Dissertations / Theses on the topic 'Airway'
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Williams, Adele. "Polymeric airway mucins in equine recurrent airway obstruction." Thesis, University of Manchester, 2014. https://www.research.manchester.ac.uk/portal/en/theses/polymeric-airway-mucins-in-equine-recurrent-airway-obstruction(14c6bee5-5406-4b7a-a9b5-495443c7c635).html.
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In healthy airways, mucus forms part of the innate immune response protecting the respiratory epithelium from damage by pathogens and environmental debris (Rose and Voynow, 2006). Conversely, in many respiratory diseases, mucus becomes part of the airway disease pathology. Mucus hypersecretion along with reduced clearance can cause blockage of the small airways, impairing gas exchange, promoting inflammation and becoming a culture medium for bacterial colonisation (Thornton et al., 2008). Recurrent airway obstruction (RAO) is a common yet poorly understood equine chronic respiratory disease where such altered mucus properties and clearance have been identified as major factors in the disease pathology (Davis and Rush, 2002; Gerber et al., 2000; Kaup et al., 1990; Robinson, 2001). The gel-forming mucins are largely responsible for the transport properties of mucus. The major equine airway gel-forming mucin in health is Muc5b and to a lesser extent Muc5ac; produced in specialised respiratory epithelial goblet cells and sub-mucosal glands (Rousseau et al., 2011b). Changes in mucin relative and net amounts and their macromolecular properties and interactions have been attributed to the altered physical properties of airway mucus in airways disease (Groneberg et al., 2002a; Jefcoat et al., 2001; Kirkham et al., 2002; Robinson et al., 2003; Sheehan et al., 1995).The project investigates the biochemical properties of mucins present in mucus from healthy horses and horses with RAO. This project identifies the anatomical presence of mucin-producing goblet cells and glands in fixed tissues from the respiratory tracts of healthy horses and subsequently examines mucin-production sites in respiratory tracts from horses with RAO. Finally the project investigates a methodology for the study of mucin production in airway cells harvested from live horses suffering from RAO.Our investigations confirmed that horses with RAO have more endotracheal mucus than healthy controls, and that Muc5b is the predominant mucin with Muc5ac also present in RAO horse mucus, both during symptomatic disease and when horses are asymptomatic. Mucins are produced in epithelial goblet cells and sub-mucosal glands dispersed throughout the length and circumference of the equine trachea and bronchi. Goblet cell hyperplasia occurs in symptomatic exposed RAO horse airways, although goblet cells are smaller than in asymptomatic RAO horse airways. Exposure to a dusty stable environment is associated with more goblet cells per length of bronchial compared to tracheal epithelium in all horses. RAO horses have larger sub-mucosal glands containing more mucin than control horses. Primary epithelial cell cultures grown at an air liquid interface are an alternative approach to study equine airway mucus, although the use of this culture system is in its early stages. We have developed novel ways to harvest equine airway epithelial cells (tracheal brushing) and shown it is possible to freeze cells collected via tracheal epithelial brushing in 20 % FBS and then culture to ALI at a later date.
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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.
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Shebani, Eyman. "Ultrastructural Studies of the Airway Epithelium in Airway Diseases." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-6632.
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Hamilton, Nicholas J. I. "Tissue-engineering airway mucosa for airway reconstruction and transplantation." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/1572383/.
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Conventional therapies are unable to treat a subset of patients with upper airway stenosis. To overcome this, tissue-engineered tracheas have been trialled as a means of replacing the damaged section of airway. All examples have suffered from poor mucosalisation following implantation which results in infection, mucostasis and airway obstruction. The aim of this thesis was to investigate methods of regenerating a respiratory mucosal graft that could be used as part of a tracheal transplant. The relationship of the extracellular matrix to human respiratory epithelial cells (HBECs) was examined to establish the optimal protein composition of the mucosal scaffold. Collagen IV was demonstrated to be the leading adhesive protein acting via the integrin α2β1 and a Src and FAK mediated intracellular pathway. Laminin was shown to play a key role in promoting HBEC proliferation and was dependent on an integrin pathway containing the subunit β1. This study compared biological, biomimetic and synthetic scaffolds for their ability to support and differentiate a respiratory epithelial layer. Decellularised dermis was shown to be the optimal scaffold and a differentiated respiratory layer with mucocilary function was achieved in-vitro. The implantation of this engineered respiratory mucosa proved more challenging with loss of differentiation markers following grafting in rabbits and mice. An alternative strategy was developed whereby basal epithelial cells were encased in collagen and successfully grafted onto the surface of decellularised trachea. This represents the most effective method for re-epithelising an allogenic trachea before or after transplantation and could also be used to reline other parts of the upper airway.
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Korpela, Antti. "Healing of airway anastomoses and stenting of airway stenosis." Helsinki : University of Helsinki, 2000. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/korpela/.
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Tao, Florence C. Y. "Mechanisms of altered airway smooth muscle calcium signalling in airway hyperresponsiveness." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0022/NQ50267.pdf.
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Tao, Florence C. Y. 1968. "Mechanisms of altered airway smooth muscle calcium signalling in airway hyperresponsiveness." Thesis, McGill University, 1998. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=35949.
