Relevant bibliographies by topics / Airway remodelling

Academic literature on the topic 'Airway remodelling'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Airway remodelling"

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Bergeron, Céline, Meri K. Tulic, and Qutayba Hamid. "Airway Remodelling in Asthma: From Benchside to Clinical Practice." Canadian Respiratory Journal 17, no. 4 (2010): e85-e93. http://dx.doi.org/10.1155/2010/318029.

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Airway remodelling refers to the structural changes that occur in both large and small airways relevant to miscellaneous diseases including asthma. In asthma, airway structural changes include subepithelial fibrosis, increased smooth muscle mass, gland enlargement, neovascularization and epithelial alterations. Although controversial, airway remodelling is commonly attributed to an underlying chronic inflammatory process. These remodelling changes contribute to thickening of airway walls and, consequently, lead to airway narrowing, bronchial hyper-responsiveness, airway edema and mucous hypersecretion. Airway remodelling is associated with poor clinical outcomes among asthmatic patients. Early diagnosis and prevention of airway remodelling has the potential to decrease disease severity, improve control and prevent disease expression. The relationship between structural changes and clinical and functional abnormalities clearly deserves further investigation. The present review briefly describes the characteristic features of airway remodelling observed in asthma, its clinical consequences and relevance for physicians, and its modulation by therapeutic approaches used in the treatment of asthmatic patients.
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Kolahian, Saeed, and Reinoud Gosens. "Cholinergic Regulation of Airway Inflammation and Remodelling." Journal of Allergy 2012 (January 16, 2012): 1–9. http://dx.doi.org/10.1155/2012/681258.

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Acetylcholine is the predominant parasympathetic neurotransmitter in the airways that regulates bronchoconstriction and mucus secretion. Recent findings suggest that acetylcholine regulates additional functions in the airways, including inflammation and remodelling during inflammatory airway diseases. Moreover, it has become apparent that acetylcholine is synthesized by nonneuronal cells and tissues, including inflammatory cells and structural cells. In this paper, we will discuss the regulatory role of acetylcholine in inflammation and remodelling in which we will focus on the role of the airway smooth muscle cell as a target cell for acetylcholine that modulates inflammation and remodelling during respiratory diseases such as asthma and COPD.
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Royce, Simon G., Anna M. Tominaga, Matthew Shen, Krupesh P. Patel, Brooke M. Huuskes, Rebecca Lim, Sharon D. Ricardo, and Chrishan S. Samuel. "Serelaxin improves the therapeutic efficacy of RXFP1-expressing human amnion epithelial cells in experimental allergic airway disease." Clinical Science 130, no. 23 (October 20, 2016): 2151–65. http://dx.doi.org/10.1042/cs20160328.

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We have identified combination cell-based therapies that effectively treat the airway inflammation and airway remodelling (structural changes) that contribute to airway obstruction and related airway hyperresponsiveness in murine chronic allergic airways.
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Chetta, Alfredo, and Dario Olivieri. "Role of Inhaled Steroids in Vascular Airway Remodelling in Asthma and COPD." International Journal of Endocrinology 2012 (2012): 1–6. http://dx.doi.org/10.1155/2012/397693.

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In chronic obstructive airway diseases, such as asthma and chronic obstructive pulmonary disease (COPD), changes in bronchial microvasculature are present in response to inflammatory stimuli. Vascular changes may significantly contribute to airway wall remodelling. Angiogenesis and vascular leakage are prevalent in asthma, while vasodilation and vascular leakage dominate in COPD. An endothelial dysfunction may be present both in asthma and in COPD. Vascular changes may occur simultaneously with the thickening of the airway wall and the narrowing of the bronchial lumen. Consequently, pharmacological control of bronchial vascular remodelling may be crucial for symptom control in asthma and COPD. In asthmatic airways, inhaled steroids can downregulate vascular remodelling by acting on proangiogenic factors. Additionally, studies on combination therapy with long-actingβ2-agonists and inhaled steroids have provided evidence of a possible synergistic action on components of vascular remodelling in asthma. In COPD, there is less experimental evidence on the effect of inhaled steroids on airway microvascular changes. Importantly, vascular endothelial growth factor (VEGF), the most specific growth factor for vascular endothelium, is crucially involved in the pathophysiology of airway vascular remodelling, both in asthma and COPD. The inhibition of VEGF and its receptor may be useful in the treatment of the vascular changes in the airway wall.
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O'Sullivan, Michael J., Thien-Khoi N. Phung, and Jin-Ah Park. "Bronchoconstriction: a potential missing link in airway remodelling." Open Biology 10, no. 12 (December 2020): 200254. http://dx.doi.org/10.1098/rsob.200254.

