Dissertations / Theses on the topic 'Airway smooth muscle'
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IJpma, Gijs. "Airway smooth muscle dynamics." AUT University, 2010. http://hdl.handle.net/10292/941.
Full textDu, Youhua. "Airway smooth muscle response to vibrations." AUT University, 2006. http://hdl.handle.net/10292/974.
Full textChin, Leslie Yee Mann. "Airway smooth muscle in health and disease." Thesis, University of British Columbia, 2010. http://hdl.handle.net/2429/27650.
Full textJia, Yanlin. "Nitric oxide and airway smooth muscle responsiveness." Thesis, McGill University, 1995. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=29052.
Full textNO is known to be synthesized from L-arginine in a reaction catalyzed by NO synthase (NOS). Liver cytochrome P450 also catalyzes the oxidative cleavage of C=N bonds of compounds containing a -C(NH$ sb2$)NOH function, producing NO in vitro. We hypothesized that the biosynthesis of NO in airway smooth muscle cells could result from P450 enzymes acting on appropriate substrates. NO can be synthesized in a number of lung cell types. However, to date, no constitutive form of NOS activity has been found in airway smooth muscle cells. We next examined the possibility that airway smooth muscle itself might be able to synthesize NO. Formamidoxime, a compound containing the -C(NH$ sb2$)NOH function, was found to produce NO in cultured airway smooth muscle cells. As well, formamidoxime relaxed pre-contracted trachealis and cyclic GMP accumulation in airway smooth muscle cells in culture. These effects were inhibited by P450 inhibitors but not by NOS inhibitors. Thus, an L-arginine-independent pathway for production of NO was demonstrable in airway smooth muscle cells. This NO production was catalyzed by P450 but not by NOS.
In conclusion, my studies have demonstrated an important role for endogenous NO production in determining the airway responsiveness of normal rats to inhaled cholinergic agonists. This mechanism contributes to strain-related differences in airway responsiveness in the rat.
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.
Full textTao, 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.
Full textLei, Min. "Airway smooth muscle orientation using en-face dissection." Thesis, McGill University, 1995. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=22759.
Full textLe, Jeune Ivan Robert. "Phosphodiesterase 4D5 in human airway smooth muscle cells." Thesis, University of Nottingham, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.408054.
Full textOpazo, 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.
Full textIn 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.
Lau, Justine Y. "Novel genes associated with airway smooth muscle proliferation in asthma." Connect to full text, 2008. http://hdl.handle.net/2123/5134.
Full textTitle from title screen (viewed Aug. 11, 2009) Submitted in fulfilment of the requirements for the degree of Doctor of Philosophy to the Discipline of Pharmacology, Faculty of Medicine. Degree awarded 2009; thesis submitted 2008. Includes bibliographical references. Also available in print form.
Stretton, Colin David. "Neuropeptide interactions with autonomic control of airway smooth muscle." Thesis, Imperial College London, 1990. http://hdl.handle.net/10044/1/46568.
Full textHalayko, Andrew John. "Characterization of determinants of airway smooth muscle cell heterogeneity." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq23606.pdf.
Full textClayton, Robert Alan. "The effect of hypoxia on airway smooth muscle function." Thesis, University of Glasgow, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244358.
Full textGavrila, Adelina. "Modulating steroid insensitive pathways in airway smooth muscle cells." Thesis, University of Leicester, 2016. http://hdl.handle.net/2381/37616.
Full textWhicker, Susan D. "Pharmacological studies of [beta]-adrenoceptors in airway smooth muscle." Thesis, The University of Sydney, 1990. https://hdl.handle.net/2123/26279.
Full textPascoe, 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.
Full textMedicine, Faculty of
Medicine, Department of
Experimental Medicine, Division of
Graduate
Wikström, Jonsson Eva. "Functional characterisation of receptors for cysteinyl leukotrienes in smooth muscle /." Stockholm, 1998. http://diss.kib.ki.se/1998/91-628-2897-5.
