Rozprawy doktorskie na temat „Airway remodelling”
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Leggett, Julian James. "Airway remodelling in asthma". Thesis, Queen's University Belfast, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.485059.
Pełny tekst źródłaBoustany, Sarah. "Mechanisms of Airway Remodelling". Thesis, The University of Sydney, 2008. http://hdl.handle.net/2123/3577.
Pełny tekst źródłaBoustany, Sarah. "Mechanisms of Airway Remodelling". University of Sydney, 2008. http://hdl.handle.net/2123/3577.
Pełny tekst źródłaAsthma is an inflammatory disease characterised by tissue remodelling. A prominent feature of this remodelling is an increase in the number and size of the blood vessels- formed from pre-existing capillaries – angiogenesis (Siddiqui et al., 2007; Wilson, 2003). This is triggered by many different endogenous angiogenic stimulators such as vascular endothelial growth factor (VEGF), and inhibited by endogenous angiogenic inhibitors such as tumstatin. Tumstatin is the non-collagenous domain (NC1) of the collagen IV α3 chain which, when cleaved, inhibits endothelial cell proliferation and induces apoptosis. Experiments described in this thesis have for the first time demonstrated the absence of tumstatin in the airways of individuals with asthma and lymphangioleiomyomatosis (LAM) as well as the functional responses to tumstatin as an angiogenic inhibitor, both in vitro and in vivo, in the airway. Although tumstatin was absent from the airways of asthmatic and LAM individuals it was present in the airways of individuals with no airways disease, chronic obstructive pulmonary disease, bronchiectasis and cystic fibrosis. No significant difference was seen in the levels of the Goodpasture Binding Protein (GPBP), a phosphorylating protein responsible for the alternate folding of tumstatin, between asthmatic, LAM and individuals with no airways disease. The αvβ3 integrin, reported to be necessary for the activity of tumstatin, as well as the individual αv and β3 sub-units were shown to be equally expressed in the airways of all patient groups. Co-localisation of tumstatin, VEGF and the αvβ3 integrin was seen in the disease free airways, however, a different pattern of VEGF and the αvβ3 integrin expression was observed in asthmatic and LAM airways with minimal co-localisation. Tumstatin was detected in serum and bronchoalveolar lavage fluid (BAL-f) samples from asthmatics and individuals with no airway disease, however there was no significant difference in the level of expression between the two groups. It was demonstrated that the tumstatin detected in the serum and BAL-f samples from asthmatics and individuals with no airway disease was part of the whole collagen IV α3 chain and not in its free and potentially active form. The ability of recombinant tumstatin to inhibit tube formation and proliferation of primary pulmonary endothelial cells was demonstrated for the first time. Further, the functional response of tumstatin was demonstrated in vivo in a mouse model of allergic airway disease. Tumstatin inhibited angiogenesis in the airway and decreased airway hyperresponsiveness. Whether there is potential for tumstatin, or a derivative thereof, to be of therapeutic value in airways diseases in which angiogenesis is a component should be the subject of future studies.
Zhao, Jingyue. "Th17 responses in airway inflammation and airway remodelling". Thesis, King's College London (University of London), 2011. http://kclpure.kcl.ac.uk/portal/en/theses/th17-responses-in-airway-inflammation-and-airway-remodelling(94ca2e63-6304-4694-998e-b40747ca0f9a).html.
Pełny tekst źródłaMcConnell, William David. "Mediators of airway remodelling in asthma". Thesis, University of Southampton, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.288445.
Pełny tekst źródłaBeckett, P. A. "Pharmacology of airway remodelling in asthma". Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596514.
Pełny tekst źródłaGrainge, Christopher. "Determinants of airway remodelling in asthma". Thesis, University of Southampton, 2010. https://eprints.soton.ac.uk/384164/.
Pełny tekst źródłaHilliard, Thomas Norman. "Airway inflammation and remodelling in cystic fibrosis". Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.427686.
Pełny tekst źródłaDaud, Tariq. "The role of WNT5a in airway remodelling in asthmatic airway epithelial repair". Thesis, University of Leicester, 2018. http://hdl.handle.net/2381/42778.