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The pathophysiological origins of airway hyperresponsiveness (AHR) in asthma are unknown. The objectives of this thesis were to establish an association between AHR in an animal model of asthma and altered contractility of airway smooth muscle (ASM) and to elucidate changes in contractile signalling that could account for any observed differences in ASM contractility. The Fisher strain of rat is spontaneously hyperresponsive to methacholine inhalation challenge relative to Lewis rats. These inbred rat strains provide a model with which to study genetically-determined variations in airway smooth muscle that may underlie AHR. Fisher rats were found to be also hyperresponsive to serotonin (5-HT) in vivo compared to Lewis rats, indicating that their AHR is not agonist specific the narrowing capacity and velocity of contraction of Fisher intraparenchymal airways in cultured explants were also greater than explanted. Lewis intraparenchymal airways in response to 5-HT. In addition, 5-HT stimulated higher Ca2+ transients in Fisher than Lewis ASM, in parallel with their rank order of intraparenchymal airway responsiveness. These results suggest that ASM contractility may be determined by the extent of Ca2+ mobilization in airway myocytes. To examine the mechanism of enhanced intracellular Ca2+ mobilization in Fisher ASM, the role of the inositol (1,4,5)trisphospbate (Ins (1,4,5)P 3) pathway in determining interstrain differences in ASM Ca2+ was studied. 5-HT produced higher levels of Ins (1,4,5)P3 in Fisher than Lewis ASM. This appeared to be caused by a lower expression and activity in Fisher ASM of the type I and II 5-phosphatases which inactivate Ins (1,4,5)P3. Inhibition of 5-phosphatase activity increased Ins (1,4,5)P3-mediated Ca2+ release in ASM from both strains of rat, equalizing Ca2+ signals between Lewis and Fisher ASM. Since Ins (1,4,5)P3 receptor sensitivity to Ins (1,4,5)P 3 was found to be similar between the two rat strains, the differences in 5-phosphatas
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Kölbeck, Karl-Gustav. "Nasal and bronchial airway reactivity in allergic and non allergic airway inflammation /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-428-3/.
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Opazo, Saez Anabelle M. (Anabelle Marjorie). "Airway responsiveness to methacholine and airway smooth muscle in the guinea pig." Thesis, McGill University, 1991. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=60629.
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The purpose of this study was two-fold: (1) to examine the relationship between the amount of airway smooth muscle and the airway responsiveness to inhaled aerosolized methacholine (MCh) in guinea pigs, and (2) to characterize the distribution of airway narrowing following MCh.In summary: (1) the quantity of airway smooth muscle (ASM) does not appear to determine differences in maximal bronchoconstriction among normal guinea pigs; the lack of a correlation between responsiveness and amount of ASM may be explained by the heterogenous distribution of bronchoconstriction among the airways studied or the modality of challenge; (2) the sensitivity to MCh appears to be related to differences in the amount of ASM in intraparenchymal cartilaginous airways; (3) variability in the EC$ sb{50}$ may also reflect differences in airway cross-sectional area; (4) lung resistance appears to be a good measure of constriction since the morphometric measure of airway narrowing correlated well with resistance; (5) the heterogeneity of airway narrowing does not appear to be determined by differences in ASM.
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Wang, Jiahua. "The role of airway epithelium in airway inflammation and effect of corticosteroids." Thesis, Queen Mary, University of London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300175.
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Yu, Chia-Chen S. M. Massachusetts Institute of Technology. "A microfluidic mucosal airway model to study airway mucosal function and pathogenesis." Thesis, Massachusetts Institute of Technology, 2016. http://hdl.handle.net/1721.1/107373.
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Thesis: S.M., Massachusetts Institute of Technology, Department of Electrical Engineering and Computer Science, 2016.Cataloged from PDF version of thesis.
Includes bibliographical references (pages 64-67).
Airway mucus hypersecretion or impaired clearance is one of the key pathophysiological features of airborne infection, allergy and severe respiratory diseases. As foreign particles enter the lungs, the airway becomes inflamed and excessive amount of mucus is generated in response. However, little is known about the role of mucus in regulating the passage of potentially harmful particles. In this thesis, we develop a novel in-vitro microfluidic system which closely models the biophysiological properties of the airway system. Our system accommodates co-current flow of aerosol and mucus and reproduces the key physiology of molecular and particle transport into a mucus barrier. A stable air-mucus interface with physiological clearance rate of mucus is achieved by optimizing device structural parameters. Evaporation-driven concentration is observed and limits our system to be used to model particle delivery to the nose and larger airways. With this platform, we hope to perform systematic permeability studies with diseased and normal mucus to develop a detailed understanding of the respiratory mucus permeability towards selected allergens. We envision the device to serve as a broad platform to identify key properties of mucus that may guide the way to improved airway disease diagnosis and treatment.
by Chia-Chen Yu.
S.M.
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Daud, Tariq. "The role of WNT5a in airway remodelling in asthmatic airway epithelial repair." Thesis, University of Leicester, 2018. http://hdl.handle.net/2381/42778.
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Asthma is heterogeneous disease characterised by distinct tissue molecular phenotypes (Choy et al, 2015). However, the process of repair and remodelling remains ambiguous in this context. Although previous reports have shown elevated protein and mRNA expression of WNT5a, there is limited evidence in the literature to the major source of and function of WNT5a in asthma. Furthermore, WNT5a acting through the non-canonical axis exhibits functional cross talk with TGF-β1, which may influence repair and remodelling in asthma. We sought to evaluate protein expression of WNT5a and TGF-β1 in bronchial biopsies from a previously described cohort of subjects (9 healthy and 23 asthmatics) in whom aggregate gene signature profiles for Th2 and Th17 activity from tissue homogenates were available. After observing co-localised protein expression of both WNT5a and TGF-b1 in the epithelium, further investigations in BEAS-2B cells as a basal cell wound repair model were undertaken. We observed increased WNT5a protein expression pattern in vivo in asthma. WNT5a protein expression was significantly elevated in the epithelium in Th17 gene expression high asthmatic biopsies and the lamina propria, but not the airway smooth muscle bundle. We found a significant correlation and colocalisation of protein expression between TGF-β1 and WNT5a immunostaining in the epithelium suggestive of crosstalk. Further evidence supportive of cross talk was that both TGF-β1 and WNT5a were shown to induce SMAD2/3 nuclear translocation, which was inhibited by BOX-5 (a WNT5a inhibitor). Furthermore, WNT5a increased [Ca2+]I suggestive of noncanonical pathway engagement. Lastly, both WNT5a and TGF-β1 dual stimulation increased wound closure in BEAS-2B cells. Finally, stimulation of BEAS-2B cells with either TGF-β1 or WNT5a increased the expression of epithelial-mesenchymal transition (EMT) markers. WNT5a protein is increased in the airway epithelium in patients with asthma displaying a mucosal Th17-dependent gene signature. Additionally, we show potential in vitro evidence of TGF-β1-WNT5a cross talk via the SMAD2/3 axis, promoting EMT and epithelial wound closure. This study potentially highlights a novel crosstalk pathway between WNT5a-TGF-β1 as a possible epithelial repair mechanism employed in asthma that warrants further molecular and functional characterisation.