Full textDechert, Melissa A. "Signaling through p21-activated kinase 1 in airway smooth muscle /." abstract and full text PDF (UNR users only), 2002. http://0-gateway.proquest.com.innopac.library.unr.edu/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3090865.
Full textRhoden, Kerry J. "Neural and neuropeptide control of airway smooth muscle in vitro." Thesis, Imperial College London, 1990. http://hdl.handle.net/10044/1/46524.
Full textLau, Justine Yeeman, and jlau@med usyd edu au. "Novel genes associated with airway smooth muscle proliferation in asthma." University of Sydney, 2008. http://hdl.handle.net/2123/5134.
Full textIt is well recognised that both genetic and environmental factors determine an individual’s predisposition to asthma. In recent years, the airway smooth muscle (ASM) cell has come to the attention of researchers to, not merely be a contractile cell of the airway, but one that orchestrates events affecting airway remodelling and proliferation. Experiments described in this thesis have, for the first time, examined genes that are associated with various aspects of the pathogenesis of asthma by using the candidate gene approach and a genome wide search. Genes have not only been identified to be differentially expressed in ASM cells derived from asthmatic and non-asthmatic participants, but have also been linked with a functional consequence of asthma. The three genes found to be differentially regulated between ASM cells derived from asthmatic and non-asthmatic participants were Peroxisome Proliferator-Activated Receptor- gamma (PPARγ), mimecan and fibulin-1. Expression of the anti-proliferative transcriptional factor PPARγ, found by the candidate gene approach, was elevated in ASM cells derived from asthmatic participants. Whilst elevated, the anti-proliferative effect of PPARγ was absent in ASM cells derived from asthmatic participants. By microarray analysis, mimecan, an anti-proliferative agent was identified. Mimecan levels, although not different basally in ASM cells, were upregulated by transforming growth factor β (TGFβ) only in asthmatic derived ASM cells. Silencing mimecan, by the use of specific oligonucleotides, increased proliferation of ASM cells. This suggested that by increasing mimecan expression, the proliferation of ASM cells may be halted. Fibulin-1, also found by microarray analysis and the final gene examined in this thesis, was found in elevated levels in BAL fluid, serum and ASM cells obtained from asthmatic participants. In addition, ASM cells derived from asthmatic participants, for the first time were shown to have faster wound healing rates compared with nonasthmatics. The elevated fibulin-1 levels in ASM cells derived from asthmatic participants, in the presence of TGFβ, were demonstrated to contribute to this increased wound healing. Specifically, fibulin-1 was found to affect wound healing by increasing proliferation rather than migration. The current available treatments for asthma, target the contractility and inflammatory conditions in the airway. Through this thesis, novel genes discovered to be associated with proliferation may be potential therapeutic targets to treat asthma. In particular, the fibulin-1 gene is outstandingly promising, as it was shown that silencing fibulin-1 resulted in slower wound healing rates through decreased cell proliferation, to possibly inhibit the airway remodelling observed in asthma, and furthermore, corticosteroid therapy was demonstrated not to affect to this gene.
Binnion, Amy Margaret. "Regulation of chemokine expression in human airway smooth muscle cells." Thesis, University of Nottingham, 2010. http://eprints.nottingham.ac.uk/11344/.
Full textBillington, Charlotte K. "Muscarinic M2 receptor signalling in human airway smooth muscle cells." Thesis, University of Nottingham, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.342489.
Full textKong, Kok Choi. "Sphingosine 1-phosphate signalling in guinea pig airway smooth muscle." Thesis, University of Strathclyde, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248742.
Full textLatourelle, Jeanne C. (Jeanne Catherine) 1976. "Dynamic equilibration of airway smooth muscle length during physiological loading." Thesis, Massachusetts Institute of Technology, 2000. http://hdl.handle.net/1721.1/89295.