Pełny tekst źródłaZheng, Ling 1958. "Airway inflammation and remodelling post human lung transplantation". Monash University, Dept. of Medicine, 2002. http://arrow.monash.edu.au/hdl/1959.1/8099.
Pełny tekst źródłaFaiz, Alen. "Novel gene candidates for Airway Remodelling in Asthma". Thesis, The University of Sydney, 2014. http://hdl.handle.net/2123/10448.
Pełny tekst źródłaSammut, David. "Airway remodelling in asthma : aspects of airway wall thickness and extracellular matrix production". Thesis, University of Southampton, 2010. https://eprints.soton.ac.uk/404048/.
Pełny tekst źródłaKhan, Nazmin. "The role of anaphylatoxins in asthma and airway remodelling". Thesis, King's College London (University of London), 2012. https://kclpure.kcl.ac.uk/portal/en/theses/the-role-of-anaphylatoxins-in-asthma-and-airway-remodelling(ee2de1d0-eb02-4b19-b546-2d4c26d4bbef).html.
Pełny tekst źródłaDavies, Elizabeth R. "Elucidating the role of ADAM33 in airway inflammation and remodelling in asthma". Thesis, University of Southampton, 2014. https://eprints.soton.ac.uk/415835/.
Pełny tekst źródłaCampbell, Gaynor Anne. "In vitro investigations of transforming growth factor-β2 induced airway wall remodelling". Thesis, University of Manchester, 2011. https://www.research.manchester.ac.uk/portal/en/theses/in-vitro-investigations-of-transforming-growth-factor2-induced-airway-wall-remodelling(788cb4e3-e92d-419f-bef2-ebd01887eb8b).html.
Pełny tekst źródłaLai, Dilys. "Modulation of airway smooth muscle secretory responses by components of airway wall extracellular matrix : relevance to remodelling in asthma". Thesis, King's College London (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.411028.
Pełny tekst źródłaMcMillan, Sarah Jane. "Allergen-induced airway remodelling : investigating the role of Th2 cells and matrix metalloproteinases". Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.415191.
Pełny tekst źródłaLabram, Briony. "Defining the molecular and cellular mechanisms regulating Aspergillus fumigatus regulated airway wall remodelling in asthma". Thesis, University of Manchester, 2017. https://www.research.manchester.ac.uk/portal/en/theses/defining-the-molecular-and-cellular-mechanisms-regulating-aspergillus-fumigatus-regulated-airway-wall-remodelling-in-asthma(2f97458e-c053-464f-8a97-cd10cceea187).html.
Pełny tekst źródłaKariyawasam, Harsha Hemantha. "Airway remodelling and transforming growth factor (TGF)-β superfamily signalling in allergen-induced asthma". Thesis, Imperial College London, 2007. http://hdl.handle.net/10044/1/8641.
Pełny tekst źródłaKaruyawasan, Harsha Hemantha. "Airway remodelling and transforming growth factor (TGF)-B superfamily signalling in allergen-induced asthma". Thesis, Imperial College London, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.497534.
Pełny tekst źródłaBerair, Rachid. "Airway structural remodelling in asthma : functional relevance and suitability as a target for therapy". Thesis, University of Leicester, 2018. http://hdl.handle.net/2381/41264.
Pełny tekst źródłaSalmon, Michael. "Mechanisms of airway cell proliferation and pulmonary inflammation induced by ozone and allergen in Brown-Norway rats". Thesis, Imperial College London, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.313031.
Pełny tekst źródłaTam, Anthony. "The impact of female sex hormones on cigarette smoke-induced airway remodelling and mucus production". Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/55846.
Pełny tekst źródłaMedicine, Faculty of
Medicine, Department of
Experimental Medicine, Division of
Graduate
Moir, Lyn Margaret. "Airway wall structural remodelling : studies on smooth muscle phemotype and contractility in isolated small bronchioles". Thesis, King's College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.405168.
Pełny tekst źródłaGribben, Elaine. "The role of glycosaminoglycans in neprilysin regulation and the remodelling of tissues in the airway". Thesis, Glasgow Caledonian University, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.688253.
