Auswahl der wissenschaftlichen Literatur zum Thema „Pulmonary arterial hyperreactivity“
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Zeitschriftenartikel zum Thema "Pulmonary arterial hyperreactivity"
Cardouat, G., M. Douard, L. Roubenne, C. Bouchet, Z. Kmecová, P. Robillard, C. Guignabert et al. „NGF induces pulmonary arterial hyperreactivity through Connexin 43 increased expression“. Revue des Maladies Respiratoires 38, Nr. 6 (Juni 2021): 582. http://dx.doi.org/10.1016/j.rmr.2021.02.029.
Der volle Inhalt der QuelleCardouat, G., M. Douard, L. Roubenne, S. Kmecova, P. Robillard, C. Guignabert, L. Tu et al. „NGF induces pulmonary arterial hyperreactivity through Connexin 43 increased expression“. Archives of Cardiovascular Diseases Supplements 12, Nr. 2-4 (Oktober 2020): 213. http://dx.doi.org/10.1016/j.acvdsp.2020.03.036.
Der volle Inhalt der QuelleBouchet, Clement, Guillaume Cardouat, Matthieu Douard, Paul Robillard, Roger Marthan, Christelle Guibert und Véronique Freund-Michel. „Short-term mechanisms activated by NGF to induce pulmonary arterial hyperreactivity“. Archives of Cardiovascular Diseases Supplements 14, Nr. 2 (Juni 2022): 157–58. http://dx.doi.org/10.1016/j.acvdsp.2022.04.147.
Der volle Inhalt der QuelleBouchet, C., G. Cardouart, M. Douard, Z. Kmecova, P. Robillard, F. Delcambre, R. Marthan, P. Berger, C. Guibert und V. Freund-Michel. „Short-term mechanisms activated by NGF to induce pulmonary arterial hyperreactivity“. Revue des Maladies Respiratoires 40, Nr. 2 (Februar 2023): 129. http://dx.doi.org/10.1016/j.rmr.2022.11.041.
Der volle Inhalt der QuelleHinton, M., L. Mellow, A. J. Halayko, A. Gutsol und S. Dakshinamurti. „Hypoxia induces hypersensitivity and hyperreactivity to thromboxane receptor agonist in neonatal pulmonary arterial myocytes“. American Journal of Physiology-Lung Cellular and Molecular Physiology 290, Nr. 2 (Februar 2006): L375—L384. http://dx.doi.org/10.1152/ajplung.00307.2005.
Der volle Inhalt der QuellePeták, Ferenc, Tibor Z. Janosi, Carole Myers, Fabienne Fontao und Walid Habre. „Impact of elevated pulmonary blood flow and capillary pressure on lung responsiveness“. Journal of Applied Physiology 107, Nr. 3 (September 2009): 780–86. http://dx.doi.org/10.1152/japplphysiol.00157.2009.
Der volle Inhalt der QuelleSmith, Kelly J., George B. Mallory, Steven H. Abman und Dunbar D. Ivy. „AIRWAY HYPERREACTIVITY AFTER ILOPROST INHALATION IN PEDIATRIC PATIENTS WITH PULMONARY ARTERIAL HYPERTENSION“. Chest 130, Nr. 4 (Oktober 2006): 156S. http://dx.doi.org/10.1378/chest.130.4_meetingabstracts.156s-b.
Der volle Inhalt der QuelleMichel, R. P., und T. S. Hakim. „Increased resistance in postobstructive pulmonary vasculopathy: structure-function relationships“. Journal of Applied Physiology 71, Nr. 2 (01.08.1991): 601–10. http://dx.doi.org/10.1152/jappl.1991.71.2.601.
Der volle Inhalt der QuelleAzamar-Solis, Brizeida, Yahveth Cantero-Fortiz, Juan Carlos Olivares-Gazca, Jesús Mauricio Olivares-Gazca, Gisela Berenice Gómez-Cruz, Iván Murrieta-Álvarez, Guillermo J. Ruiz-Delgado und Guillermo J. Ruiz-Argüelles. „Primary Thrombophilia in Mexico XIII: Localization of the Thrombotic Events in Mexican Mestizos With the Sticky Platelet Syndrome“. Clinical and Applied Thrombosis/Hemostasis 25 (01.01.2019): 107602961984170. http://dx.doi.org/10.1177/1076029619841700.