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Tiklová, Katarína. "Airway maturation in Drosophila." Doctoral thesis, Stockholms universitet, Wenner-Grens institut, 2011. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-62419.
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Tubes are a fundamental unit of organ design. Most of our major organs like the lung, kidney and vasculature are composed primarily of tubes. To identify fundamental biological principles of tubular organ formation we used the respiratory organ of Drosophila melanogaster, the trachea.This work dissects embryonic trachea maturation. Three precise epithelial transitions occur during airway maturation. A secretion burst deposits proteins into the lumen; then luminal material is cleared and finally liquid is removed. We identified the cellular mechanisms behind these transitions. Sar1 and γCOP are required for protein secretion, matrix assembly and tube expansion. Rab5-dependent endocytic activity internalizes and clears luminal contents. The data show how programmed transitions in cellular activities form functional airways, and may reflect a general mechanism in respiratory organ morphogenesis.We further focused on tube size regulation. We identified Melanotransferrin, a new component of septate junctions that limits tracheal tube elongation. MTf is a lipid- modified, iron-binding protein attached to epithelial cell membranes, similarly to its human homologue. We show that septate junction assembly during epithelial maturation relies on endocytosis and apicolateral recycling of iron-bound MTf. Mouse MTf complements the defects of Drosophila MTf mutants. This provides the first genetic model for the functional dissection of MTf in epithelial morphogenesis. In the last part, we describe two genes, which are selectively involved in tube diameter expansion. Obst-A and Gasp are closely related proteins with characteristic chitin-binding domains. They are strongly expressed in the trachea at the time of lumen expansion. The single and double mutants cause a tube diameter reduction, whereas their overexpression leads to its increase. We propose that Obst-A and Gasp organize luminal matrix assembly and thereby regulate the extent of tube diameter expansion.At the time of the doctoral defense, the following paper was unpublished and had a status as follows: Paper 4: Manuscript.
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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.
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Asthma management places significant financial demands on health services. With increased understanding of the mediators involved in asthma pathophysiology more specific agents could be developed for treatment. We studied the effects of oxidant injury- on adult asthmatic cells in vitro and showed asthmatic epithelium more susceptible to oxidative stress at high concentrations of hydrogen peroxide. Cell death occurred via caspase independent apoptosis. However, at lower doses of hydrogen peroxide proliferation was observed suggesting a biphasic response. We investigated levels of Matrix Metalloproteinase-9 (MMP-9) and its inhibitor Tissue Inhibitor of Matrix Metalloproteinase-1 (TIMP-1) in the induced sputum, bronchial wash and bronchoalveolar lavage fluid (BALF) of adult asthmatics and their correlation to- their respective immunostaining in bronchial biopsies. Bronchoalveolar lavage fluid in asthmatics demonstrates significantly raised TIMP-1 levels suggesting derangement in extracellular matrix turnover. Involvement of TIMP-1 in asthma pathophysiology is further supported by the finding that TIMP-1 immunostaining correlated with markers of asthma severity. In contrast no such relationship was observed with MMP-9, suggesting an imbalance between MMP-9 and TIMP-1 may be important in remodelling 'of the airway in asthma. Increased Epithelial Growth Factor (EGF) staining was observed within the basal • controls. However, no difference in EGF levels between asthmatics and controls in epithelial layer and in submucosal macrophages of asthmatics compared to either BALF or bronchial wash was found. In the 'asthmatic subjects studied response. In conclusion, this data suggests the epithelial response to increased Epithelial Growth Factor Receptor (EGFR) correlated positively with PC20 suggesting that in mild asthma increased EGFR represents an appropriate repair EGFR expression in mild asthma appears appropriate. In summary, asthmatic bronchial epithelium demonstrates an altered response to oxidative stress. This thesis further supports the evidence for abnormal epithelial cell response in asthma to oxidative stress and an imbalance in matrix turnover in the asthmatic airway.
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IJpma, Gijs. "Airway smooth muscle dynamics." AUT University, 2010. http://hdl.handle.net/10292/941.
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The current study aims to investigate the relative contributions of each of the processes that govern airway smooth muscle mechanical behaviour. Studies have shown that breathing dynamics have a substantial effect on airway constriction in healthy and diseased subjects, yet little is known about the dynamic response of the main instigator of airway constriction, Airway Smooth Muscle (ASM). In this work several models are developed to further the understanding of ASM dynamics, particularly the roles and interactions of the three dominant processes in the muscle: contractile dynamics, length adaptation and passive dynamics. Three individual models have been developed, each describing a distinct process or structure within the muscle. The first is a contractile model which describes the contractile process and the influence of external excitation on contractile behaviour. The second model incorporates the contractile model to describe length adaptation, which includes the reorganisation and polymerisation of contractile elements in response to length changes. The third model describes the passive behaviour of the muscle, which entails the mechanical behaviour of all non-contractile components and processes. As little data on the passive dynamics of the muscle was available in the literature, a number of experiments were conducted to investigate relaxed ASM dynamics. The experimental data and mathematical modelling showed that passive dynamics plays not only a dominant role in relaxed ASM, but contributes considerably to the dynamics of contracted muscle as well. A novel theory of sequential multiplication in passive ASM is proposed and implemented in a mathematical model. Experiments and literature validated the model simulations. Further integration of the models and improved force control modelling of length adaptation is proposed for future study. It is likely that the coupling of the models presented here with models describing other airway wall components will provide a more complete picture of airway dynamics, which will be invaluable for understanding respiratory disease.
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Reale, Riccardo. "Microfluidic airway on-chip." Thesis, University of Southampton, 2017. https://eprints.soton.ac.uk/420762/.
