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Littérature scientifique sur le sujet « Pulmonary Pathophysiology »

Auteur : Grafiati

Publié le 4 juin 2021

Mis à jour le 19 février 2022

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Articles de revues sur le sujet "Pulmonary Pathophysiology"

Cherniack, Neil S. "Pulmonary Pathophysiology." Annals of Internal Medicine 131, no. 5 (September 7, 1999): 399. http://dx.doi.org/10.7326/0003-4819-131-5-199909070-00022.

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Gonzalez, Norberto C. "PULMONARY PATHOPHYSIOLOGY." Shock 11, no. 2 (February 1999): 152. http://dx.doi.org/10.1097/00024382-199902000-00018.

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Grippi, Michael A. "PULMONARY PATHOPHYSIOLOGY." Shock 5, no. 4 (April 1996): 311. http://dx.doi.org/10.1097/00024382-199604000-00013.

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Chamarthy, Murthy R., Asha Kandathil, and Sanjeeva P. Kalva. "Pulmonary vascular pathophysiology." Cardiovascular Diagnosis and Therapy 8, no. 3 (June 2018): 208–13. http://dx.doi.org/10.21037/cdt.2018.01.08.

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Gao, Yuansheng, and J. Usha Raj. "Pathophysiology of Pulmonary Hypertension." Colloquium Series on Integrated Systems Physiology: From Molecule to Function 9, no. 6 (November 22, 2017): i—104. http://dx.doi.org/10.4199/c00158ed1v01y201710isp078.

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Angerio, Allan D., and Peter A. Kot. "Pathophysiology of pulmonary edema." Critical Care Nursing Quarterly 17, no. 3 (November 1994): 21–26. http://dx.doi.org/10.1097/00002727-199411000-00004.

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Higenbottam, Tim. "Pathophysiology of Pulmonary Hypertension." Chest 105, no. 2 (February 1994): 7S—12S. http://dx.doi.org/10.1378/chest.105.2_supplement.7s.

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Klayton, Ronald J. "PULMONARY PATHOPHYSIOLOGY — THE ESSENTIALS." Military Medicine 158, no. 2 (February 1, 1993): A9. http://dx.doi.org/10.1093/milmed/158.2.a9a.

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Shibuya, Kazutoshi, Chikako Hasegawa, Shigeharu Hamatani, Tsutomu Hatori, Tadashi Nagayama, Hiroko Nonaka, Tsunehiro Ando, and Megumi Wakayama. "Pathophysiology of pulmonary aspergillosis." Journal of Infection and Chemotherapy 10, no. 3 (2004): 138–45. http://dx.doi.org/10.1007/s10156-004-0315-5.

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Matthay, Michael A. "Pathophysiology of Pulmonary Edema." Clinics in Chest Medicine 6, no. 3 (September 1985): 301–14. http://dx.doi.org/10.1016/s0272-5231(21)00366-x.

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Thèses sur le sujet "Pulmonary Pathophysiology"

Walsh, Robert Leo. "Leukocyte elastase and anti-elastases in pulmonary emphysema." Title page, contents and abstract only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09phw2261.pdf.

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Includes bibliographical references (leaves 218-249) The preferred theory to explain the aetiology of emphysema points to an imbalance in the protease-antiprotease systems within the lung with human leukocyte elastase and [alpha]1-protease inhibiter being the main candidates. Examines some aspects of this theory.

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Muzaffar, Saima. "Reactive oxygen species and the pathophysiology of adult respiratory distress syndrome." Thesis, University of Bristol, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271916.

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Tauriainen, M. Peter. "Negative pressure pulmonary edema, a clinical review and study of its pathophysiology." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq23521.pdf.

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Otsuka, Kojiro. "Sputum YKL-40 Levels and Pathophysiology of Asthma and Chronic Obstructive Pulmonary Disease." Kyoto University, 2012. http://hdl.handle.net/2433/152498.

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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.

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Bibliography: leaves 168-184. The work in this study encompasses oxygen free radical related inflammation in the peripheral lung and in lung cells. Animal and human studies have been used. Methods include cell culture with function studies, protein chemistry, animal and human physiology, and cell and lung structure through histopathology, and various forms of electron microscopy. The work resulting from this thesis has formed an important basis for understanding acute and chronic lung injury.

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Mittal, Manish [Verfasser]. "Role of NADPH oxidases and KDR channels in the pathophysiology of hypoxia induced pulmonary hypertension / Manish Mittal." Gießen : Universitätsbibliothek, 2009. http://d-nb.info/1060563207/34.

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Mason, Nicholas. "Mechanisms of altitude-related cough." Doctoral thesis, Universite Libre de Bruxelles, 2012. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209711.

