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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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7

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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8

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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9

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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10

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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11

Diller, Gerhard-Paul. "Pathophysiologic correlates of exercise intolerance in adults with pulmonary hypertension and congenital heart disease." Thesis, Imperial College London, 2009. http://hdl.handle.net/10044/1/11341.

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Adult congenital heart disease (ACHD) patients have markedly depressed exercise capacity. This thesis examined (i) the prevalence of chronotropic incompetence, its relationship to symptoms and exercise capacity and its prognostic value in ACHD patients; (ii) investigated exercise capacity in patients with Eisenmenger syndrome and assessed survival prospects in this cohort as well as risk factors for mortality. In addition, clinical effects of Bosentan (a pulmonary vasodilator) were examined during longer-term follow-up. (iii) Mathematical modelling studies were employed to assess the impact of
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12

Schulze-Neick, Ingram. "Postoperative pulmonale Hypertension nach Korrektur angeborener Herzfehler Behandlung, Pathophysiologie, und vaskulo-bronchiale Interaktionen /." [S.l.] : [s.n.], 2002. http://deposit.ddb.de/cgi-bin/dokserv?idn=965753859.

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13

Parajuli, Nirmal [Verfasser]. "The role of nitric oxide synthases in the pathophysiology of chronic obstructive pulmonary disease / by Nirmal Parajuli." 2009. http://d-nb.info/1000411672/34.

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Schulze-Neick, Ingram [Verfasser]. "Postoperative pulmonale Hypertension nach Korrektur angeborener Herzfehler : Behandlung, Pathophysiologie, und vaskulo-bronchiale Interaktionen / von Ingram Schulze-Neick." 2002. http://d-nb.info/965753859/34.

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15

Robitaille, Genevieve. "Étude du rôle de l’auto-antigène nucléaire centromérique B (CENP-B) et des auto-anticorps anti-CENP-B dans l’activation des cellules musculaires lisses vasculaires : Implication potentielle dans la pathophysiologie de la sclérose systémique." Thèse, 2009. http://hdl.handle.net/1866/3142.

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La sclérose systémique (ScS) est une maladie auto-immune dont l’un des principaux auto-anticorps, dirigé contre la protéine centromérique B (CENP-B), est fortement associé à l’hypertension artérielle pulmonaire, l’une des causes majeures de décès dû à la ScS. L’hypertension résulte de l’occlusion progressive des vaisseaux suite à une hyperactivation des cellules musculaires lisses (CML) de la paroi vasculaire. Cependant, les facteurs responsables de ce remodelage vasculaire restent inconnus. Plusieurs études récentes ont démontré que certains auto-antigènes possèdent des fonctions biologiques
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16

Li, Pin. "Effects of carbon nanotubes on airway epithelial cells and model lipid bilayers : proteomic and biophysical studies." Thesis, 2014. http://hdl.handle.net/1805/5968.

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Indiana University-Purdue University Indianapolis (IUPUI)<br>Carbon nanomaterials are widely produced and used in industry, medicine and scientific research. To examine the impact of exposure to nanoparticles on human health, the human airway epithelial cell line, Calu-3, was used to evaluate changes in the cellular proteome that could account for alterations in cellular function of airway epithelia after 24 h exposure to 10 μg/mL and 100 ng/mL of two common carbon nanoparticles, singleand multi-wall carbon nanotubes (SWCNT, MWCNT). After exposure to the nanoparticles, label-free quantitative
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