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In asthma, progressive structural changes of the airway wall are collectively termed airway remodelling. Despite its deleterious effect on lung function, airway remodelling is incompletely understood. As one of the important causes leading to airway remodelling, here we discuss the significance of mechanical forces that are produced in the narrowed airway during asthma exacerbation, as a driving force of airway remodelling. We cover in vitro , ex vivo and in vivo work in this field, and discuss up-to-date literature supporting the idea that bronchoconstriction may be the missing link in a comprehensive understanding of airway remodelling in asthma.
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Royce, Simon G., Amelia Sedjahtera, Chrishan S. Samuel, and Mimi L. K. Tang. "Combination therapy with relaxin and methylprednisolone augments the effects of either treatment alone in inhibiting subepithelial fibrosis in an experimental model of allergic airways disease." Clinical Science 124, no. 1 (September 7, 2012): 41–51. http://dx.doi.org/10.1042/cs20120024.

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Although CSs (corticosteroids) demonstrate potent effects in the control of airway inflammation in asthma, many patients continue to experience symptoms and AHR (airway hyper-responsiveness) despite optimal treatment with these agents, probably due to progressive airway remodelling. Identifying novel therapies that can target airway remodelling and/or airway reactivity may improve symptom control in these patients. We have demonstrated previously that the anti-fibrotic hormone RLN (relaxin) can reverse airway remodelling (epithelial thickening and subepithelial fibrosis) and AHR in a murine model of AAD (allergic airways disease). In the present study, we compared the effects of RLN with a CS (methylprednisolone) on airway remodelling and AHR when administered independently or in combination in the mouse AAD model. Female mice at 6–8 weeks of age were sensitized and challenged to OVA (ovalbumin) over a 9-week period and treated with methylprednisolone, RLN, a combination of both treatments or vehicle controls. Methylprednisolone was administered intraperitoneally on the same day as nebulization for 6 weeks, whereas recombinant human RLN-2 was administered via subcutaneously implanted osmotic mini-pumps from weeks 9–11. RLN or methylprednisolone alone were both able to significantly decrease subepithelial thickness and total lung collagen deposition; whereas RLN but not methylprednisolone significantly decreased epithelial thickness and AHR. Additionally, combination therapy with CS and RLN more effectively reduced subepithelial collagen thickness than either therapy alone. These findings demonstrate that RLN can modulate a broader range of airway remodelling changes and AHR than methylprednisolone and the combination of both treatments offers enhanced control of subepithelial fibrosis.
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Wang, Kimberley C. W., Timothy D. Le Cras, Alexander N. Larcombe, Graeme R. Zosky, John G. Elliot, Alan L. James, and Peter B. Noble. "Independent and combined effects of airway remodelling and allergy on airway responsiveness." Clinical Science 132, no. 3 (February 2, 2018): 327–38. http://dx.doi.org/10.1042/cs20171386.