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The original work presented in this thesis investigates some of the mechanisms that may be responsible for the aetiology of altitude-related cough. Particular attention is paid to its relationship to the long recognised, but poorly understood, changes in lung volumes that occur on ascent to altitude. The literature relevant to this thesis is reviewed in Chapter 1.Widespread reports have long existed of a debilitating cough affecting visitors to high altitude that can incapacitate the sufferer and, on occasions, be severe enough to cause rib fractures (22, 34, 35). The prevalence of cough at altitude has been estimated to be between 22 and 42% at between 4200 and 4900 m in the Everest region of Nepal (10, 29). Traditionally the cough was attributed to the inspiration of the cold, dry air characteristic of the high altitude environment (37) but no attempts were made to confirm this aetiology. In the first formal study of cough at high altitude, nocturnal cough frequency was found to increase with increasing altitude during a trek to Everest Base Camp (5300 m) and massively so in 3 climbers on whom recordings were made up to 7000 m on Everest (8). After 9 days at 5300 m the citric acid cough threshold, a measure of the sensitivity of the cough reflex arc, was significantly reduced compared with both sea level and arrival at 5300 m.During Operation Everest II, a simulated climb of Mount Everest in a hypobaric chamber, the majority of the subjects were troubled above 7000 m by pain and dryness in the throat and an irritating cough despite the chamber being maintained at a relative humidity of between 72 and 82% and a temperature of 23ºC (18). This argued against the widely held view that altitude-related cough was due to the inspiration of cold, dry air. In the next major hypobaric chamber study, Operation Everest III, nocturnal cough frequency and citric acid cough threshold were measured on the 8 subjects in the study. The chamber temperature was maintained between 18 and 24ºC and relative humidity between 30 and 60% (24). This work is presented in Chapter 2 and, demonstrated an increase in nocturnal cough frequency with increasing altitude which immediately returned to control values on descent to sea level. Citric acid cough threshold was reduced at 8000 m compared to both sea level and 5000 m values. Changes in citric acid cough threshold at lower altitudes may not have been detected because of the constraints on subject numbers in the chamber. The study still however demonstrated an increase in clinical cough and a reduction in the citric acid cough threshold at extreme altitude, despite controlled environmental conditions, and thus refuted the long held belief that altitude-related cough is solely due to the inspiration of cold, dry air. If altitude-related cough is not simply due to the inspiration of cold, dry air, other possible aetiologies are:•\ Doctorat en Sciences médicales info:eu-repo/semantics/nonPublished

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Yoshioka, Eliane Muta. "Alterações pulmonares e sistêmicas em modelo de lesão pulmonar aguda de etiologia pulmonar e extra pulmonar após ventilação mecânica de curto prazo." Universidade de São Paulo, 2010. http://www.teses.usp.br/teses/disponiveis/5/5144/tde-03092010-144329/.