Full textComer, Brian S. "Cyclooxygenase-2 expression in asthmatic human airway smooth muscle cells." Thesis, University of South Alabama, 2014. http://pqdtopen.proquest.com/#viewpdf?dispub=3608829.
Full textAsthmatic human airway smooth muscle cells (hASMCs) exhibit enhanced expression of numerous cytokine-responsive genes but this trend has not been observed for cyclooxygenase-2 (COX-2) expression despite knowledge that conserved regulatory mechanisms exist for cytokine-responsive gene expression. Enhanced expression of cytokine-responsive genes in asthmatic hASMCs has been attributed to differences in histone post-translational modifications and microRNA (miR or miRNA) expression. COX-2 expression is of interest because it serves as a model cytokine-responsive gene and is regulated by epigenetic mechanisms. In other cell types, miR-146a represses COX-2 and Interleukin (IL)-1β expression, directly and indirectly, respectively. Due to sequence homology, miR-146b is predicted to repress the expression of COX-2 and IL-1β. I investigated COX-2 expression in asthmatic and non-asthmatic hASMCS treated with cytomix (IL-1β, tumor necrosis factor (TNF)-α, and interferon (IFN)-γ). Also, I chose to compare histone acetylation, transcription factor binding, and miR-146a/b expression in asthmatic and non-asthmatic hASMCs to identify any correlations with COX-2 expression. A major goal of this project was to help identify new treatment targets for asthma therapeutics . I hypothesized that asthmatic hASMCs treated with cytomix express more COX-2 and secrete more prostaglandinE2 (PGE2) than non-asthmatic hASMCs due to differences in COX-2 epigenetic regulation. It is reported here that asthmatic hASMCs treated with cytomix expressed more COX-2 (mRNA/protein), and secreted more PGE2 than non-asthmatic hASMCs. Histone H3/H4 pan-acetylation at the COX-2 promoter did not increase with cytomix treatment and was not different in asthmatic and non-asthmatic hASMCs. Treatment of hASMCs with cytomix increased RNA Polymerase II and nuclear factor-κB binding at the COX-2 promoter with no difference between asthmatic and non-asthmatic hASMCs. Treatment of hASMCs with cytomix increased miR-146a and miR-146b expression with greater miR-146a expression in asthmatic. MiR-146a/b expression in asthmatic hASMCs treated with cytomix did not negatively correlate with COX-2 expression. These results led me to investigate whether miR-146a/b were capable of negatively regulating COX-2 and IL-1β expression in hASMCs. MiR-146a and miR-146b mimics reduced COX-2 and IL-1β mRNA/protein, and PGE2 secretion in hASMCs. MiR-146a and miR-146a/b combination inhibition increased COX-2 and pro-IL-1β protein in hASMCs but not miR-146b inhibition alone. In conclusion, elevated miR-146a expression and histone acetylation are not responsible for increased COX-2 expression in asthmatic hASMCs. MiR-146a is a minor negative regulator of COX-2 and IL-1β expression in hASMCs at physiological expression levels but mimics are capable of antagonizing cytokine-responsive gene expression profoundly. These results coupled with other evidence from the literature indicate that miR-146a/b should be investigated in animal models of asthma to determine if they are relevant asthma drug target in patients that do not respond to current anti-inflammatory therapies.
Norris, Brandon Anthony. "Development and maintenance of force and stiffness in airway smooth muscle." Thesis, University of British Columbia, 2015. http://hdl.handle.net/2429/54875.
Full textMedicine, Faculty of
Medicine, Department of
Experimental Medicine, Division of
Graduate
Pasternyk, Stephanie Marika 1983. "Effect of extracellular matrix and mechanical strain on airway smooth muscle." Thesis, McGill University, 2009. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=111560.
Full textStyhler, Angela. "Proliferative response of airway smooth muscle cells to macrophage-derived products." Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=22812.
Full textJoubert, Philippe. "Expression and function of chemokine receptors on airway smooth muscle cells." Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103385.