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Organs-on-chip are a new class of in vitro devices aimed at improving the predictivity of preclinical drug testing models by integrating physiologically relevant features in cell culture devices using microfabrication techniques. In human bodies, epithelial tissues are the first line of defence against the external environment and act as barriers by expressing inter-cellular protein complexes called tight junctions (TJ). The epithelial physical barrier has selective permeability properties which can experimentally be measured by electrical means. In this thesis, the design, simulation, modelling, optimisation, fabrication and experimental characterisation of a novel organ-on-chip device for epithelial cell culture and epithelial barrier monitoring are described. In the device, cells are cultured on top of a nanoporous support, fed by constant perfusion of growth medium and barrier properties are monitored in real-time with integrated coplanar Pt/Pt-black electrodes. Finite element method (FEM) simulations were used to develop a new coplanar electrode design which achieved greater sensitivity (45-fold) compared to the other coplanar designs presented in the literature. This design was formed by 2 circular segments electrodes divided by a polymeric septum. The high sensitivity of the novel electrode design enabled the measurement of epithelial electrical properties directly at the air-liquid interface (ALI) and was used to monitor disruptions in the barrier properties of primary bronchial epithelial cells (PBECs) cultured on commercial supports (Transwell®) induced by a calcium chelator (EGTA). The measured barrier disruption was comparable to those measured by standard systems without requiring a submerged culture. The microfluidic device was used to monitor the establishment of the physical barrier under submerged conditions for 6 days of the human bronchial epithelial cell line (16HBE14o-) and disruption of the physical barrier induced by stimulation with a viral mimic (poly(I:C)). All results were comparable to the ones measured by standard systems. This platform is an easy-to-manufacture alternative to available systems with the unique potential to enable the real-time epithelial barrier monitoring under submerged or ALI conditions.
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Kottyan, Leah Claire. "Airway Acidification in Asthma." University of Cincinnati / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1280778640.
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Crump, Gwyn N. "Caffeine and airway resistance." [Tampa, Fla.] : University of South Florida, 2004. http://purl.fcla.edu/fcla/etd/SFE0000559.
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Crump, Gwyn N. M. D. "Caffeine and Airway Resistance." Scholar Commons, 2004. https://scholarcommons.usf.edu/etd/1002.
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This study investigated the effect of caffeine on airway resistance. The subjects were drawn from volunteers (18-90 years old) in good health, with no major cardiopulmonary conditions.
We found no association between the consumption of a single cup of the caffeinated beverage coffee and a decrease in airway resistance within one hour in a normal sample of subjects as measured by impulse oscillometry nor with conventional spirometry . It appears that any possible bronchodilatory effect of the caffeine from a single cup of coffee in a normal population is below the limit of detection of spirometry and impulse oscillometry or is not sufficiently expressed in the one hour time frame of the study.
The study did validate currently accepted methods of using the Jaeger impulse oscillometry (IOS) measurement for use at the University of South Florida (USF). The impulse oscillometry technique was found to be a useful adjunct to conventional pulmonary function testing. Conventional pulmonary function testing provides a useful measure of a person's ability to breathe yet is difficult to perform and only indirectly guides the physician to the diagnosis of the pathology behind the person's breathing difficulties. The impulse oscillometry technique may help the physician to noninvasively determine the location of a pulmonary obstruction by measurement of the dynamics of sound wave travel through the airways of the lungs.
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Boustany, Sarah. "Mechanisms of Airway Remodelling." Thesis, The University of Sydney, 2008. http://hdl.handle.net/2123/3577.
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Asthma 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.
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Boustany, Sarah. "Mechanisms of Airway Remodelling." University of Sydney, 2008. http://hdl.handle.net/2123/3577.
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Doctor of Philosophy (PhD)Asthma 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.
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Noble, Peter Beresford. "Regulation of airway narrowing by dynamic and static mechanical loads." University of Western Australia. School of Biomedical and Chemical Sciences, 2006. http://theses.library.uwa.edu.au/adt-WU2006.0050.
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[Truncated abstract] The extent to which an airway narrows is strongly influenced by mechanical loads on airway smooth muscle (ASM). This thesis considers both dynamic and static mechanical loads. Dynamic load describes the time varying load on airways produced by oscillatory breathing movements. Static load is that present at a fixed lung volume ie. without breathing. In the intact lung static load principally comprises the pressure across the airway wall, that is transmural pressure (Ptm), and elastic after-load arising from distortion of airway and lung tissue by the narrowing airway. The experiments performed in this thesis were designed to answer several outstanding questions relating to how dynamic and static loads regulate airway narrowing. Dynamic load from breathing movements cyclically stretches ASM, which produces a number of physiological and cellular effects. For example in ASM strips a period of cyclical stretch reduces subsequent ASM contraction. However the response of the whole airway to dynamic load may differ from isolated ASM where non-muscle tissue also contributes. The first aim of this thesis was to characterise the response of the whole airway to dynamic load and determine whether the airway wall modifies the effects produced by ASM length cycling. Static after-loads restrict ASM shortening providing a limit to airway narrowing. Two primary sources of airway wall load include cartilage and the mucosal membrane which contribute to airway compliance. The relative importance of cartilage and mucosa to airway wall compliance and airway narrowing is unclear. ... Results demonstrate that airway narrowing is restricted by Ptm but not by parenchymal elastic after-load. The major findings of this thesis are: (1) dynamic loads produced by breathing movements regulate airway responsiveness through cyclical airway expansion and elongation; (2) the reported effects of cyclical stretch on ASM contraction differs in situ 8 possibly due to modification by one or more biomechanical or physiological properties of the airway wall; (3) parenchymal elastic after-loads, previously thought to be important during bronchoconstriction, do not restrict airway narrowing. Given the absence of an effect of parenchymal elastic after-load on airway narrowing, the static mechanical load on ASM therefore comprises Ptm and airway wall stiffness, with important contributions from cartilage and mucosa depending on lung volume.
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Pascoe, Christopher Daniel. "Mechanical and molecular contribution of airway smooth muscle to airway hyperresponsiveness in asthma." Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/51862.