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A inflamação pulmonar pode variar de acordo com o sitio primário da injuria e poder ser afetado pelo estresse mecânico gerado pela ventilação mecânica. (VM) Objetivos: estudar as eventuais diferenças na reposta pulmonar e sistêmica na lesão pulmonar aguda pulmonar (LPA P ) e extra pulmonar (LPA Exp) após ventilação mecânica. Métodos: Camundongos BALB/c foram divididos em doze grupos. Os grupos controle pulmonar (CP) e extra pulmonar (C Exp) receberam solução salina (SAL) ou Lipopolissacarideo (LPS) via intratraqueal (IT) ou intraperitoneal (IP) respectivamente. Os grupos foram submetidos ou não a simples manobra de pressurização (SMP) até 45 cm H2O. Resultados: Os grupos LPAP e LPAExp não ventilados apresentaram o mesmo nível de inflamação; uma diferença estatisticamente significativa na densidade de células inflamatórias foi observada no grupo LPA P VM (3,84±1,28 cels/2) comparado ao grupo LPA Exp VM ((1,75±0,14 cels/2), p=0,013. O mesmo foi observado na LPA P SMP (2,92±0,44 cels/2) comparado ao LPA Exp SMP (1,46±0,23 cels/2), p<0,0001. LPAP mostrou estatisticamente significante aumento no El (56,19 ± 12,26 cm H2O) em comparação ao LPA Exp SMP (26,88 ± 36,38 cm H2O) após SMP (p = 0,029). Nenhuma diferença estatisticamente significante foi observada no estresse oxidativo no rim. Conclusão: Observamos um padrão diferente da resposta inflamatória e mecânica pulmonar comparando LPA pulmonar e extra-pulmonar submetido à ventilação mecânica de curto prazo. Embora a ventilação mecânica represente uma ferramenta essencial para estabilizar o paciente critico, é necessário individualizar a abordagem do tratamento ventilatório Lung inflammation may vary according to the primary site of injury and may be affected by the mechanical stress generated by mechanical ventilation (MV). Objectives: to address possible differences in lung and systemic responses in pulmonary and extra pulmonary ALI after mechanical ventilation. Methods: BALB/c mice were divided in twelve groups of six animals. In pulmonary and extrapulmonary control or ALI groups received either saline or LPS (intratracheally instilled or intraperitoneally injected), respectively. Ventilated groups were either recruited or not with a single recruitment maneuver (SRM) reaching 45 cm H2O. Results: At baseline ALI P and ALI EXP non ventilated groups presented the same level of inflammation; a statistically significant difference in density of inflammatory cells was noted in ALI P MV (3,84±1,28 cells/2) compared to ALI EXP MV (1,75±0,14 cells/2), p=0,013. The same was observed in ALI P SRM (2,92±0,44 cells/2) compared to ALI EXP SRM (1,46±0,23 cells/2) ventilated groups (p<0,0001). ALI P showed a statistically significant increase in El (56,19 ± 12,26 cm H2O) in comparison to ALI EXP (26,88 ± 36,38 cm H2O) after SRM (p = 0,029). No statistical differences were observed in kidney oxidative stress. Conclusion: We observed a different pattern of response in lung inflammation and mechanics comparing pulmonary and extra pulmonary ALI, submitted to short term mechanical ventilation. Although mechanical ventilation represents a fundamental tool to stabilize critical patients, it is essential to individualize the approach of the ventilatory treatment

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Rondelet, Benoît. "Médiation humorale de l'hypertension artérielle pulmonaire dans un modèle de cardiopathie congénitale à shunt systémo-pulmonaire chez le porcelet en croissance." Doctoral thesis, Universite Libre de Bruxelles, 2008. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210373.

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Aissa, Jamal. "Pathophysiologie et pharmacologie cardio-pulmonaire et inflammatoire du PAF-ACETHER." Paris 5, 1993. http://www.theses.fr/1993PA05CD07.

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Le paf-acéther (paf) est un médiateur pro inflammatoire dérivé du métabolisme des lipides constitutifs des membranes cellulaires. Nous avons étudié les effets physiothologiques du paf dans le domaine cardio-pulmonaire et lors d'une inflammation locale et articulaire. L'injection de ce médiateur dans la circulation pulmonaire chez la brebis induit une thrombocytopénie et une leucopénie immédiate puis une accumulation leucocytaire pulmonaire décelable à la 5ème minute. On observe une hypertension pulmonaire indépendante du thromboxane B2 (TxB2). Toutes les réponses induites par le paf sont inhibées par un antagoniste spécifique de ce médiateur, le WEB 2086. L'administration du complexe héparine-protamine chez le lapin s'accompagne d'une production transitoire de paf associée à une thrombocytopénie et à une leucopénie et d'une production retardée mais prolongée de TxB2. L'effet protecteur du BN 52021, autre antagoniste spécifique du paf, sur la trombocytopénie et le niveau plasmique du TxB2 indique d'une part que le paf exerce un rôle précoce au niveau cellulaire, d'autre part que la production de TxB2 est partiellement médiée par le paf. Notre travail a également montré l'implication du paf dans l'arthrite induite par la carragénie chez le lapin, notamment dans sa phase aiguë. Un antagoniste spécifique du paf, le BN 50730, exerce une action préventive et curative sur l'arthrite. Dans le modèle du granulome inflammatoire induit par la carragénine chez le rat, le paf est produit in situ au cours de la phase aiguë mais également au cours du passage à la phase chronique ce qui suggère son implication à cette étape de la réaction inflammatoire. L'action du paf doit se concevoir en fonction de ses nombreux effets cellulaires et de ses interrelations avec d'autres médiateurs de l'inflammation. Les effets bénéfiques des antagonistes des récepteurs au paf pourraient représenter une alternative thérapeutique et un intérêt clinique, notamment dans l'inflammation chronique.

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Livres sur le sujet "Pulmonary Pathophysiology"

Pulmonary pathophysiology. Philadelphia: Lippincott, 1995.

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Pulmonary pathophysiology: The essentials. 7th ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins, 2008.

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B, West John, ed. Pulmonary pathophysiology--the essentials. 4th ed. Baltimore: Williams & Wilkins, 1992.

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West, John B. (John Burnard), ed. Pulmonary pathophysiology: The essentials. 8th ed. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins Health, 2012.