Full textFor the first time, this work describes the expression of chemokine receptors by ASMC. We have shown that eotaxin, an important chemokine in asthma, induces migration of ASMC through the activation of CCR3. Although CCR3 expression is not regulated by Th2 cytokines in vitro, ASMC isolated from asthmatic patients expressed intrinsically higher levels of the surface receptor when compared to controls. We also describe the expression of CCR1 by ASMC, a receptor involved in airway remodelling in an animal model of asthma. We reported the expression of CCR1 mRNA in biopsies obtained from mild, moderate and severe asthmatics and showed that mild group express the highest level of CCR1. We also confirmed that ASMC express the receptor in vivo and showed that stimulation of this receptor with its ligands induces intra-cellular calcium mobilization, which confirms its functionality. Regulation of CCR1 on ASMC was also assessed using proinflammatory, Th1 and Th2 cytokines. We found that TNF-alpha and to a lesser extent, IFN-gamma, upregulated CCR1 mRNA and protein expression, while Th2 cytokines had no effect. The effect of these two cytokines was totally suppressed by either dexamethasone or mithramycin.
Collectively, our results demonstrate the expression of functional C-C chemokine receptors by ASMC. Interestingly, we have shown that CCR3 activation mediates ASMC migration and provides a new possible mechanism for the increased smooth muscle mass observed in asthmatic patients. Although the exact function of the CCR1 expressed by ASMC is unknown, our results suggest an involvement in asthma pathogenesis, possibly through airway remodelling.
Woodman, Lucy. "Cellular interactions of airway smooth muscle and human lung mast cells." Thesis, University of Leicester, 2009. http://hdl.handle.net/2381/7382.
Full textSweeney, David. "Human airway smooth muscle cell Ca2+ dynamics in asthma and health." Thesis, University of Leicester, 2011. http://hdl.handle.net/2381/10130.
Full textStocks, Joanne. "The production of soluble angiogenic factors by human airway smooth muscle." Thesis, University of Nottingham, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.430617.
Full textNguyen, Trang Thi Bao. "Modulation of human airway smooth muscle proliferation by the extracellular matrix." Thesis, King's College London (University of London), 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406267.
Full textDarby, Peter James. "Isolation and characterization of caveolae from canine airway and intestinal smooth muscle." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/NQ66199.pdf.
Full textRobins, Stephanie. "The p38 MAPK pathway in human airway smooth muscle: roles in asthma." Thesis, McGill University, 2011. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=97233.
Full textL'asthme est une maladie inflammatoire dont les glucocorticoïdes constituent le principal traitement via le contrôle de la voie p38 MAPK. Les cellules musculaires lisses bronchiques (CLM) jouent un rôle clé dans la physiopathologie de l'asthme notamment dans le remodelage des voies aériennes via leur capacité à proliférer, migrer et sécréter des médiateurs inflammatoires. La stimulation des CLM avec du TNFα entraine une activation des voies MAPK ERK et p38, induisant l'expression des gènes GM-CSF, IL-1β, IL-33 et CXCL8. L'activation de la voie MAPK ERK est importante dans la migration des neutrophiles exposée à du milieu conditionné provenant de CLM stimulées par TNFα via son rôle sur l'expression de CXCL8. En contrepartie, la voie p38 MAPK joue un rôle important dans la migration des CLM en réponse à CXCL12, un chimiokine élevée dans les bronches de patients asthmatiques. Ces résultats ont mis en évidence un rôle important et divergeant des MAPKs dans les CLM dans la pathophysiologie de l'asthme sevère.
Freyer, Anette M. S. "The effect of extracellular matrix on human airway smooth muscle cell phenotype." Thesis, University of Nottingham, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.415554.
Full textCorteling, Randolph Lee. "The role of TRPC channels in human airway smooth muscle cell homeostasis." Thesis, University of Nottingham, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.403290.