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Airway remodelling and allergic inflammation are key features of airway hyperresponsiveness (AHR) in asthma; however, their interrelationships are unclear. The present study investigated the separate and combined effects of increased airway smooth muscle (ASM) layer thickness and allergy on AHR. We integrated a protocol of ovalbumin (OVA)-induced allergy into a non-inflammatory mouse model of ASM remodelling induced by conditional and airway-specific expression of transforming growth factor-α (TGF-α) in early growth response-1 (Egr-1)-deficient transgenic mice, which produced thickening of the ASM layer following ingestion of doxycycline. Mice were sensitised to OVA and assigned to one of four treatment groups: Allergy – normal chow diet and OVA challenge; Remodelling – doxycycline in chow and saline challenge; Allergy and Remodelling – doxycycline in chow and OVA challenge; and Control – normal chow diet and saline challenge. Airway responsiveness to methacholine (MCh) and histology were assessed. Compared with the Control group, airway responsiveness to MCh was increased in the Allergy group, independent of changes in wall structure, whereas airway responsiveness in the Remodelling group was increased independent of exposure to aeroallergen. The combined effects of allergy and remodelling on airway responsiveness were greater than either of them alone. There was a positive relationship between the thickness of the ASM layer with airway responsiveness, which was shifted upward in the presence of allergy. These findings support allergy and airway remodelling as independent causes of variable and excessive airway narrowing.
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Redington. "Fibrosis and airway remodelling." Clinical & Experimental Allergy 30 (June 2000): 42–45. http://dx.doi.org/10.1046/j.1365-2222.2000.00096.x.

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Boulet, L.-P., and P. J. Sterk. "Airway remodelling: the future." European Respiratory Journal 30, no. 5 (November 1, 2007): 831–34. http://dx.doi.org/10.1183/09031936.00110107.

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Lloyd, C. M., and D. S. Robinson. "Allergen-induced airway remodelling." European Respiratory Journal 29, no. 5 (May 1, 2007): 1020–32. http://dx.doi.org/10.1183/09031936.00150305.

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Dissertations / Theses on the topic "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.

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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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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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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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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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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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Grainge, Christopher. "Determinants of airway remodelling in asthma." Thesis, University of Southampton, 2010. https://eprints.soton.ac.uk/384164/.

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Hilliard, 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.

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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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Zheng, 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.

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Books on the topic "Airway remodelling"

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G, Stewart Alastair, ed. Airway wall remodelling in asthma. Boca Raton: CRC Press, 1997.

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Stewart, A. G. AIRWAY WALL REMODELLING in ASTHMA. Edited by Alastair G. Stewart. CRC Press, 2020. http://dx.doi.org/10.1201/9781003068792.

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Stewart, A. G. Airway Wall Remodelling in Asthma. Taylor & Francis Group, 2020.

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Stewart, A. G. Airway Wall Remodelling in Asthma. Taylor & Francis Group, 2020.

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Stewart, A. G. Airway Wall Remodelling in Asthma. Taylor & Francis Group, 2020.

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Stewart, A. G. Airway Wall Remodelling in Asthma. Taylor & Francis Group, 2020.

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Airway Wall Remodelling in Asthma (Handbooks in Pharmacology and Toxicology). Informa Healthcare, 1996.

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(Editor), Clive Page, and Judith Black (Editor), eds. Airways and Vascular Remodelling in Asthma and Cardiovascular Disease: Implications for Therapeutic Intervention. Academic Press, 1994.

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Book chapters on the topic "Airway remodelling"

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Pelaia, Girolamo, Alessandro Vatrella, and Rosario Maselli. "Airway Remodelling in Asthma." In Asthma: Targeted Biological Therapies, 17–25. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-46007-9_3.

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Holgate, Stephen T., and Donna E. Davies. "Airways Remodelling." In New Drugs for Asthma, Allergy and COPD, 39–43. Basel: KARGER, 2001. http://dx.doi.org/10.1159/000062126.

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Hiemstra, Pieter S., Xinhui Wu, P. Padmini S. J. Khedoe, and Reinoud Gosens. "The role of altered stem cell function in airway and alveolar repair and remodelling in COPD." In Lung Stem Cells in Development, Health and Disease, 322–39. Sheffield, United Kingdom: European Respiratory Society, 2021. http://dx.doi.org/10.1183/2312508x.10010620.

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Bai, Tony R., Clive R. Roberts, and P. D. Paré. "Airway Remodelling." In Asthma, 475–86. Elsevier, 1998. http://dx.doi.org/10.1016/b978-012079027-2/50108-8.

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James, Alan L. "Relationship Between Airway Wall Thickness and Airway Hyperresponsiveness." In AIRWAY WALL REMODELLING in ASTHMA, 1–27. CRC Press, 2020. http://dx.doi.org/10.1201/9781003068792-1.

