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Auswahl der wissenschaftlichen Literatur zum Thema „Lungs Pathophysiology“
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Zeitschriftenartikel zum Thema "Lungs Pathophysiology"
Bland, Richard D. „Pathophysiology of Neonatal Lung Injury“. International Journal of Technology Assessment in Health Care 7, S1 (Januar 1991): 56–60. http://dx.doi.org/10.1017/s0266462300012514.
Der volle Inhalt der QuelleSundar, Isaac K., Hongwei Yao, Michael T. Sellix und Irfan Rahman. „Circadian molecular clock in lung pathophysiology“. American Journal of Physiology-Lung Cellular and Molecular Physiology 309, Nr. 10 (15.11.2015): L1056—L1075. http://dx.doi.org/10.1152/ajplung.00152.2015.
Der volle Inhalt der Quellevan Zanden, Judith E., Henri G. D. Leuvenink, Erik A. M. Verschuuren, Michiel E. Erasmus und Maximilia C. Hottenrott. „A translational rat model for ex vivo lung perfusion of pre-injured lungs after brain death“. PLOS ONE 16, Nr. 12 (02.12.2021): e0260705. http://dx.doi.org/10.1371/journal.pone.0260705.
Der volle Inhalt der QuelleLevvey, Bronwyn, Kovi Levin, Miranda Paraskeva, Glen Westall und Gregory Snell. „Donation after Brain Death versus Donation after Circulatory Death: Lung Donor Management Issues“. Seminars in Respiratory and Critical Care Medicine 39, Nr. 02 (26.03.2018): 138–47. http://dx.doi.org/10.1055/s-0037-1615820.
Der volle Inhalt der QuelleNaramala, Srikanth, Sharmi Biswas, Sreedhar Adapa, Vijay Gayam, Romeo C. Castillo, Srinadh Annangi und Venu Madhav Konala. „Pleomorphic Pulmonary Manifestations of IgG4-Related Disease“. Case Reports in Rheumatology 2019 (20.08.2019): 1–4. http://dx.doi.org/10.1155/2019/7572869.
Der volle Inhalt der QuelleAgraval, Hina, und Hong Wei Chu. „Lung Organoids in Smoking Research: Current Advances and Future Promises“. Biomolecules 12, Nr. 10 (12.10.2022): 1463. http://dx.doi.org/10.3390/biom12101463.
Der volle Inhalt der QuelleDas, Mita, W. Michael Zawada, James West und Kurt R. Stenmark. „JNK2 regulates vascular remodeling in pulmonary hypertension“. Pulmonary Circulation 8, Nr. 3 (02.05.2018): 204589401877815. http://dx.doi.org/10.1177/2045894018778156.
Der volle Inhalt der QuelleFrétaud, Maxence, Delphyne Descamps, Daphné Laubreton, Marie-Anne Rameix-Welti, Jean-François Eléouët, Thibaut Larcher, Marie Galloux und Christelle Langevin. „New Look at RSV Infection: Tissue Clearing and 3D Imaging of the Entire Mouse Lung at Cellular Resolution“. Viruses 13, Nr. 2 (28.01.2021): 201. http://dx.doi.org/10.3390/v13020201.
Der volle Inhalt der QuelleRaredon, Micha Sam Brickman, Taylor Sterling Adams, Yasir Suhail, Jonas Christian Schupp, Sergio Poli, Nir Neumark, Katherine L. Leiby et al. „Single-cell connectomic analysis of adult mammalian lungs“. Science Advances 5, Nr. 12 (Dezember 2019): eaaw3851. http://dx.doi.org/10.1126/sciadv.aaw3851.
Der volle Inhalt der QuelleMeyerowitz, Glen, und Igor Barjaktarevic. „369 The impact of asymmetric lung injury on gas and pressures distribution in a mechanical ventilation model with implementation of compartmentalized inspiratory hold“. Journal of Clinical and Translational Science 6, s1 (April 2022): 69. http://dx.doi.org/10.1017/cts.2022.209.
Der volle Inhalt der QuelleDissertationen zum Thema "Lungs Pathophysiology"
McLennan, Geoffrey. „Oxygen toxicity and radiation injury to the pulmonary system“. Title page, index and forward only, 1997. http://web4.library.adelaide.edu.au/theses/09PH/09phm164.pdf.
Der volle Inhalt der QuelleMcNamara, Tracy Renee. „Chlamydia pneumoniae and airways inflammation : an investigation of the host cell-pathogen relationship /“. Title page, table of contents and abstract only, 2004. http://web4.library.adelaide.edu.au/theses/09PH/09phm4791.pdf.