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This thesis focuses on the mechanical and molecular role of airway smooth muscle (ASM) in asthma with the aim to determine the contribution of ASM to both asthma and airway hyperresponsiveness (AHR). The first three chapters involve studies probing the mechanical properties of tracheal ASM strips and how these may contribute to the development of AHR. They will aim to show that ASM can contribute to AHR without fundamental changes to the tissue. Specifically, the first chapter investigated the ASMs response to force oscillations mimicking breathing maneuvers under levels of activation that induce force adaptation, a phenomenon potentially seen in asthmatics. It shows that force adaptation can persist under conditions that mimic breathing maneuvers and therefore could contribute to AHR and ASM hypercontractility. The second chapter investigated the role of tone in limiting the strain imposed on ASM by breathing maneuvers and the subsequent response of ASM to those strains. The stiffening of muscle in response to agonist precedes force development and acts to decrease the strain applied to the ASM. As strain decreased, the effect on the muscle contractility was blunted. Interestingly, a prior history of oscillations induced a bronchoprotective effect in the strip and caused a two times greater decline in force than would normally be expected by the small strains indicating that prior DIs are effective in limiting the responsiveness of the ASM to agonist. The third chapter investigated whether the ASM is intrinsically responsible for the bronchoprotective effect of deep inspirations (DIs). This study showed that simulated prior DIs can increase the compliance of the muscle to subsequent DIs, and although the effect on a single strip of muscle is small, the effect at the whole lung level may be sufficient to explain the bronchoprotective effect of DIs. The final chapter describes the molecular phenotype of ASM in asthma at both the gene and protein level. Proteins involved in contraction were found not to be significantly altered in asthmatics; however a host of proteins involved in cytoskeletal structure were changed and could explain why asthmatic ASM is stiffer and less responsive to DIs.Medicine, Faculty of
Medicine, Department of
Experimental Medicine, Division of
Graduate
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Sammut, 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/.
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Liu, Jia Clinical School Prince of Wales Hospital Faculty of Medicine UNSW. "Nitric oxide in airway inflammation." Publisher:University of New South Wales. Clinical School - Prince of Wales Hospital, 2009. http://handle.unsw.edu.au/1959.4/43678.
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Exhaled breath condensate (EBC) is a non-invasive method of investigating airway inflammation associated with nitric oxide (NO) and the metabolites nitrite/nitrates (NOx) in diseases such as chronic obstructive pulmonary disease (COPD), but some of the variables affecting the results are unknown. It was hypothesised that 1) EBC would be influenced by lung volumes and the type of EBC collection device; 2) fractional exhaled NO (FENO) and EBC NOx in COPD patients would be altered by smoking and glucocorticosteroids (GCS); 3) cigarette smoke could contribute to the EBC NOx concentration while it may also decrease FENO indirectly by converting airway NO to NOx. It was found that EBC volume was significantly correlated with both tidal volume and minute volume. Comparing four EBC collection devices demonstrated greater efficiency with the ECoScreen?? than siliconised glass tubes or RTube?? but it gave factitiously high NOx levels. Total EBC protein levels over a 10-minute collection were significantly higher using the ECoScreen?? than either glass or RTube?? devices. A cross-sectional study of 96 COPD patients and 80 age-matched control subjects demonstrated that FENO levels in COPD patients were significantly higher than normal subjects when comparing either the combined groups or appropriate two subgroups: ex-smokers and smokers. GCS treatment demonstrated no significant effect on either FENO levels or EBC NOx, but EBC NOx was elevated in smokers. In vitro, cigarette smoke extract (CSE) induced significantly higher NOx and asymmetric dimethylarginine (ADMA) levels in A549 cells when compared with control media. The anti-oxidant, NAC pre-treatment partially reversed the elevated NOx levels but not the ADMA levels. This thesis is the first to report FENO and EBC NOx in COPD patients in an appropriate sample size to be able to evaluate each subgroup, and the increased EBC NOx levels found in smokers in vivo was consistent with the elevated NOx level in response to CSE observed in vitro. These data indicate that smoking-related airway inflammation and activation of the NO pathway are complex with both an increase in ADMA, NO, NOx and may be regulated by oxidative stress rather than the nitric oxide synthase (NOS) pathway.
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Bálint, Tibor Sándor. "Dynamics of the upper airway." Thesis, University of Warwick, 2001. http://wrap.warwick.ac.uk/66409/.
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Fluid—structure interaction problems occur in everyday life, from medicine to aerospace engineering. One of the general questions from the field of bio-engineering is related to the interaction of a flexible cantilevered plate embedded in a channel flow. Further examining this problem, the motivation for the current study is the desire to elucidate the instability mechanisms of the upper airway with a view to understanding the medical conditions of snoring and obstructive sleep apnoea/hypopnea (OSAH). Snoring is caused by fluttering motions of the soft palate. OSAH involves complete or partial blockage of the airway due to a flow-induced collapse of the pharynx and/or large deflections of the soft palate thereby restricting the air flow to the lungs. The present work addresses the interaction of a flexible plate with viscous channel flow at Reynolds numbers up to 1500, which is about half of the typical Reynolds numbers for the maximal inspiratory flow rate of 0.001m3/s. To perform this investigation, a stable numerical simulation methodology for fluid—structure interaction was developed. To this end a computational model is constructed in which the fluid and flexible plate equations are solved concurrently. The Navier-Stokes equations are solved using an explicit finite-element method while the equations of motion of the plate are solved using an implicit finite-difference method; the latter permits plate deformations to evolve without prescription. A rapid mesh generator able to cope with an arbitrarily deforming geometry of the coupled problem has been implemented. Each of the fluid and solid computational elements of the method has been tested against a variety of unit and benchmark cases. The coupled model has then been used to perform a series of numerical simulations. For flow through both (oral and nasal) airways, the palate experiences a flutter-type of instability caused by a phase shift between the pressure difference across the plate and its motion. This yields an irreversible flow of energy into the plate. In contrast, when one airway is blocked, the plate loses its stability essentially due to divergence. In this case, a deformation is amplified because the pressure forces on the plate exceed the restorative structural forces in the plate; the amplification then serves to increase the force imbalance and further deflection growth ensues. Throughout the time series the full coupling method allows for unrestricted interaction between the viscous fluid flow and the flexible cantilevered plate. The computational model developed here holds much promise for the study of real, spatially varying, geometries and temporal variation of the mean flow. Moreover, the methodology can readily be extended to a similar configuration but with flexible channel walls more realistically representing the pharynx.
