Relevant bibliographies by topics / Airway smooth muscle

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Airway smooth muscle'

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

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Journal articles on the topic "Airway smooth muscle"

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Martin, J. G., A. Opazo-Saez, T. Du, R. Tepper, and D. H. Eidelman. "In vivo airway reactivity: predictive value of morphological estimates of airway smooth muscle." Canadian Journal of Physiology and Pharmacology 70, no. 4 (April 1, 1992): 597–601. http://dx.doi.org/10.1139/y92-076.

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Airway responsiveness to methacholine and other bronchoconstrictors is highly variable within and among species. The aim of the experiments in this report was to evaluate the importance of the quantity of airway smooth muscle as a determinant of intra- and inter-species variability in airway responsiveness. To do this we established concentration–response curves to methacholine in a sample of normal guinea pigs as well as in rat, rabbit, and dog. After challenge we excised the lungs for the quantitation of smooth muscle by morphometry. Animals were anesthetized with pentobarbital and mechanically ventilated using a Harvard ventilator. Aerosols of methacholine were administered in progressively doubling concentrations from 0.0625 to 256 mg/mL for a period of 30 s for each concentration. The maximal response, determined from pulmonary resistance (RL), and the concentration of methacholine required to effect 50% of the maximal RL were determined. After provocation testing the lungs were removed and fixed with 10% Formalin. Midsagittal sections and parahilar sections were stained with hematoxylin–phloxine–saffron for microscopic examination of smooth muscle. The images of all airways in the sections were traced using a camera lucida side-arm attachment and digitized using commercial software. The area of the airway wall occupied by smooth muscle was determined and standardized for airway size by dividing it by the square of the epithelial basement membrane length. The variability in airway smooth muscle in the intraparenchymal airways was significantly greater between than within individual guinea pigs (n = 13). This was not true of extraparenchymal airways. There was a significant relationship between the quantity of airway smooth muscle in the intraparenchymal cartilaginous airways and the EC50 but not the maximal value of resistance (Rmax). In contrast there was a statistically significant positive correlation between Rmax and airway smooth muscle for all species. There was also a significant inverse correlation between EC50 and airway smooth muscle for all species. We conclude that airway smooth muscle appears to be an important determinant of inter-animal differences in sensitivity of guinea pigs to aerosolized methacholine. Smooth muscle also appears to be a determinant of interspecies differences in both sensitivity and maximal responses to methacholine.Key words: airways responsiveness, mechanical determinants, limited bronchoconstriction, methacholine, morphometry.
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Dowell, Maria L., Tera L. Lavoie, Julian Solway, and Ramaswamy Krishnan. "Airway smooth muscle." Current Opinion in Pulmonary Medicine 20, no. 1 (January 2014): 66–72. http://dx.doi.org/10.1097/mcp.0000000000000011.

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Mitzner, Wayne. "Airway Smooth Muscle." American Journal of Respiratory and Critical Care Medicine 169, no. 7 (April 2004): 787–90. http://dx.doi.org/10.1164/rccm.200312-1636pp.

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Rodger, I. W. "Airway smooth muscle." British Medical Bulletin 48, no. 1 (1992): 97–107. http://dx.doi.org/10.1093/oxfordjournals.bmb.a072545.

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Stephens, N. L. "Airway Smooth Muscle." Lung 179, no. 6 (December 1, 2001): 333–73. http://dx.doi.org/10.1007/s004080000073.

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Gallos, George, Elizabeth Townsend, Peter Yim, Laszlo Virag, Yi Zhang, Dingbang Xu, Matthew Bacchetta, and Charles W. Emala. "Airway epithelium is a predominant source of endogenous airway GABA and contributes to relaxation of airway smooth muscle tone." American Journal of Physiology-Lung Cellular and Molecular Physiology 304, no. 3 (February 1, 2013): L191—L197. http://dx.doi.org/10.1152/ajplung.00274.2012.