Der volle Inhalt der QuelleOhar, Jill A., Kemberly S. Waller und Thomas E. Dahms. „Platelet-activating Factor Induces Selective Pulmonary Arterial Hyperreactivity in Isolated Perfused Rabbit Lungs“. American Review of Respiratory Disease 148, Nr. 1 (Juli 1993): 158–63. http://dx.doi.org/10.1164/ajrccm/148.1.158.
Der volle Inhalt der QuelleDissertationen zum Thema "Pulmonary arterial hyperreactivity"
Bouchet, Clement. „Expression et rôle du facteur de croissance des nerfs NGF dans l’hypertension pulmonaire“. Electronic Thesis or Diss., Bordeaux, 2024. http://www.theses.fr/2024BORD0092.
Der volle Inhalt der QuellePulmonary hypertension (PH) is a severe disease characterized by an increase in mean pulmonary arterial pressure over 20mmHg at rest, compared with 14mmHg in healthy individuals. Ultimately, PH leads to right heart failure and death. In the absence of any curative treatment, identification of new therapeutic targets is a major challenge. In this context, a better understanding of PH development and progression is crucial. In our laboratory, one target of interest is the nerve growth factor or NGF, overexpressed in pulmonary arteries both in experimental and human PH, and playing a significant role in three major PH features: pulmonary arterial inflammation, reactivity and remodeling.First, we focused on possible mechanisms activated in PH that may contribute to NGF pulmonary arterial increased expression. We showed that pro-inflammatory cytokines whose expression are increased in PH, such as interleukin-1β (IL-1β) or Tumor necrosis factor-α, as well as oxidative stress can increase NGF expression and secretion by pulmonary arterial endothelial cells - EC- or smooth muscle cells -CML-. We showed that this secretion involved Transforming growth factor β1, which is secreted by both ECs and SMCs, and then acts in an autocrine manner on these cells to stimulate NGF secretion.We then studied the role of NGF in two major PH features: pulmonary arterial hyperreactivity and inflammation.Regarding hyperreactivity first, we showed that a chronic treatment with NGF (24h) led to pulmonary arterial hyperreactivity, by enhancing activity of connexin-43-dependent gap junctions in SMCs. In parallel, we showed that a shorter treatment with NGF (1h) also led to led to pulmonary arterial hyperreactivity, but in a connexin-43-independent manner, with deregulation of intracellular calcium signaling and increased sensitization of the contractile apparatus in SMCs.Regarding the link between NGF and inflammation, our results showed that in vivo, in a rat model of PH, a preventive treatment with anti-NGF blocking antibodies reduced pulmonary arterial monocyte/macrophage infiltration and inflammasome protein expression as well as both circulating and pulmonary levels of IL-1β. In vitro, we showed that NGF is able to attract monocytes, and that IL-1β plays an important role in pulmonary arterial remodeling, inflammation and endothelial dysfunction.In conclusion, this work has highlighted mechanisms contributing to NGF increased expression in PH and confirmed its involvement in the progression of the disease. The overall results obtained further support NGF as a therapeutic target of interest in this disease
Konferenzberichte zum Thema "Pulmonary arterial hyperreactivity"
Cardouat, guillaume, Matthieu Douard, Lukas Roubenne, Zuzana Kmecová, Paul Robillard, Christophe Guignabert, Ly Tu et al. „NGF induces pulmonary arterial hyperreactivity through connexin 43 increased expression“. In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.3565.
Der volle Inhalt der QuelleBOUCHET, Clement, Guillaume Cardouat, Matthieu Douart, Paul Robillard, Roger Marthan, Bernard Muller, Christelle Guibert und Veronique Freund-Michel. „Short-term mechanisms activated by NGF to induce pulmonary arterial hyperreactivity“. In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa585.
Der volle Inhalt der QuelleSikarwar, Anurag S., K. T. Santhosh und Shyamala Dakshinamurti. „Inhibition Of Palmitoylation Normalizes Hyperreactivity Of The Pulmonary Arterial Thromboxane Receptor In Hypoxic Pulmonary Hypertension“. In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5034.
Der volle Inhalt der QuelleDouard, Matthieu, Paul Robillard, Juliette Deweirdt, Isabelle Baudrimont, Mathilde Dubois, Roger Marthan, Jean-Pierre Savineau, Bernard Muller, Christelle Guibert und Veronique Freund-Michel. „Late Breaking Abstract - NGF induces pulmonary arterial hyperreactivity through increased connexin-43 expression: potential role in pulmonary hypertension“. In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.oa3274.
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