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Inglis, Timothy J. J. "Colonisation of the ventilated airway." Thesis, University of Southampton, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.259486.
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McIlwaine, Patricia Margaret. "Airway clearance in cystic fibrosis." Thesis, Ulster University, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.625501.
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This thesis overviews and highlights a body of work performed at the BC Children's Hospital, Vancouver, Canada between 1986 and 2013, and involving travel to Belgium, Denmark and the United Kingdom. It is based on five articles published by McIlwaine on research and development in the use of various airway clearance techniques for the treatment of cystic fibrosis, namely: Autogenic Drainage; Positive Expiratory Pressure; Oscillating Positive Expiratory Pressure; and High Frequency Chest Wall Oscillation. The thesis comprises of seven chapters, including the introduction. Chapter 2 presents the physiological evidence and theories to support each technique. Chapter 3 describes various types of airway clearance studies based on the published studies submitted by McIlwaine and discusses barriers and challenges related to each study design. A clinical research pathway for future airway clearance studies is proposed. Chapter 4 examines the use of outcome measures for each stage of the pathway. Chapter 5 is based on the most recent published paper by McIlwaine, and offers an overview on how to optimise designing a multi-centre clinical airway clearance study, identifying challenges and barriers to performing such a study. The work presented in this thesis has contributed to research by furthering an understanding of the physiology upon which various airway clearance techniques are based, as well as providing guidance on the use of appropriate outcome measures. The published papers underlying the thesis have validated the airway clearance techniques of Autogenic Drainage and positive Expiratory Pressure and have in-validated the use of Oscillating PEP using Flutter and High Frequency Chest Wall Oscillation, in the treatment of cystic fibrosis. Outcomes of this work have lead to a change in clinical practice, in Europe and N. America, and have had a direct and positive effect in decreasing the burden of care in people living with cystic fibrosis.
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Marshall, Ian. "Acoustic reflectometry for airway measurement." Thesis, University of Edinburgh, 1993. http://hdl.handle.net/1842/19987.
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Wood, Lorna J. "The role of bone marrow progenitor cells in allergen-induced airway hyperresponsiveness and airway inflammation." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0028/NQ51023.pdf.
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Lee, Lewis On Hang. "Development of Simulation Platform for Oropharyngeal Airway Placement and Design Evaluation of the Bardo Airway." DigitalCommons@CalPoly, 2012. https://digitalcommons.calpoly.edu/theses/901.
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Off-label use of traditional Oropharyngeal Airway (OPA) as a bite-block, and the subsequential procedure of force exertion of the device by physician has caused many cases of patient’s teeth damage and monetary loss, as the patient’s incisors were damaged while clenching on the OPA during an adverse scenario called “Emergency Clenching”. To remedy this harmful situation, Bardo OPA was developed by Dr. Theodore Burdumy. The Bardo airway has unique design to transfer the clenching force from incisor to the molar. However, the Bardo OPA is one-sized, and cannot fit most of the patients like the commonly-used OPAs, such as the Berman and Gudel OPA, which have a spectrum of sizes to ensure fit. In this project, a Computer Assisted Design (CAD) simulation platform was developed to simulate the scenario where OPA is placed in a patient’s oral cavity. CAD – related technique and tools, such as 3D scanner (ScanStudio HD), RapidWorks, SolidWorks and Mimics were utilized to create the models used to construct the platform. The purpose of this platform is to generate data to support the development of additional sizes and other modification to improve the current design of the Bardo OPA. MRI sets of nine (9) patients were obtained and converted into STL mesh models. Berman and Guedel OPA were used as the standard for comparison against the Bardo OPA. It was found that the Bardo OPA was able to fit into all sample patients’ models, while these models were fitted with Berman and Guedel OPA of 70-90mm (Small to medium adult) sizes. It can only be concluded that the Bardo is compatible with these OPA sizes and there was not enough evidence to show the need for additional sizes. Nevertheless, some functional features of the Bardo OPA were found potentially harmful to the patients or ineffective. Three approaches were suggested to improve the design of the Bardo to achieve better safety and efficacy.
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Kleine-Brüggeney, Maren. "A cross-over comparison of the laryngeal mask airway Supreme and the laryngeal mask airway I-gel in a simulated difficult airway scenario in anasthetized patients /." [S.l.] : [s.n.], 2009. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.
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Nilsson, Harriet. "Studies of Tight Junctions and Airway Surface Liquid in Airway Epithelium with Relevance to Cystic Fibrosis." Doctoral thesis, Uppsala universitet, Institutionen för medicinsk cellbiologi, 2009. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-99411.
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Cystic fibrosis (CF) is a multi-organ autosomal recessive disease of fluid-transporting epithelia, due to a mutation in the gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. CFTR is a cAMP-regulated Cl-channel involved in various regulatory processes. Salt and water transport depend on CFTR and the epithelial sodium channel (ENaC), operating in concert with the paracellular pathway through the tight junctions (TJ). The ionic composition of the ASL has been assumed to be altered in CF, resulting in a fatal accumulation of viscous mucus in the airways. ASL samples were collected from tracheal and nasal fluid in normal and transgenic CF mice and from the fluid covering the apical surface of normal bronchial cells (16HBE14o-) and a CF human bronchial cell line (CFBE41o-). Analysis of the elemental content of the ASL was performed by X-ray microanalysis. The ASL contained more Na and Cl in CFTR-deficient or DF508-CFTR-containing cells than in control cells with wild- type CFTR. The relation between osmolarity and TJ permeability was examined by the addition of salt or sugar (295-700 mOsm) to 16HBE14o- cells, where the integrity of TJ was evaluated by transepithelial electrical resistance (TEER) measurements. Studies of interaction between the activity of CFTR, TJ and cytoskeleton were performed in CFBE41o-, plasmid corrected CFBE41o- (CFBE41o pCep4), and 16HBE14o- cells exposed to an inhibitor of CFTR (CFTRinh-172). The TJ were investigated by determining the paracellular permeability to lanthanum ions or with [14C] mannitol. Cytoskeletal changes were evaluated by immunofluorescence. Hyperosmotic stress resulted in opening of TJ. Inhalation of hypertonic salt or sugar solutions may open TJ, leading to enhanced paracellular water transport and increased ASL volume, diluted mucus and enhanced mucociliary clearance. This may explain the beneficial effect of this treatment for CF-patients. In healthy airway epithelial cells, inhibition of CFTR by CFTRinh-172 resulted in an increased TEER, whereas stimulation of CFTR by IBMX/forskolin caused a decrease. The paracellular permeability was inversely proportional to TEER. Immunofluorescence revealed a disorganization of cytoskeletal proteins in CF-cells. These results point toward a possible interaction between the activity of CFTR and TJ protein complex, presumably via the cytoskeleton.