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Bradding, Peter, Anthony E. Redington, and Stephen T. Holgate. "Airway Wall Remodelling in the Pathogenesis of Asthma: Cytokine Expression in the Airways." In AIRWAY WALL REMODELLING in ASTHMA, 29–63. CRC Press, 2020. http://dx.doi.org/10.1201/9781003068792-2.

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Li, Xun, and John W. Wilson. "Fibrogenic Cytokines in Airway Fibrosis." In AIRWAY WALL REMODELLING in ASTHMA, 111–38. CRC Press, 2020. http://dx.doi.org/10.1201/9781003068792-4.

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Goldie, Roy G., and Janet M. H. Preuss. "Epithelial Function and Airway Responsiveness." In AIRWAY WALL REMODELLING in ASTHMA, 139–78. CRC Press, 2020. http://dx.doi.org/10.1201/9781003068792-5.

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Panettieri, Reynold A. "Regulation of Growth of Airway Smooth Muscle by Second Messenger Systems." In AIRWAY WALL REMODELLING in ASTHMA, 269–93. CRC Press, 2020. http://dx.doi.org/10.1201/9781003068792-10.

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Stewart, Alastair G., Paul R. Tomlinson, and Leslie Schachte. "Regulation of Airway Smooth Muscle Proliferation by β2-Adrenoceptor Agonists." In AIRWAY WALL REMODELLING in ASTHMA, 295–330. CRC Press, 2020. http://dx.doi.org/10.1201/9781003068792-11.

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Conference papers on the topic "Airway remodelling"

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Kermode, Jessica A., Nathan J. Brown, Kate M. Hardaker, Claude S. Farah, Norbert Berend, Gregory G. King, and Cheryl M. Salome. "Airway Remodelling Increases Ventilation Heterogeneity In Peripheral Airways In Asthma." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a2180.

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Wang, Kimberley, Timothy Le Cras, Alexander Larcombe, Graeme Zosky, Alan James, and Peter Noble. "Transforming growth factor alpha produces airway remodelling and reduces airway distensibility." In ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa386.

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Wilson, Susan, Jonathan Ward, Helen Rigden, Ana Sousa, Julie Corfield, Peter Sterk, K. Fan Chung, et al. "Airway remodelling in the U-BIOPRED severe asthma cohort." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa899.

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Ricciardolo, Fabio L. M., Anna Folino, Vitina Carriero, Michela Bullone, and Michael Pieper. "Cholinergic muscarinic receptors and airway remodelling in severe asthma." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa4402.

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James, A. L., J. Elliot, A. Cairncross, T. Mauad, M. J. Abramson, K. McKay, F. H. Y. Green, and P. B. Noble. "Site-Specific Remodelling of the Airway Smooth Muscle in Asthma." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a4407.

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Sze, Marc, Soraya Utokaparch, John E. McDonough, John Gosselink, W. M. Elliott, Vivien Wong, Don D. Sin, James C. Hogg, and Richard Hegele. "Airway Inflammation And Remodelling In COPD: Relationship To Viral Infections." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a1018.

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Jonigk, Danny, Kais Hussein, Katharina Theophile, Marlene Merk, Lavinia Maegel, Jens Gottlieb, Stefan Fischer, et al. "Aberrant Expression Of Bone Morphogenetic Proteins In Fibrotic Airway Remodelling." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a2083.

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Ierodiakonou, Despo, Dirkje S. Postma, Elizabeth E. Torr, Gerard H. Koppelman, Jorrit Gerritsen, Nick H. Ten Hacken, Wim Timens, H. M. Boezen, Judith M. Vonk, and I. Sayers. "Urokinase Plasminogen Activator Receptor (uPAR) Gene Polymorphisms And Airway Remodelling In Asthma." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a6827.

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Stölting, H., S. A. Walker, F. Puttur, S. Saglani, and C. M. Lloyd. "Epidermal growth factor receptor in airway remodelling during allergic airway disease – divergent roles during early life and adulthood?" In ERS Lung Science Conference 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/23120541.lsc-2021.19.

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Johnson, J. R., and R. E. Bignold. "The Matricellular Protein Periostin Is Produced by Pericytes and Contributes to Airway Wall Remodelling in Allergic Airway Disease." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a3304.

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