Der volle Inhalt der QuelleChan, Ching Eunice, und 陳清. „Pathogenetic role of aberrant promoter methylation in lung cancer“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39557819.
Der volle Inhalt der QuelleSmedley, Jeremy Vance. „A Combined In Vivo and In Vitro Approach to the Study of Endotoxemia in Swine“. Thesis, Virginia Tech, 2000. http://hdl.handle.net/10919/33947.
Der volle Inhalt der QuelleMaster of Science
Kerckx, Yannick. „Modeling nitric oxide production and transport in the human lung“. Doctoral thesis, Universite Libre de Bruxelles, 2009. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210324.
Der volle Inhalt der Quelle\
Doctorat en sciences, Spécialisation physique
info:eu-repo/semantics/nonPublished
Bondue, Benjamin. „Role of chemerin and its receptor ChemR23 in the physiopathology of inflammatory lung diseases“. Doctoral thesis, Universite Libre de Bruxelles, 2010. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209992.
Der volle Inhalt der QuelleAccording to these elements, and to the role of neutrophils in the physiopathology of many inflammatory lung diseases and in the generation of active chemerin, we began in 2007 to study the role of chemerin and its receptor ChemR23 in inflammatory lung diseases. We first characterized the mouse chemerin/ChemR23 system, and described that this system was very similar to the human one, in terms of distribution, pharmacology and functional properties. We then used wild type mice (WT) and mice invalidated for the receptor (ChemR23-/-) in various models of inflammatory lung diseases, including asthma, lung fibrosis, viral pneumonia, and acute lung injury.
Whereas the asthma and lung fibrosis models did not allow to demonstrate a significant role of the chemerin/ChemR23 system (possibly as a result of the lack of production of active chemerin in these models), infection by either the Pneumonia Virus of Mice (PVM), the mouse counterpart of human RSV, or by a murinized H1N1 influenza strain resulted in a significantly higher mortality rate in ChemR23-/- mice as compared to their WT counterparts. Using the PVM-induced pneumonia model, we observed that the excessive mortality of knock-out mice is caused by an inadequate and excessive innate immune response characterized by a massive recruitment of neutrophils to the lungs, associated with a delayed viral clearance and lower type I IFN synthesis. This latter observation suggested an impairment of pDC recruitment, according to the important contribution of pDCs to the production of type I IFNs in viral diseases, and the role of chemerin in the recruitment of these cells. We indeed confirmed a lower recruitment of pDCs in the lung of infected ChemR23-/- mice, as compared to WT mice. However, experiments of adoptive transfert and depletion of pDCs failed to proof a link between impaired pDC recruitment and the excessive morbidity and mortality observed in ChemR23-invalidated mice.
In parallel, we studied the role of the chemerin/ChemR23 system in the control of innate immune responses, by using a model of acute lung injury caused by the intra-tracheal instillation of bacterial lipopolysaccharide (LPS). In this model, administration of recombinant chemerin together with LPS in WT mice resulted in a significant (about 50%) reduction of neutrophil recruitment to both lung parenchyma and airways. Assessment of pro-inflammatory cytokines and chemokines in broncho-alveolar lavage fluids confirmed this anti-inflammatory effect of chemerin, which was ChemR23-dependent, as the inflammatory response of ChemR23-/- mice was unaffected by chemerin. In our hands, chemerin does not modulate macrophage functions, in contrast to data recently published by other groups, attributing anti-inflammatory effects of chemerin or chemerin-derived peptide to the modulation of macrophage activation and phagocytosis. Other hypotheses that could take our observations into account are presently investigated, including an immunomodulatory role of chemerin on lung epithelial or endothelial cells, and/or the ChemR23-dependent recruitment of subtypes of macrophages or other myeloid cells endowed with immunosuppressive properties.
In conclusion, our studies characterized the mouse chemerin/ChemR23 system and highlighted the role of this system in the physiopathology of some inflammatory lung diseases. Our results suggest that the chemerin/ChemR23 system might be considered as a potential therapeutic target for the development of future anti-infectious and anti-inflammatory therapies, particularly for viral pneumonia, which represent a major public health problem, as well as for acute respiratory distress syndrome (ARDS) following severe acute lung injuries.