Pełny tekst źródłaHossain, Mohammed Imran. "Chlamydia pneumoniae infection of Dentritic cells and its role in asthma exacerbations". Thesis, Queensland University of Technology, 2014. https://eprints.qut.edu.au/70453/3/Mohammed_Hossain_Thesis.pdf.
Pełny tekst źródłaCunningham, Jason Owen. "Variation in airway remodelling genes and their role on asthma severity in children and young adults". Thesis, University of Sussex, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.590080.
Pełny tekst źródłaAlrifai, Mohammed [Verfasser], i Holger [Akademischer Betreuer] Garn. "Resolution of airway remodelling in a mouse model of chronic allergic asthma / Mohammed Alrifai ; Betreuer: Holger Garn". Marburg : Philipps-Universität Marburg, 2019. http://d-nb.info/1183909020/34.
Pełny tekst źródłaHartley, Ruth Angela. "Using quantitative computed tomography to provide important and novel insights into airway remodelling in asthma and COPD". Thesis, University of Leicester, 2017. http://hdl.handle.net/2381/39959.
Pełny tekst źródłaNaveed, Shams-un-nisa. "Matrix metalloproteinase-1 mediated extra-cellular matrix remodelling contributes to airway smooth muscle growth and asthma severity". Thesis, University of Nottingham, 2018. http://eprints.nottingham.ac.uk/50577/.
Pełny tekst źródłaPrabhala, Pavan. "The impact of precise MKP-1 regulation and modulation on cytokine expression in asthma and airway remodelling". Thesis, The University of Sydney, 2016. http://hdl.handle.net/2123/14954.
Pełny tekst źródłaBrodlie, Malcolm James. "Development of a primary airway epithelial cell culture model and explanted tissue archive to study the role of neutrophilic inflammation and airway remodelling in cystic fibrosis lung disease". Thesis, University of Newcastle Upon Tyne, 2011. http://hdl.handle.net/10443/1228.
Pełny tekst źródłaNath, Puneeta. "Investigation of T-helper type 2 cytokines and the mitogen-activated protein kinase pathway in the modulation of bronchial hyperresponsiveness, airway inflammation and remodelling". Thesis, Imperial College London, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.417857.
Pełny tekst źródłaSalgado, Daniel Cauduro. "Distribuição de colágeno na concha nasal inferior de pacientes com rinite alérgica ou idiopática". Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/5/5143/tde-12012015-104722/.
Pełny tekst źródłaINTRODUCTION: Despite our knowledge about nasal conchae fibrosis and basement membrane thickening in allergic rhinitis, there are no descriptive studies on nasal mucosa behavior in patients with idiopathic rhinitis. The aim of our study was to describe possible changes in the basement membrane and lamina propria of the inferior concha in patients with idiopathic or allergic rhinitis, in addition to a quantitative study of collagen fibers in this site. METHODS: The inferior nasal concha obtained from 28 patients submitted to bilateral turbinectomy was examined - 14 with allergic rhinitis and 14 with idiopathic rhinitis; analyzing the collagen area, the basement membrane thickness and the collagen fibrils diameter using optical microscopy (Hematoxylin-eosin and Picrosirius-hematoxylin staining), electron microscopy and immunohistochemistry for laminin and collagen IV. RESULTS: 1) patients with allergic rhinitis had a significantly larger area of the nasal concha occupied by collagen than the group with idiopathic rhinitis. 2) the basement membrane of patients with allergic rhinitis was significantly thicker. 3) the reticular lamina of the basement membrane of patients with allergic rhinitis had collagen fibrils with diameters which were smaller than those from patients with idiopathic rhinitis. 4) there were no significant differences between the groups concerning the distribution of laminin and collagen IV. CONCLUSIONS: Alterations to the nasal mucosa that happen in allergic rhinitis are characterized by basement membrane thickening and fibrosis. In idiopathic rhinitis the patients\' mucosae were structurally similar to those from normal patients
Lederlin, Mathieu. "Etude de l’atténuation scanographique de la paroi bronchique dans l’imagerie de l’inflammation et du remodelage des voies aériennes". Thesis, Bordeaux 2, 2011. http://www.theses.fr/2011BOR21905.