Full textMorris, Gavin Edward. "Mechanisms of airway smooth muscle activation by agonists of toll-like receptors." Thesis, University of Sheffield, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.425196.
Full textMcVicker, Clare Geldard. "Calcium influx mechanisms during mediator-induced responses in human airway smooth muscle." Thesis, King's College London (University of London), 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404814.
Full textChang, Po-Jui. "Investigation of corticosteroid responsiveness in airway smooth muscle cells of severe asthma." Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/11590.
Full textInouye, David Shoichi. "Perturbed equilibria of myosin binding in airway smooth muscle and its implications in airway hyperresponsiveness and asthma." Thesis, Massachusetts Institute of Technology, 2000. http://hdl.handle.net/1721.1/9372.
Full text"September 1999."
Includes bibliographical references (leaves 139-145).
In asthma, the key effector driving acute airway narrowing is thought to be airway smooth muscle (ASM); as the muscle surrounding the airways shortens, the airway lumen narrows. Airway hyperresponsiveness (AHR) - the excessive narrowing of the airways - is one of the cardinal features of asthma. Yet, the mechanism(s) regulating the airway lumenal radius, and perhaps the failure of these mechanisms to prevent excessive airway constriction, remains largely unexplained. This thesis shows that the regulation of ASM length corresponds to a dynamically equilibrated steady-state, not the static mechanical equilibrium that had been previously assumed. This dynamic steady state requires as an essential feature a continuous supply of external mechanical energy (derived from tidal lung inflations) that act to perturb the interactions of myosin with actin, drive the molecular state of the system far away from thermodynamic equilibrium, and bias the muscle toward lengthening. This mechanism leads naturally to the suggestion that excessive airway narrowing in asthma may be associated with the destabilization of that dynamic process and its resulting collapse back to static equilibrium. With this collapse the muscle undergoes a phase transition and virtually freezes at its static equilibrium length. This mechanism may help to elucidate several unexplained phenomena including the multi-factorial origins of AHR, how allergen sensitization leads to AHR, and the inability in asthma of deep inspiration to relax ASM.
by David Shoichi Inouye.
Ph.D.
Anaparti, Vidyanand. "Role of N-methyl-D-aspartate receptors in the regulation of human airway smooth muscle function and airway responsiveness." American Physiological Society, 2015. http://hdl.handle.net/1993/30657.
Full textOctober 2015
Hallsworth, Matthew Pearce. "GM-CSF and eosinophil survival in asthma." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341883.
Full textSvensson, Holm Ann-Charlotte B. "Platelets and airway remodeling : Mechanisms involved in platelet-induced fibroblast and airway smooth muscle cell proliferation in vitro." Doctoral thesis, Linköpings universitet, Farmakologi, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:liu:diva-61623.
Full textSwyngedouw, Nicholas Eric. "The influence of interleukin-13 on force generation in airway smooth muscle tissue." Thesis, University of British Columbia, 2016. http://hdl.handle.net/2429/58763.
Full textMedicine, Faculty of
Pathology and Laboratory Medicine, Department of
Graduate
Cavers, Andrew. "Mechanical strain bioreactor design and assessment for culture of human airway smooth muscle." Thesis, University of British Columbia, 2016. http://hdl.handle.net/2429/59236.
Full textApplied Science, Faculty of
Graduate
Wilson, Louise Elizabeth. "Ontogenic changes in porcine pulmonary vascular and airway smooth muscle responsiveness in vitro." Thesis, University of Edinburgh, 1995. http://hdl.handle.net/1842/27700.
Full textWang, Ying. "Phenotypic modulations of cultured canine airway smooth muscle cells and growth-arrested cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ32279.pdf.
Full textMa, Xuefei. "Heterogeneity of airway smooth muscle cells and its implications in pathogenesis of asthma." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp02/NQ32004.pdf.
Full textGhaffar, Omar. "Constitutive and cytokine-stimulated expression of eotaxin by human airway smooth muscle cells." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0024/MQ50776.pdf.
Full text