Les agents chimioattractants jouent un rôle fondamental dans l’initiation des réponses immunes en régulant le trafic et la fonction des populations leucocytaires. Leurs récepteurs constituent dès lors des cibles d’intérêt pour le développement de traitements contre les maladies inflammatoires et le cancer. Le laboratoire d’accueil a identifié le récepteur ChemR23, exprimé à la surface des cellules dendritiques myéloïdes (mDCs) et plasmacytoïdes (pDCs) immatures, des macrophages, des cellules NK, des adipocytes, et des cellules endothéliales. Le ligand endogène du récepteur ChemR23, la chémérine, est présent en abondance dans divers échantillons pathologiques d’origine inflammatoire. La chémérine est produite sous la forme d'un précurseur inactif, la prochémérine, qui nécessite pour devenir active le clivage protéolytique de six ou sept acides aminés à son extrémité carboxy-terminale. La chémérine induit le chimiotactisme des macrophages et des DCs immatures, et en particulier des pDCs immatures en accord avec l’expression plus importante de ChemR23 par les pDCs. Les pDCs jouent un rôle immunorégulateur important en pathologie pulmonaire, en particulier dans la physiopathologie des pneumonies virales, par leur capacité à produire d’importantes quantités d’interféron (IFN) de type I.
Compte tenu de ces éléments et du rôle des polynucléaires neutrophiles dans de nombreuses pathologies pulmonaires, ainsi que dans la génération de chémérine active à partir de son précurseur, nous avons débuté en octobre 2007, l’étude du rôle de la chémérine et de son récepteur ChemR23 dans le contrôle des pathologies pulmonaires inflammatoires. Nous avons tout d’abord caractérisé le système chémérine/ChemR23 chez la souris et avons montré que ce système présentait des caractéristiques similaires à celles décrites chez l’homme, en termes de distribution, de pharmacologie et de propriétés fonctionnelles.
Ensuite, nous avons comparé des souris sauvages et invalidées pour le récepteur ChemR23 (ChemR23-/-) dans divers modèles de pathologies pulmonaires. Les modèles d’asthme et de fibrose pulmonaire induite par instillation de bléomycine ou de silice n’ont pas permis de mettre en évidence un rôle important du couple chémérine/ChemR23, peut-être en raison de l’absence de génération de forme active de chémérine dans ces modèles. En revanche, l’administration de deux agents viraux différents, le PVM (Pneumonia Virus of Mice), l’équivalent murin du RSV humain, et un virus de l’influenza H1N1 murinisé, a résulté en un taux de mortalité 40% plus élevé pour les souris ChemR23-/- par rapport à leurs homologues sauvages. En utilisant le modèle de pneumonie induite par le PVM, nous avons montré que cette différence de mortalité est causée par une réponse immune inappropriée et excessive, associée à une réduction de l’élimination du virus, ainsi qu’à un déficit de synthèse d’IFN de type I. Les pDCs, dans un contexte d’infection virale, sont capables de synthétiser d’importantes quantités d’IFN de type I, et nous avons mis en évidence un déficit relatif de recrutement en pDCs chez les souris ChemR23-/- infectées. Néanmoins, les expériences de transfert adoptif et de déplétion de pDCs n’ont pas permis de lier ce défaut de recrutement à l’excès de morbidité et de mortalité observé chez les souris ChemR23-/- infectées.
En parallèle, le rôle de ce couple ligand-récepteur dans le contrôle des réponses immunitaires innées a été étudié dans un modèle de pneumopathie aiguë induite par instillation intra-trachéale de lipopolysaccharide (LPS). Dans ce modèle, l’administration simultanée de chémérine recombinante avec le LPS entraîne chez les souris sauvages une diminution significative (environ 50%) du nombre de polynucléaires neutrophiles recrutés dans les voies aériennes et dans le parenchyme pulmonaire, ainsi qu’une importante diminution de synthèse de cytokines pro-inflammatoires. Cet effet anti-inflammatoire de la chémérine est dépendant de ChemR23, et ne semble pas être secondaire à un effet de la chémérine sur l’activation des macrophages, contrairement à certaines données publiées récemment par d’autres groupes. D’autres hypothèses permettraient cependant de prendre en compte ces observations, notamment un effet de la chémérine sur les cellules épithéliales et/ou endothéliales pulmonaires, ainsi que sur le recrutement de sous-populations de macrophages ou d’autres cellules myéloïdes possédant des propriétés immunosuppressives. Des expériences complémentaires ont été initiées afin de tester ces hypothèses.