Pełny tekst źródłaAsthma and chronic obstructive pulmonary disease (COPD) are frequent conditions characterized by two main pathological changes: bronchial inflammation and remodelling. Pathological examination requires invasive biopsy, which is rarely performed in routine. Therefore there is a great interest in developing non-invasive methods that would lead to more precise phenotyping of patients and the development of new targeted treatments. Computed tomography (CT) can provide a quantitative morphometry-based analysis of the airways. These morphometric parameters have been shown to correlate with functional obstruction but are poorly used in routine practice due to their lack of standardisation. The aim of our studies was to investigate the value of CT attenuation-based parameters in humans and animals. In asthma and COPD, we have shown that the wall attenuation value had diagnostic performances comparable to those of morphometric parameters, correlated better with functional obstructive indexes, and could be a marker of remodelling in asthma. In asthmatic mice, peribronchial attenuation values extracted from respiratory-gated micro-CT images correlate with remodeling. Therefore, the concept of bronchial wall attenuation seems to be promising for assessing non-invasively airways remodeling. Further studies are required to ensure the full reproducibility of these methods
Abdelsadik, Ahmed Mohammed Khalil [Verfasser]. "Hypoxia induces processes related to inflammation and remodelling in the airways of the fruit fly Drosophila melanogaster / Ahmed Mohammed Khalil Abdelsadik". Kiel : Universitätsbibliothek Kiel, 2012. http://d-nb.info/1021342610/34.
Pełny tekst źródłaEapen, MS. "Understanding cellular changes and mediators of airway remodelling in COPD". Thesis, 2018. https://eprints.utas.edu.au/28492/1/Eapen_whole_thesis.pdf.
Pełny tekst źródłaSoltani, Abhari A. "Airway remodelling in smokers with or without chronic obstructive pulmonary disease (COPD) and the effects of inhaled corticosteroids on remodelling in COPD". Thesis, 2010. https://eprints.utas.edu.au/10766/1/Amir_Soltani_whole%20_thesis.pdf.
Pełny tekst źródłaSohal, SS. "Epithelial activation in chronic obstructive pulmonary disease (COPD)". Thesis, 2010. https://eprints.utas.edu.au/10765/34/Sohal_whole%20_thesis.pdf.
Pełny tekst źródłaHaw, Tatt Jhong. "Investigation of pathogenesis of chronic obstructive pulmonary disease". Thesis, 2016. http://hdl.handle.net/1959.13/1318484.
Pełny tekst źródłaChronic Obstructive Pulmonary Disease (COPD) affects more than 64 million people globally and is primarily caused by cigarette smoke (CS) exposure. It is the third leading cause of morbidity and mortality worldwide and imposes significant socioeconomic burden worldwide. COPD is a chronic lung disease characterised by chronic pulmonary inflammation, airway remodelling and emphysema. These pathologies consequently culminate in progressive lung function decline and airflow limitation. Current therapies for the management of COPD are largely ineffective. They provided symptomatic relief to patients and do not target the underlying causal factors of COPD. Hence, there is a lack of effective treatments and an urgent need for research into the identification and development of therapeutic strategies in treating COPD. The lack of effective treatments is due to the poor understanding of immunological processes and mechanisms that underpin the pathogenesis of COPD. Our laboratory has recently established a murine experimental model of COPD by exposing mice to nose-only inhalation of tightly regulated dose of CS. Importantly, our CS-induced model of COPD recapitulates the hallmark features of human disease in a relatively short period of time. Thus, this allows us to investigate and examine the immunological processes and mechanisms that underpin the pathogenesis of COPD. The aims of the studies described in this thesis were to identify and elucidate immunological processes that underpin the pathogenesis of COPD. The first study identified a novel role for tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) in promoting CS-induced COPD. TRAIL and its receptors were increased by CS exposure in mice and in lung samples from human COPD patients. TRAIL-deficient mice or wild-type (WT) mice treated with neutralising TRAIL monoclonal antibodies had significantly reduced CS-induced pulmonary inflammation, expression of pro-inflammatory mediators, emphysema-like alveolar enlargement and improved lung function. The second study investigated the role of Toll-like receptor (TLR)2 and TLR4 