature led to decreased proliferation and increased apoptosis of PAH-PASMC in a BRD4-dependant manner. In addition, pharmacological or molecular inhibition of BRD4 reversed established PAH in a rat model of the disease. In conclusion, these studies showed a key role for DNA damage signaling and epigenetic mechanisms in PAH pathophysiology. Our studies also offer new therapeutic perspectives for patients with PAH.
Maitre, Bernard. "Rôle du système des IGF ans le contrôle de la prolifération des cellules épithéliales de l'alvéole pulmonaire : étude au cours du développement du poumon et lors des processus de lésion-réparation alvéolaires." Paris 5, 1996. http://www.theses.fr/1996PA05CD24.
Повний текст джерелаZhai, Ruoyang. "Effects of sevoflurane in the treatment of Acute Respiratory Distress Syndrome : a translational approach." Electronic Thesis or Diss., Université Clermont Auvergne (2021-...), 2023. http://www.theses.fr/2023UCFA0077.
Повний текст джерелаAcute respiratory distress syndrome (ARDS) is a major cause of respiratory failurewith a high mortality rate. It is characterized by diffuse alveolar damage, alveolar edema, and hypoxemic respiratory loss which cause heavy healthcare costs. Currently, available treatments for ARDS remain primarily supportive, and no pharmacological approach is successfully translated into clinical application. There are two major processes during the physiopathological development of ARDS that lead to the formation of lung edema:alveolar barrier dysfunction and the impairment of alveolar fluid clearance following alveolar epithelial injury and inflammation. The receptor for advanced glycation end products (RAGE) was indicated to be involved during those processes, with the high potential of its soluble form as a biomarker for ARDS diagnostic and prognostic. Volatile halogenated agents, such as sevoflurane or isoflurane, are increasingly used in intensive care units as sedative agents with their ideal intrinsic characteristics as a sedative. Furthermore, numerous pre-clinical and clinical studies indicate its lung protective effects for ARDS patients.However, its mechanisms of such beneficial effects remain to be clarified.The main objectives of this thesis work are multiple, through experimental andtranslational in vivo and in vitro models of ARDS, to1) Asses the beneficial lung protective effects of sevoflurane in ARDS, including its effects on ARDS physiological features, lung fluid clearance, and alveolar permeability.2) Investigate the precise mechanism of observed effects of sevoflurane, including mechanistic studies and involved proteins' function and expression.3) Explore the role of RAGE in lung epithelial injury and repair and its eventualmediation role of the beneficial effects of sevoflurane.During this thesis work, we advanced from many angles: First, our work found in ourA549 cells wound healing model, the important role of RAGE in the lung injury repairprocess, as its ligand, HMGB1, and AGEs promoted RAGE-dependent wound healing oflung alveolar epithelial cells, which is possible through enhanced cell migration and proliferation.Secondly, our work in murine in vitro and in vivo ARDS models, animprovement of experimental features, with decreased indices of permeability and preserved epithelial structures in cells and mice, by at least in a part, increasing expression of ZO-1 and the inhibition of RhoA activity and pMLC as well as actin cytoskeleton rearrangement following lung epithelial injury. Additionally, RAGE may play a mediating role in the effects of sevoflurane on acute lung injury. Furthermore, our work in porcine in vivo ARDS models confirmed the lung protective effects of sevoflurane on ARDS features, with improved oxygenation, restored alveolar permeability, and improved AFC. Our study suggests theprotective effect of sevoflurane on AFC may be explained by the restoration of impaired lung expression of epithelial channels AQP-5, Na, K, ATPase, and ENaC during ARDS.Taken together, this thesis work explained more precisely the protective effects ofhalogenated agents and the new revelation of its potential mechanism, and hence supports the high interest in the use of inhaled sedation in intensive care for ARDS patients. This work may give some new insights for research on the effects of sevoflurane on ARDS and its resolution.Keywords: Acute respiratory distress syndrome; Sevoflurane; Lung epithelial barrierfunction; Lung wound repair; Alveolar fluid clearance; Epithelial channels: Junction proteins;Intracellular pathways; Receptor for advanced glycation end-products
Menoni, Hervé. "La réparation par excision de base d’une lésion oxydative sur des matrices nucléosomales." Lyon, École normale supérieure (sciences), 2008. http://www.theses.fr/2008ENSL0487.