En conclusion, après avoir caractérisé le système chémérine/ChemR23 chez la souris, nos études ont permis de mettre en évidence le rôle de ce couple ligand/récepteur dans la physiopathologie de certaines pneumopathies inflammatoires, ouvrant ainsi de nouvelles perspectives thérapeutiques, en particulier pour le traitement des pneumopathies virales, qui constituent un problème de santé publique majeur, ainsi que des syndromes de détresse respiratoire aiguë (ARDS).
Doctorat en Sciences médicales
info:eu-repo/semantics/nonPublished
Vanderstocken, Gilles. „Caractérisation du rôle des nucléotides extracellulaires et du récepteur purinergique P2Y2 dans la physiopathologie des maladies pulmonaires inflammatoires“. Doctoral thesis, Universite Libre de Bruxelles, 2012. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209591.
Der volle Inhalt der Quellehealth problem. As a consequence, investigating the immune mechanisms that contribute to
the pathogenesis of these diseases is essential to identify candidate targets for the
development of new therapeutic drugs. Furthermore, over the past 20 years, the growing awareness
that purinergic signalling events shape the immune and inflammatory responses to infection and
allergic reactions warranted the development of animal models to assess their importance in vivo in
acute lung injury and chronic airway diseases. The field of purinergic inflammation formulated the
unifying concept that ATP is released as a «danger signal» to induce inflammatory responses upon
binding purinergic receptors.
According to these elements, we began in 2007 to evaluate lung inflammation in mice deficient for
the P2Y2 purinergic receptor in TH2 and TH1 models. The most convincing evidence that the P2Y2
receptor is engaged during alarm situations comes from studies related to cystic fibrosis and asthma.
Indeed, chronic respiratory diseases are commonly associated with elevated airway ATP
concentrations, as reported in cystic fibrosis, but also in idiopathic pulmonary fibrosis and chronic
obstructive pulmonary disease (COPD) patients, and they are raised by allergens in asthmatic
patients.
First, we demonstrated a significant role of the P2Y2R in a TH2-ovalbumin(OVA)-induced asthma
model. We observed that eosinophil accumulation, a distinctive feature of lung allergic inflammation,
was defective in OVA-treated P2Y2-deficient mice compared with OVA-treated wild type animals.
Interestingly, the upregulation of VCAM-1 was lower on lung endothelial cells of OVA-treated P2Y2
knockout mice compared with OVA-treated wild type animals. Adhesion assays demonstrated that
the action of UTP on leukocyte adhesion through the regulation of endothelial VCAM-1 was
abolished in P2Y2-deficient lung endothelial cells. Additionally, the level of soluble VCAM-1, reported
as an inducer of eosinophil chemotaxis, was strongly reduced in the bronchoalveolar lavage fluid of
P2Y2-deficient mice.
Secondly, we studied the consequences of P2Y2R loss in lung inflammation initiated after pneumonia
virus of mice (PVM) infection in collaboration with the group of Pr. Daniel Desmecht (ULg). We
demonstrated here that P2Y2
-/-
mice display a severe increase in morbidity and mortality rate in
response to PVM. Lower survival of P2Y2
-/-
mice was not correlated with excessive inflammation
despite the higher level of neutrophil recruiters in their broncho-alveolar fluids. Interestingly, we
observed lower numbers of dendritic cells, CD4
+
T cells and CD8
+
T cells in P2Y2
-/-
mice compared to
P2Y2
+/+
infected lungs. Lower level of IL-12 and higher level of IL-6 in broncho-alveolar fluid support
an inhibition of Th1 response in P2Y2
-/-
mice. Quantification of DC recruiter expression revealed
comparable IP-10 and MIP-3&
Doctorat en Sciences biomédicales et pharmaceutiques
info:eu-repo/semantics/nonPublished
Wang, Jianpu. „Pathophysiology and treatment of chlorine gas-induced lung injury : an experimental study in pigs /“. Linköping : Univ, 2004. http://www.bibl.liu.se/liupubl/disp/disp2004/med877s.pdf.
Der volle Inhalt der QuelleTiev, Kiet Phong. „Rôle du monoxyde d'azote dans la physiopathologie des atteintes pulmonaires de la sclérodermie systémique“. Thesis, Paris Est, 2008. http://www.theses.fr/2008PEST0081.