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Pulmonary pathophysiology: The essentials. 3rd ed. Baltimore: Williams & Wilkins, 1987.

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B, West John, ed. Pulmonary pathophysiology--the essentials. 5th ed. Baltimore, Md: Williams & Wilkins, 1998.

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Pulmonary pathophysiology: A clinical approach. 3rd ed. New York: McGraw-Hill Medical, 2010.

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Workshop on "Chronic Pulmonary Hyperinflation" (1988 Montescano, Italy). Chronic pulmonary hyperinflation. London: Springer-Verlag, 1989.

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Pulmonary circulation: Diseases and their treatment. 3rd ed. London: Hodder Arnold, 2011.

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Bittar, E. Edward. Pulmonary biology in health and disease. Edited by Springer-Verlag. New York: Springer, 2002.

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Chapitres de livres sur le sujet "Pulmonary Pathophysiology"

Kaul, Sunny. "Pathophysiology." In Managing Chronic Obstructive Pulmonary Disease, 1–12. West Sussex, England: John Wiley & Sons Ltd, 2008. http://dx.doi.org/10.1002/9780470697603.ch1.

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Vanzeller, Mafalda, Marta Drummond, and João Carlos Winck. "Chronic respiratory failure – pathophysiology." In Pulmonary Rehabilitation, 399–408. Second edition. | Boca Raton : CRC Press, [2020] | Preceded by Pulmonary rehabilitation / Claudio F. Donner, Nicolino Ambrosino, Roger Goldstein. 2005.: CRC Press, 2020. http://dx.doi.org/10.1201/9781351015592-41.

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Rabinovitch, Marlene. "Pulmonary Vascular Pathophysiology." In Pediatric Cardiovascular Medicine, 71–80. Oxford, UK: Wiley-Blackwell, 2012. http://dx.doi.org/10.1002/9781444398786.ch5.

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Lajoie, Annie C., Vincent Mainguy, SéBastien Bonnet, and Steeve Provencher. "Pulmonary vascular diseases." In Applied Respiratory Pathophysiology, 119–47. Boca Raton : CRC Press, [2017]: CRC Press, 2017. http://dx.doi.org/10.1201/9781315177052-7.

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Milot, Julie, and Mathieu Morissette. "Chronic obstructive pulmonary disease." In Applied Respiratory Pathophysiology, 97–118. Boca Raton : CRC Press, [2017]: CRC Press, 2017. http://dx.doi.org/10.1201/9781315177052-6.

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Schols, Annemie M. W. J., and Emiel F. M. Wouters. "Pulmonary rehabilitation." In Recent Advances in the Pathophysiology of COPD, 167–87. Basel: Birkhäuser Basel, 2004. http://dx.doi.org/10.1007/978-3-0348-7939-2_11.

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Schrump, David S. "Pulmonary Malignancies: Pathophysiology and Treatment." In Principles and Practice of Geriatric Surgery, 406–32. New York, NY: Springer New York, 2001. http://dx.doi.org/10.1007/978-1-4757-3432-4_29.

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Rizzo, Alicia N., Dustin R. Fraidenburg, and Jason X. J. Yuan. "Pulmonary Vascular Physiology and Pathophysiology." In PanVascular Medicine, 4057–77. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-37078-6_202.

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Rizzo, Alicia N., Dustin R. Fraidenburg, and Jason X. J. Yuan. "Pulmonary Vascular Physiology and Pathophysiology." In PanVascular Medicine, 1–26. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-37393-0_202-1.

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Mitani, Yoshihide. "Pathophysiology and Genetics: BMPR2." In Diagnosis and Treatment of Pulmonary Hypertension, 115–24. Singapore: Springer Singapore, 2017. http://dx.doi.org/10.1007/978-981-287-840-3_9.

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Actes de conférences sur le sujet "Pulmonary Pathophysiology"

Zhao, Y. C., S. E. Rees, S. Andreassen, and S. Kjaergaard. "Simulation of Pulmonary Pathophysiology During Spontaneous Breathing." In 2005 IEEE Engineering in Medicine and Biology 27th Annual Conference. IEEE, 2005. http://dx.doi.org/10.1109/iembs.2005.1615892.

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Ghanem, M., A. Justet, M. Jaillet, M. Hachem, T. Boghanim, A. Vadel, A. Mailleux, and B. Crestani. "Involvement of FGFR4 in Pulmonary Fibrosis Pathophysiology." 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.a4220.