Повний текст джерелаNucleic bases, the support of our genetic information, can be oxidized at any time. The main oxidative lesion , the 8-oxoG, has to be removed from our genome through the base excision repair pathway in order to fight its mutational effect. The glycolase OGG1, which initiate the repair of this lesion has to deal with chromatin. The fist level of this complex structure of DNA can inhibit or be transparent depending on the process involved. We're showing that base excision repair of an 8-oxoG is strongly inhibited by the nucleosome. An ATP-dependant chromatin remodeling without eviction of the octamer or displacement of the nucleosome is possible for the repair of the lesion inside the nucleosome. The excision of 8-oxoG in the linker DNA is inhibited by the secondary structure of the chromatin. The eviction of histone H1 by a histone chaperon facilitate the excisionof 8-oxoG
Plantier, Laurent. "Réparation alvéolaire et emphysème pulmonaire : rôle des systèmes d'alvéologénèse." Phd thesis, Université Paris-Est, 2008. http://tel.archives-ouvertes.fr/tel-00462142.
Повний текст джерелаNabeyrat, Elodie. "Acide rétinoïque et réparation de l'épithélium de l'alvéole pulmonaire." Paris 5, 1999. http://www.theses.fr/2000PA05N052.
Повний текст джерелаPignarre, Louis-Frédéric. "Les obligations en nature et de somme d'argent en droit privé : essai de théorisation à partir d'une distinction." Montpellier 1, 2005. http://www.theses.fr/2005MON10068.
Повний текст джерелаFournier, Clément. "Monitorep monitorage intra-thoracique optique de la réparation pulmonaire in vivo." Mémoire, Université de Sherbrooke, 2009. http://savoirs.usherbrooke.ca/handle/11143/1514.
Повний текст джерелаVedrenne, Nicolas. "Rôles de différentes populations d'astrocytes dans les mécanismes de réparation après lésion du système nerveux central." Limoges, 2013. http://www.theses.fr/2013LIMO330D.
Повний текст джерелаAstrocytes play a key role in central nervous system (CNS) repair, particularly during the formation of the glial scar. After a severe CNS injury, an important extracellular matrix deposition produced by activated astrocytes limits the extension of the lesion but impairs axonal growth impeding the restoration of altered physiological functions. A better understanding of the scar tissue formation and of remodelling processes could therefore help to define new therapeutic approaches. To address this problem, two models in vitro and in vivo have been developped. In vitro, the sedimentation field flow fractionation method allowed us to quickly enrich cortical cell cultures in astrocytes. In addition, this technique was used to isolate different astrocyte populations. One expresses the α-smooth muscle actin isoform and contracts, thus showing a myofibroblast phenotype wich is usually observed in the majority of organs after damage. Another wich strongly expresses vimentin, forms neurospheres wich are able to generate the three major cell types of the CNS (neurons, oligodendrocytes and astrocytes), demonstrating capacities of neural stem cells. In vivo, the model of controlled cortical impact in rats was developped and characterized in order to reproduce the pathophysiology of traumatic brain injury. Using this model, we have shown that treatment with an antisense oligonucleotide directed against TGF-β1 mRNA enables a better functional and cognitive recovery
Книги з теми "Réparation de lésion pulmonaire"
Essai n° 482: Toxicologie génétique: Lésion et réparation d'ADN - Synthèse non programmée de l'ADN (UDS) sur cellules de mammifère - in vitro. OECD, 1986. http://dx.doi.org/10.1787/9789264071452-fr.
Повний текст джерела