Der volle Inhalt der QuelleInterstitial lung disease (ILD) has become the main cause of death in systemic sclerosis (SSc). In ILD, immune activation leads to strong nitric oxide (NO) output by inducible NO synthase. Increased the whole fractional rate of NO in exhaled air has been reported in SSc patients with ILD and suggested that exhaled NO can be an accurate none-invasive marker of early alveolar inflammation in order to initiate in time treatment. The two compartment-model method partitioned exhaled NO into alveolar concentration (CANO) and conducting airway flux, We hypothesized that overproduction of NO in the lung eventually leads to ILD in SSc. We have found that CANO is significantly increased in SSc patients as compared with healthy controls. We have also demonstrated that high levels of CANO were related to alveolitis and the severity of ILD in SSc. Moreover, we have found that ILD could be ruled in (positive predictive value > 95%) when CANO = 10.8 ppb, and ruled out when CANO values = 3.8 ppb (negative predictive value > 95%). The two-compartment model neglected the trumpet shape of airway tree and the axial diffusion of NO that the advanced “trumpet model” takes account. We have found that CANO levels assessed by the two models were comparable (rho=0,98, p<0.001). Finally, we have found that the serum ability to induce lung fibroblast proliferation and myofibroblast transition was increased in SSc patients with high levels of CANO (>5ppb) as compared to SSc patients with low levels of CANO (=5ppb) and healthy controls. Our findings suggest a possible link between alveolar inflammation, and lung fibrosis in SSc. 1624 caractères avec espace
Ridings, Philip Charles. „An investigation into the role of selectins in the pathophysiology of sepsis and sepsis-induced acute lung injury“. Thesis, University of Southampton, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266390.
Der volle Inhalt der QuelleBücher zum Thema "Lungs Pathophysiology"
Pulmonary pathophysiology: A clinical approach. 3. Aufl. New York: McGraw-Hill Medical, 2010.
Den vollen Inhalt der Quelle findenPulmonary pathophysiology. Philadelphia: Lippincott, 1995.
Den vollen Inhalt der Quelle findenG, Crystal Ronald, und West John B, Hrsg. The Lung: Scientific foundations. New York: Raven Press, 1991.
Den vollen Inhalt der Quelle findenWest, John B. (John Burnard), Hrsg. Pulmonary pathophysiology: The essentials. 8. Aufl. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins Health, 2012.
Den vollen Inhalt der Quelle findenPulmonary pathophysiology: The essentials. 3. Aufl. Baltimore: Williams & Wilkins, 1987.
Den vollen Inhalt der Quelle findenPulmonary pathophysiology: The essentials. 7. Aufl. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins, 2008.
Den vollen Inhalt der Quelle findenB, West John, Hrsg. Pulmonary pathophysiology--the essentials. 5. Aufl. Baltimore, Md: Williams & Wilkins, 1998.
Den vollen Inhalt der Quelle findenB, West John, Hrsg. Pulmonary pathophysiology--the essentials. 4. Aufl. Baltimore: Williams & Wilkins, 1992.
Den vollen Inhalt der Quelle findenAdvances in surgical pathology: Lung cancer. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins, 2011.
Den vollen Inhalt der Quelle findenAnalytical lung pathology. Berlin: Springer-Verlag, 1992.
Den vollen Inhalt der Quelle findenBuchteile zum Thema "Lungs Pathophysiology"
Christian, Couture. „Lung cancer“. In Applied Respiratory Pathophysiology, 207–22. Boca Raton : CRC Press, [2017]: CRC Press, 2017. http://dx.doi.org/10.1201/9781315177052-11.
Der volle Inhalt der QuelleGeneviève, Dion, Cormier Yvon und Boulet Louis-Philippe. „Interstitial lung diseases“. In Applied Respiratory Pathophysiology, 177–205. Boca Raton : CRC Press, [2017]: CRC Press, 2017. http://dx.doi.org/10.1201/9781315177052-10.
Der volle Inhalt der QuelleHenske, Elizabeth P., Souheil El-Chemaly, Thomas N. Darling, Angelo M. Taveira-DaSilva und Joel Moss. „Pathophysiology of Lymphangioleiomyomatosis“. In Diffuse Cystic Lung Diseases, 101–20. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-63365-3_5.
Der volle Inhalt der QuelleFinsterer, U., und K. Peter. „Pathophysiologie thoraxchirurgischer Eingriffe“. In Lunge und Mediastinum, 107–15. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-662-08433-5_11.
Der volle Inhalt der QuelleKroegel, C., M. Mohorn und P. R. Grahmann. „Pathophysiologie der Lunge“. In Springer Lehrbuch, 201–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-57115-2_14.
Der volle Inhalt der QuelleWard, Chris, Rhys Jones, Mellissa Friel, Eoin Hunt und Des Murphy. „Pathophysiology in the Lung“. In Reflux Aspiration and Lung Disease, 55–69. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-90525-9_5.