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Lammers, Steven R., Phil H. Kao, Lian Tian, Kendall Hunter, H. Jerry Qi, Joseph Albietz, Stephen Hofmeister, Kurt Stenmark, and Robin Shandas. "Quantification of Elastin Residual Stretch in Fresh Artery Tissue: Impact on Artery Material Properties and Pulmonary Hypertension Pathophysiology." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206793.

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Pulmonary arterial hypertension (PAH) is characterized as a chronic elevation in mean pulmonary artery pressure (MPAP) resulting from increased hydrodynamic resistance and decreased hydraulic capacitance of the pulmonary circulatory system. These hemodynamic changes cause the heart to operate outside optimum pump efficiency. The heart compensates for the efficiency loss through ventricular hypertrophy which, if left untreated, will continue until cardiac failure results.

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Siler, S. Q., D. Longo, J. Woodhead, C. Battista, Z. Kenz, S. Tallapaka, G. Liu, G. Generaux, S. Ermakov, and L. Shoda. "Using Quantitative Systems Pharmacology Modeling to Understand the Pathophysiology of Idiopathic Pulmonary Fibrosis." 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.a4648.

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Alamer, Amal, Rhys Jones, Chris Ward, Michael Drinnan, Alexander John Simpson, Michael Griffin, Joanne Patterson, and Ian Forrest. "Oropharyngeal swallowing pathophysiology in patients with idiopathic pulmonary fibrosis: A consecutive descriptive case series." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.3370.

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Dumas, Sébastien J., Frédéric Perros, Catherine Rucker-Martin, Elodie Gouadon, Marc J. C. Humbert, and Sylvia Cohen-Kaminsky. "Glutamate And NMDA Receptors: New Signaling Pathway Involved In The Pathophysiology Of Pulmonary Hypertension." 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.a4747.

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Alamer, A., R. Jones, C. Ward, M. Drinnan, AJ Simpson, M. Griffin, J. Patterson, and I. Forrest. "S127 Oropharyngeal swallowing pathophysiology in patients with idiopathic pulmonary fibrosis: A consecutive descriptive case series." In British Thoracic Society Winter Meeting, Wednesday 17 to Friday 19 February 2021, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2021. http://dx.doi.org/10.1136/thorax-2020-btsabstracts.132.

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He, M., K. Qing, N. Tustison, L. A. Myc, J. MacLeod, R. Nunoo-Asare, J. Cassani, et al. "Probing Early-Stage Pulmonary Pathophysiology in Young Healthy E-cigarettes Users Using Hyperpolarized 129Xe 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.a1113.

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Tan, Yan, and 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.

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Pulmonary arterial hypertension (PAH) is a group of chronic, progressive and fatal diseases, characterized by the dysfunction of the small arteries and microvasculature in the pulmonary circulation. Due to high blood pressure and high resistance in the pulmonary arteries, PAH causes detrimental damage on the lung and right heart ventricle. If left untreated, PAH quickly becomes life threatening. Although the exact pathophysiology remains unknown, there is increasing evidence suggesting that inflammation likely plays an important role in inducing and perpetuating the PAH progress. Although anti-inflammatory therapy has been shown effective in certain connective-tissue-disease-associated PAH, this approach has not been tested in other PAH conditions. The potential benefit of anti-inflammatory therapy to treat various PAH conditions could be of importance and require further study on the possible pathological mechanisms underlying the therapeutic effects.

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Lee, Namheon, Michael D. Taylor, Kan N. Hor, and Rupak K. Banerjee. "Non-Invasive Calculation of Energy Loss in Pulmonary Arteries Using 4D Phase Contrast MRI Measurement." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80525.

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The recent development of energy based endpoints, to quantify the pathophysiology of congenital heart disease such as tetralogy of Fallot (TOF), requires accurate measurement of cardiac blood flow and pressure data. Consequently, invasive cardiac catheterization is required for those measurements. In this research we used 4D phase contrast magnetic resonance imaging (PC MRI) data to determine the pressure drop non-invasively. This enables us to obtain pressure-flow variation, which, in turn, allowed us to calculate energy loss along the branch pulmonary arteries (PA). Based on our result, we believe that the hemodynamic status of the PA of a subject can be non-invasively evaluated by both pressure drop and energy loss values along the PA.

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Rapports d'organisations sur le sujet "Pulmonary Pathophysiology"

Hurt, Holcombe H., Suzanne A. Hernandez, Wallace B. Baze, Theresa M. Tezak-Reid, and Jill R. Keeler. Pathophysiologic Mechanisms of Three Pulmonary Edemagenic Compounds: The Role of Toxic Oxygen Species. Fort Belvoir, VA: Defense Technical Information Center, April 1992. http://dx.doi.org/10.21236/ada251135.

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