Academic literature on the topic 'Lung wound repair'
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Journal articles on the topic "Lung wound repair"
Kim, Sean H. J., Michael A. Matthay, Keith Mostov, and C. Anthony Hunt. "Simulation of lung alveolar epithelial wound healing in vitro." Journal of The Royal Society Interface 7, no. 49 (March 17, 2010): 1157–70. http://dx.doi.org/10.1098/rsif.2010.0041.
Full textGazdhar, Amiq, Patrick Fachinger, Coretta van Leer, Jaroslaw Pierog, Mathias Gugger, Robert Friis, Ralph A. Schmid, and Thomas Geiser. "Gene transfer of hepatocyte growth factor by electroporation reduces bleomycin-induced lung fibrosis." American Journal of Physiology-Lung Cellular and Molecular Physiology 292, no. 2 (February 2007): L529—L536. http://dx.doi.org/10.1152/ajplung.00082.2006.
Full textCrane, Meredith, Yun Xu, William L. Henry, Jorge E. Albina, and Amanda M. Jamieson. "The impact of lung infection on wound repair responses." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 61.10. http://dx.doi.org/10.4049/jimmunol.196.supp.61.10.
Full textOlsen, Colin E., Andrew E. Liguori, Yue Zong, R. Clark Lantz, Jefferey L. Burgess, and Scott Boitano. "Arsenic upregulates MMP-9 and inhibits wound repair in human airway epithelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 295, no. 2 (August 2008): L293—L302. http://dx.doi.org/10.1152/ajplung.00134.2007.
Full textGeiser, Thomas, Masanobu Ishigaki, Coretta van Leer, Michael A. Matthay, and V. Courtney Broaddus. "H2O2 inhibits alveolar epithelial wound repair in vitro by induction of apoptosis." American Journal of Physiology-Lung Cellular and Molecular Physiology 287, no. 2 (August 2004): L448—L453. http://dx.doi.org/10.1152/ajplung.00177.2003.
Full textCroasdell Lucchini, Amanda, Naomi N. Gachanja, Adriano G. Rossi, David A. Dorward, and Christopher D. Lucas. "Epithelial Cells and Inflammation in Pulmonary Wound Repair." Cells 10, no. 2 (February 5, 2021): 339. http://dx.doi.org/10.3390/cells10020339.
Full textClark, Richard A. "The Commonality of Cutaneous Wound Repair and Lung Injury." Chest 99, no. 3 (March 1991): 57S—60S. http://dx.doi.org/10.1378/chest.99.3_supplement.57s.
Full textIto, Yoko, Kelly Correll, John A. Schiel, Jay H. Finigan, Rytis Prekeris, and Robert J. Mason. "Lung fibroblasts accelerate wound closure in human alveolar epithelial cells through hepatocyte growth factor/c-Met signaling." American Journal of Physiology-Lung Cellular and Molecular Physiology 307, no. 1 (July 1, 2014): L94—L105. http://dx.doi.org/10.1152/ajplung.00233.2013.
Full textGeiser, Thomas, Pierre-Henri Jarreau, Kamran Atabai, and Michael A. Matthay. "Interleukin-1β augments in vitro alveolar epithelial repair." American Journal of Physiology-Lung Cellular and Molecular Physiology 279, no. 6 (December 1, 2000): L1184—L1190. http://dx.doi.org/10.1152/ajplung.2000.279.6.l1184.
Full textConese, Massimo, and Sante Di Gioia. "Pathophysiology of Lung Disease and Wound Repair in Cystic Fibrosis." Pathophysiology 28, no. 1 (March 10, 2021): 155–88. http://dx.doi.org/10.3390/pathophysiology28010011.
Full textDissertations / Theses on the topic "Lung wound repair"
Lai, Ju-Ping. "Phosphatase and tensin homolog deleted on chromosome Ten (PTEN) as a molecular target in lung epithelial wound repair and protection." The Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=osu1206120012.
Full textZhai, 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.
Full textAcute 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
Books on the topic "Lung wound repair"
(Editor), Geoffrey J. Bellingan, and Geoffrey J. Laurent (Editor) ;, eds. Acute Lung Injury: From Inflammation to Repair (Biomedical and Health Research). Ios Pr Inc, 2001.
Find full textFye, W. Bruce. Pioneering Open-Heart Surgery at the University of Minnesota and the Mayo Clinic. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199982356.003.0010.
Full textBook chapters on the topic "Lung wound repair"
Chegireddy, Vishwanath, Koby D. Caplan, and Joseph S. Fernandez-Moure. "Porcine Acellular Lung Matrix in Wound Healing and Hernia Repair." In Chronic Wounds, Wound Dressings and Wound Healing, 347–62. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/15695_2017_102.
Full textBoston, Patricia. "Klara Bergman." In Crossing Over, 102—C5.P108. Oxford University PressNew York, 2022. http://dx.doi.org/10.1093/med/9780197602270.003.0005.
Full textDebost, Michel. "Muscles, Strong and Weak." In The Simple Flute, 166–67. Oxford University PressNew York, NY, 2002. http://dx.doi.org/10.1093/oso/9780195145212.003.0048.
Full textConference papers on the topic "Lung wound repair"
Blokland, Kaj, David Waters, Michael Schuliga, Simon Pouwels, Chris Grainge, Steven Mutsaers, Cecilia Prêle, et al. "Alveolar epithelial wound repair is delayed by scenescent lung fibroblasts in IPF." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa596.
Full textLópez-Martínez, C., P. Martín-Vicente, R. Albillos-Almaraz, I. Lopez-Alonso, R. Rodríguez-García, M. Fernández-Rodríguez, F. E. Fernández Suárez, et al. "Impact of Tidal Ventilation on Lung Repair in Ex Vivo Wound Healing Models." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a5388.
Full textFergie, NF, DF McAuley, CM O’Kane, and AD Krasnodembskaya. "P47 Hypercapnia impairs the ability of mesenchymal stem cells to promote distal lung epithelial wound repair in ards." In British Thoracic Society Winter Meeting 2017, QEII Centre Broad Sanctuary Westminster London SW1P 3EE, 6 to 8 December 2017, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2017. http://dx.doi.org/10.1136/thoraxjnl-2017-210983.189.
Full textNita, Izabela, Cedric Vonarburg, Rolf Spirig, Sylvia Miescher, Thomas Geiser, and Amiq Gazdhar. "Alpha1-Antitrypsin reduces endoplasmic reticulum stress, inflammatory cytokines and improves wound repair in alveolar epithelial cells of fibrotic lung in vitro." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa3483.
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