Der volle Inhalt der QuelleCouture, Christian. „Embryology, anatomy, and histology of the lung“. In Applied Respiratory Pathophysiology, 1–14. Boca Raton : CRC Press, [2017]: CRC Press, 2017. http://dx.doi.org/10.1201/9781315177052-1.
Der volle Inhalt der QuelleBhat, Javeed Ahmad, Nawab John Dar und Wajid Waheed Bhat. „Asthma: Pathophysiology, Current Status, and Therapeutics“. In Chronic Lung Diseases, 25–60. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-3734-9_2.
Der volle Inhalt der QuelleGrossi, Adalberto, und PierPaolo Giomarelli. „Pathophysiology of adult RDS“. In The Surfactant System of the Lung, 183–90. London: Macmillan Education UK, 1991. http://dx.doi.org/10.1007/978-1-349-12553-1_30.
Der volle Inhalt der QuelleJohnston, Nikki. „The Pathophysiology of Gastroesophageal Reflux“. In Gastroesophageal Reflux and the Lung, 23–41. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5502-8_2.
Der volle Inhalt der QuelleKonferenzberichte zum Thema "Lungs Pathophysiology"
Jagani, Jakin, und Alexandrina Untaroiu. „A Study of TCPC-Stent Conjunction for Cavopulmonary Assist in Fontan Patients With Right Ventricular Dysfunction“. In ASME 2016 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2016. http://dx.doi.org/10.1115/imece2016-68760.
Der volle Inhalt der QuelleRomem, Ayal, Karen Lammers, Aldo T. Iacono, Mohan E. Tulapurkar, Cinthia Dranchenberg, Jeffrey D. Hasday und Alessio Fasano. „Zonulin - A Novel Player In Human Lung Pathophysiology“. In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a4266.
Der volle Inhalt der QuelleBruno, Nicoletta, Aran Singanayagam, Hugo A. Farne, Julia Aniscenko, Nicholas Glanville, Chloe J. Pyle, Dhiren F. Patel, Sebastian L. Johnston und Robert J. Snelgrove. „G-CSF drives pathophysiology of RV-induced allergic asthma exacerbations by potentiating neutrophilic inflammation and ILC2 function“. In ERS Lung Science Conference 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/23120541.lsc-2022.191.
Der volle Inhalt der QuelleTorday, John S. „Evolutionary Biology As A Cipher For Lung Physiology And Pathophysiology“. In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6416.
Der volle Inhalt der QuelleSaha, P., S. Jain, I. Mukherjee, S. Durugkar, M. Das, S. Gokhale, S. S. Sohal, V. Naidu und P. Sharma. „Effect of Long-Term Particulate Matter (PM10) Exposure on Lung Pathophysiology in Mice“. In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2887.
Der volle Inhalt der QuelleVega-Sanchez, Angel Emmanuel, Espiridión Ramos-Martínez, Ivette Buendía-Roldan, Gloría Pérez-Rubio, Ramcés Falfán-Valencia, Mayra Mejía und Jorge Rojas-Serrano. „Role of the inflammasome in the pathophysiology of antisynthetase-associated interstitial lung disease“. In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa2377.
Der volle Inhalt der QuelleBasu, S., und A. J. Halayko. „IGFBP3 Modulates Lung Pathophysiology in an Allergen -Specific Manner in Murine Models of Asthma“. In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a5609.
Der volle Inhalt der QuelleHe, M., J. MacLeod, S. J. Callahan, K. Qing, N. Tustison, M. Salerno, J. Mata et al. „Assessment of Pulmonary Pathophysiology in Lung Transplant Recipients With and Without Chronic Lung Allograft Dysfunction Using Hyperpolarized Helium-3 MRI“. In American Thoracic Society 2021 International Conference, May 14-19, 2021 - San Diego, CA. American Thoracic Society, 2021. http://dx.doi.org/10.1164/ajrccm-conference.2021.203.1_meetingabstracts.a4604.
Der volle Inhalt der QuelleTan, Yan, und Wei Tan. „Reducing Upstream Compliance Induces Downstream High Pulsatility Flow-Dependent Inflammatory Response in Pulmonary Endothelial Cells via TLR2/NF-KB Pathway“. In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80900.
Der volle Inhalt der QuelleSandler, H., B. Gerdin und T. Saldeen. „STUDIES ON THE ROLE OF THROMBOXANE IN THROMBIN-INDUCED PULMONARY INSUFFICIENCY IN THE RAT“. In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643379.
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