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Blumerich, Celeste Ann. "Comparison of Airway Response in Recurrent Airway Obstruction-Affected Horses Fed Steamed Versus Non-steamed Hay." Thesis, Virginia Tech, 2012. http://hdl.handle.net/10919/43534.
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Recurrent Airway Obstruction (RAO)-affected horses experience bronchoconstriction and airway inflammation in response to inhalation of irritants including hay molds. Steaming hay reduces fungal content, but the effect on the antigenic potential has not been investigated. We tested the hypothesis that RAO-affected horses develop less severe clinical disease when fed steamed versus non-steamed hay and this reduction coincides with decreased hay fungal content.
Six RAO-affected horses in clinical remission were divided in two groups and fed steamed or non-steamed hay for 10 days using a two-way cross-over design. Hay was steamed using a commercial hay-steamer. Clinical assessment was performed daily. Full assessment, including airway endoscopy, tracheal mucous scores and maximal change in pleural pressure, was performed on days 1, 5, and 10. Bronchial fluid sampling and cytology were performed on days 1 and 10. Hay core samples were collected pre- and post-steaming and cultured to determine fungal and bacterial concentrations.
Statistical analysis was based on data distribution and quantity and performed using SAS®. P-value <0.05 was significant.
Steaming significantly decreased the number of bacterial and fungal colony-forming-units in hay. Horses fed non-steamed hay experienced a significant increase in clinical score and a trend towards airway neutrophilia, while parameters were unchanged in horses fed steamed hay. Only horses fed non-steamed hay experienced a significant increase in tracheal mucous score. Horses fed steamed hay gained significantly more weight compared to horses fed non-steamed hay, even though the amount of hay consumed not greater on a dry matter basis.
These results indicate that steaming reduces the RAO-affected horseâ s response to hay which coincides with a reduction in viable fungal content of hay.Master of Science
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Barker, Bethan Louise. "Exploring the interplay between airway bacteria, airway inflammation, lung structure and skeletal muscle dysfunction in COPD." Thesis, University of Leicester, 2017. http://hdl.handle.net/2381/39977.
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Airway bacteria, airway inflammation, lung structure and skeletal muscle dysfunction are all recognised as important components of chronic obstructive pulmonary disease (COPD), yet the interplay between these components is not well understood. Within this thesis I present an observational study exploring relationships between airway inflammation and molecular measures of potentially pathogenic bacteria. I have shown that airway bacterial detection is associated with increased airway inflammation in stable COPD, and that this association appears to be driven by Haemophilus influenzae. I then present a cross-sectional and longitudinal study using dual energy x-ray absorptiometry measurements of body composition and have shown that airway bacterial load and inflammation are independent of body composition changes, and that loss of skeletal muscle is not associated with accelerated airway inflammation or lung function decline. Within a multi-centre exacerbation cohort study I have shown that sputum bacterial load is only weakly associated with quadriceps muscle strength in stable COPD. In addition I have shown only a small, short-lived reduction in quadriceps strength at exacerbation, suggesting that community managed exacerbations may have limited impact on long term decline in muscle and physical function in COPD patients. Finally, I present the results of a single centre study that has shown that air trapping measured using quantitative computed tomography (QCT) makes the strongest unique contribution to airflow obstruction in COPD. Moreover, H. influenzae bacterial load is related to QCT measured small airways disease, and this association is independent of the amount of neutrophilic airways inflammation. In summary, within this thesis I provide data demonstrating significant relationships between H. influenzae, airway inflammation and lung structural changes in COPD. By contrast, my findings suggest that inflammation, and in particular overspill of pulmonary inflammation is not a key pathophysiological mechanism leading to skeletal muscle depletion or dysfunction in COPD.
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McConnell, William David. "Mediators of airway remodelling in asthma." Thesis, University of Southampton, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.288445.
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Mulrennan, Siobhain A. "Diagnosis and treatment in airway inflammation." Thesis, University of Hull, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.441682.
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Siva, Roshan. "Modulation of airway inflammation in COPD." Thesis, University of Leicester, 2006. http://hdl.handle.net/2381/4732.
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Inflammation in foregut derivatives outside the lung may contribute to amplification of airway inflammation. I have shown that a management strategy aiming to minimise eosinophilic airway inflammation as well as symptoms is associated with a significant 62% reduction in the frequency of severe exacerbations of COPD. This strategy was associated with no overall increase in corticosteroid treatment; there was evidence that increased corticosteroid therapy was targeted to patients with eosinophilic airway inflammation and benefit was largely confined to these patients. I have shown an association between the sputum differential neutrophil count and airway bacterial load, and showed that a one week course of Levofloxacin significantly reduced both the % neutrophil count and bacterial load in patients with stable state COPD and bacterial load > 106 cfu/ml. I have shown that the prevalence of peptic ulcer disease increases progressively with increasing severity of COPD in miners with homogeneous risk factors for development of COPD, and that peptic ulceration was a strong and independent predictor of a low FEV1 % predicted and FEV1/FVC ratio. In another population I showed that H.Pylori seropositivity was more common in patients with COPD compared to healthy smokers matched for age and occupation.;We have shown that TREM-1 can be measured from induced sputum and is potentially a novel marker of bacterial infection and neutrophilic airway inflammation during exacerbations.;Further work is required to ensure that measurement and modulation of airway inflammation results in improved clinical outcomes, and is made more clinically viable.