in CS-induced pathogenesis of COPD. CS-induced pulmonary inflammation was largely unaltered in the absence of TLR2 or TLR4. TLR2-deficient mice had CS-induced emphysema-like alveolar enlargement, apoptosis and impaired lung function compared to normal air-exposed mice that was equivalent to CS-exposed WT mice, whilst small airway remodelling was not altered. By contrast, TLR4-deficient mice had reduced CS-induced emphysema-like alveolar enlargement, apoptosis and impaired lung function compared to WT mice. Interestingly, CS-induced small airway fibrosis, characterised by increased collagen deposition around small airways, was ablated in TLR4-deficient mice. The third study identified a previously unrecognised role for TLR7 in the pathogenesis of COPD. In the absence of TLR7, CS-induced pulmonary inflammation was not altered compared to CS-exposed WT controls. CS-induced small airway epithelial cell thickening was reduced whilst collagen deposition increased in the absence of TLR7. Importantly, CS-induced emphysema-like alveolar enlargement and apoptosis were reduced in TLR7-deficient mice. Administration of the TLR7 agonist imiquimod synergistically increased CS-induced emphysema and apoptosis. Interestingly, imiquimod-induced emphysema and apoptosis may occur through the activity of mast cell-specific proteases, in particular mouse mast cell protease-6 (mMCP-6). Crucially, antibody-mediated neutralisation of TLR7 also reduced CS-induced emphysema and apoptosis in the lungs in experimental COPD. Our novel findings indicate that TRAIL and TLRs, in particularly TLR2, TLR4 and TLR7, have critical roles in CS-induced development of COPD. TRAIL promotes CS-induced pulmonary inflammation, emphysema-alveolar enlargement and lung function impairment. TLRs have little or minor role in CS-induced pulmonary inflammation. TLR2 may protect against CS-induced emphysema and lung function impairment, whilst TLR4 and TLR7 induce these disease features of COPD. TLR4 promotes CS-induced airway fibrosis whilst TLR2 and TLR7 regulate collagen deposition around small airways. Collectively, our studies significantly advance the understanding of the immunological mechanisms that underpin the pathogenesis of COPD and may facilitate the development of novel treatments for COPD in the future.
Setlakwe, Emilie L. "Subepithelial collagen content in the peripheral airways of heaves-affected and control horses". Thèse, 2011. http://hdl.handle.net/1866/6886.
Pełny tekst źródłaExtracellular matrix remodelling is present in the human asthmatic lung, and is characterized by increased collagen or fibrosis of the subepithelial area of the airway. Heaves, a naturally occurring chronic lower airway inflammatory condition in horses shares aspects of pathophysiology with asthma, including features of airway remodelling. We thus hypothesize that airway fibrosis is a characteristic of remodelling in heaves. The aim of this study was to evaluate the presence of fibrosis in the subepithelial area of the peripheral airways of heaves-affected horses. Peripheral lung biopsies acquired under thoracoscopic guidance were obtained from 5 control and 6 heaves-affected horses, both before (T0) and after a 30 day antigenic challenge with mouldy hay and straw. Prior to the study, diseased horses were in clinical remission and exhibited no clinical signs of disease. Obtained samples were microscopically examined using picrosirius-red, a collagen specific histological staining technique. Collagen area in the subepithelial layer, e.g. the region between the airway smooth muscle and the epithelial layer was measured, and corrected for airway size using standard morphometric techniques. In comparison with controls, heaves-affected horses had an increased collagen content in the airway subepithelial area (p<0.1). No change in fibrosis of the subepithelial area was observed in diseased horses after the 30 day antigenic challenge. Peripheral airway subepithelial collagen at baseline was positively associated with maximal changes in transpulmonary pressure and pulmonary resistance in horses with heaves but not in controls. Results of this study indicate that fibrosis of the subepithelial area is present in the peripheral airways of heaves-affected horses, and may play a role in residual lung function deficits observed in diseased horses even while in clinical remission.
Koucký, Václav. "Detekce časných patofyziologických změn dýchání u dětí s chronickým plicním onemocněním". Doctoral thesis, 2020. http://www.nusl.cz/ntk/nusl-412517.
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