Bibliografie tematiche / Pulmonary Pathophysiology

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Letteratura scientifica selezionata sul tema "Pulmonary Pathophysiology"

Autore: Grafiati
Pubblicato: 4 giugno 2021
Ultima modifica: 19 febbraio 2022

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Articoli di riviste sul tema "Pulmonary Pathophysiology"

1

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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Tesi sul tema "Pulmonary Pathophysiology"

1

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.<p><p>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
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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 nã
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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 inhib
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Libri sul tema "Pulmonary Pathophysiology"

1

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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Capitoli di libri sul tema "Pulmonary Pathophysiology"

1

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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Atti di convegni sul tema "Pulmonary Pathophysiology"

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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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Abstract (sommario):
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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Abstract (sommario):
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
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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 b
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Rapporti di organizzazioni sul tema "Pulmonary Pathophysiology"

1

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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