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Du, Youhua. "Airway smooth muscle response to vibrations." AUT University, 2006. http://hdl.handle.net/10292/974.
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The main goal of this research was the in vitro investigation of the stiffness response of contracted airway smooth muscles under different external oscillations. Living animal airway smooth muscle tissues were dissected from pig tracheas and stimulated by a chemical stimulus (acetylcholine). These tissues were then systematically excited with different external vibrations. The force change was recorded to reflect the muscle stiffness change under vibration. The static and dynamic stiffness of contracted airway smooth muscles in isometric contraction were determined before, during and after vibrations. A continuum cross-bridge dynamic model (the fading memory model) was modified to accommodate smooth muscle behaviour and dynamically describes the cross-bridge kinetics. A two-dimensional finite element model (FEM) was developed to simulate longitudinal and transverse vibrations of the tissue. An empirical equation, derived from the experiments, is incorporated into the FEM. The results indicate that the stiffness of active smooth muscles can be physically reduced using external vibrations. This reduction is caused by a certain physical position change between actin and myosin. The dynamic stiffness has the tendency of decreasing as the frequency and/or amplitude of external vibration increases. However, the static stiffness decreases with an increase in the frequency and amplitude of excitation until it reaches a critical value of frequency where no variation in stiffness is observed. It is postulated that the tissue elasticity and mass inertia are the main contributors to the dynamic stiffness while the actin-myosin cross-bridge cycling is the main contributor to the static stiffness.
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Kharitonov, Sergei Alexandrovich. "Exhaled nitric oxide in airway diseases." Thesis, Imperial College London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266411.
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Saravanan, Vadivelu. "Small Airway Obstruction in Rheumatoid Arthritis." Thesis, University of Newcastle Upon Tyne, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.519460.
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Bhimrao, Sanjiv Kumar. "Airway structural changes in allergic rhinitis." Thesis, University of Southampton, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.536296.
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Beckett, P. A. "Pharmacology of airway remodelling in asthma." Thesis, University of Cambridge, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.596514.
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Patterson, R. N. "Gut-lung interactions in airway disease." Thesis, Queen's University Belfast, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.419495.
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Cushley, M. J. "Adensoine and airway calibre in man." Thesis, University of Southampton, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233287.
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Herrmann, P. "Tissue engineering of upper airway replacements." Thesis, University College London (University of London), 2016. http://discovery.ucl.ac.uk/1533028/.
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Laryngotracheal diseases cause considerable morbidity and fully functional replacement after extensive surgical resection is still missing. Regenerative medicine has made considerable progress towards clinical transplantation and offers a potentially attractive solution. To date the use of biological scaffolds is considered promising for tissue engineering, providing structural and microbiological support for cell seeding and integration in the host environment. This thesis investigates the possibility of developing a decellularization protocol suitable for the production of upper airway constructs for clinical transplantation. In the first part of this work a new decellularization protocol for tracheal tissue and laryngeal tissue of different species was developed. The novel use of vacuum technology was explored. Resultant biological scaffolds were characterised by assessment of immunogenicity (H&E staining, DNA quantification, immunohistochemistry and biocompatibility) and extra-cellular matrix architecture (histology, quantitative protein assays, SEM) and biomechanical properties. In the following part of this work the resultant porcine laryngeal scaffolds seeded with human epithelial and mesenchymal stem cells were tested in a large animal model in comparison to a synthetic scaffold. Study duration was two months. In vivo assessments included regular endoscopies with cytological brushings, CT scans and blood tests. Post-mortem analysis included histology and immunohistochemistry. The data supported the hypothesis that biological, decellularized scaffolds possess some advantages for laryngeal bioengineering compared to the synthetic scaffold tested in this thesis.
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Schorr, Raphael Avram 1976. "Essays on airport and airway congestion." Thesis, Massachusetts Institute of Technology, 2006. http://hdl.handle.net/1721.1/38246.
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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Civil and Environmental Engineering, 2006.Includes bibliographical references (p. 163-166).
Runway and airspace congestion are the primary causes of flight delays in the US. These delays cost airlines and airline customers billions of dollars per year. This thesis consists of two essays. The first essay focuses on several of the commonly proposed market-based solutions to airport congestion. Most of the literature on these market-based solutions has assumed that these remedies are justified by welfare economics, but there is relatively little focus on these justifications. We explore the economic arguments for and against using various market-based approaches to treating airport congestion. The second essay examines the relationship between aviation infrastructure pricing and congestion. Aviation taxes (and some airport fees) are currently designed to tax large aircraft more than small aircraft and flights with more passengers more than flights with few passengers. Several authors have argued that these taxes and fees create an incentive system for airlines to use small aircraft with high frequency, which exacerbates the congestion problem. We study this effect by developing a game theoretic model of airline behavior.
(cont.) Using this model, we are able to find a pure-strategy Nash equilibrium behavior for any given set of taxes and fees. These equilibrium results allow us to directly test the potential effects of changing the fees and taxes. We propose an alternative system of taxes and airport fees that charges all similar flights equally, regardless of size, revenue, or the number of passengers. We find that adopting these "flat" taxes and landing fees - i.e. aircraft of all sizes pay equal amounts - would have substantial benefits. The model predicts that the change would reduce congestion levels while making air travel more affordable.
by Raphael A. Schorr.
Ph.D.
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Hrousis, Constantine Athanasios 1970. "Computational modeling of asthmatic airway collapse." Thesis, Massachusetts Institute of Technology, 1998. http://hdl.handle.net/1721.1/32692.
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Grainge, Christopher. "Determinants of airway remodelling in asthma." Thesis, University of Southampton, 2010. https://eprints.soton.ac.uk/384164/.
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Amineh, Abbadi. "Hyaluronan Rafts on Airway Epithelial Cells." Cleveland State University / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=csu1407316041.
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