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Chronic obstructive pulmonary disease and asthma are characterized by hyperreactive airway responses that predispose patients to episodes of acute airway constriction. Recent studies suggest a complex paradigm of GABAergic signaling in airways that involves GABA-mediated relaxation of airway smooth muscle. However, the cellular source of airway GABA and mechanisms regulating its release remain unknown. We questioned whether epithelium is a major source of GABA in the airway and whether the absence of epithelium-derived GABA contributes to greater airway smooth muscle force. Messenger RNA encoding glutamic acid decarboxylase (GAD) 65/67 was quantitatively measured in human airway epithelium and smooth muscle. HPLC quantified GABA levels in guinea pig tracheal ring segments under basal or stimulated conditions with or without epithelium. The role of endogenous GABA in the maintenance of an acetylcholine contraction in human airway and guinea pig airway smooth muscle was assessed in organ baths. A 37.5-fold greater amount of mRNA encoding GAD 67 was detected in human epithelium vs. airway smooth muscle cells. HPLC confirmed that guinea pig airways with intact epithelium have a higher constitutive elution of GABA under basal or KCl-depolarized conditions compared with epithelium-denuded airway rings. Inhibition of GABA transporters significantly suppressed KCl-mediated release of GABA from epithelium-intact airways, but tetrodotoxin was without effect. The presence of intact epithelium had a significant GABAergic-mediated prorelaxant effect on the maintenance of contractile tone. Airway epithelium is a predominant cellular source of endogenous GABA in the airway and contributes significant prorelaxant GABA effects on airway smooth muscle force.
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Robinson, Philip, Mitsushi Okazawa, Tony Bai, and Peter Paré. "In vivo loads on airway smooth muscle: the role of noncontractile airway structures." Canadian Journal of Physiology and Pharmacology 70, no. 4 (April 1, 1992): 602–6. http://dx.doi.org/10.1139/y92-077.

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The degree of airway smooth muscle contraction and shortening that occurs in vivo is modified by many factors, including those that influence the degree of muscle activation, the resting muscle length, and the loads against which the muscle contracts. Canine trachealis muscle will shorten up to 70% of starting length from optimal length in vitro but will only shorten by around 30% in vivo. This limitation of shortening may be a result of the muscle shortening against an elastic load such as could be applied by tracheal cartilage. Limitation of airway smooth muscle shortening in smaller airways may be the result of contraction against an elastic load, such as could be applied by lung parenchymal recoil. Measurement of the elastic loads applied by the tracheal cartilage to the trachealis muscle and by lung parenchymal recoil to smooth muscle of smaller airways were performed in canine preparations. In both experiments the calculated elastic loads applied by the cartilage and the parenchymal recoil explained in part the limitation of maximal active shortening and airway narrowing observed. We conclude that the elastic loads provided by surrounding structures are important in determining the degree of airway smooth muscle shortening and the resultant airway narrowing.Key words: elastic loads, tracheal cartilage, airway smooth muscle shortening.
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Jiang, He, Kang Rao, Xueliang Liu, Andrew J. Halayko, Gang Liu, and Newman L. Stephens. "Early changes in airway smooth muscle hyperresponsiveness." Canadian Journal of Physiology and Pharmacology 72, no. 11 (November 1, 1994): 1440–47. http://dx.doi.org/10.1139/y94-208.

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To study asthmatic airway smooth muscle we developed a canine model of ragweed pollen sensitized, airway hyperresponsiveness because of the difficulties in obtaining human tissue. Tracheal and bronchial smooth muscles from sensitized dogs were shown to possess greater ability to shorten and higher maximum shortening velocity (Vo), both of which contribute to the excessive narrowing of airways typical of human asthma. However, maximum force production remained normal, demonstrating the dissociation between the behaviour of shortening and force. Because we found no evidence of inflammation, hypertrophy, or hyperplasia in the sensitized airway smooth muscles, we felt this is a model of early disease and should provide insight into early and perhaps primary pathogenetic mechanisms. Vo is known to be determined by actornyosin ATPase, which in smooth muscle is activated via phosphorylation of the 20-kDa myosin light chain (MLC20) by myosin light chain kinase (MLCK). Therefore, ATPase activity, MLC20 phosphorylation, and MLCK were investigated. Sensitized tracheal and bronchial smooth muscles showed significantly higher ATPase activity, and a higher level of MLC20 phosphorylation, resulting from increased MLCK activity, a consequence of the measured increase in total quantity of MLCK rather than in specific activity. Since MLCK is activated by binding with Ca2+–calmodulin complex, intracellular Ca2+ concentration and calmodulin activity were also assessed, but no difference was found between sensitized and control animals. Our study suggests that increased MLCK quantity may be the cause of airway hyperresponsiveness found in sensitized animals, and future investigation should be focused on depicting the reason for the elevated MLCK.Key words: airway hyperresponsiveness, smooth muscle, biophysics, biochemistry, early asthmatic changes.
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Halayko, Andrew J., and Newman L. Stephens. "Potential role for phenotypic modulation of bronchial smooth muscle ceils in chronic asthma." Canadian Journal of Physiology and Pharmacology 72, no. 11 (November 1, 1994): 1448–57. http://dx.doi.org/10.1139/y94-209.

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Asthma is considered to be a chronic inflammatory disease of the airways and is highlighted by excessive airway narrowing in response to various stimuli. Subepithelial fibrosis and increased airway smooth muscle mass are characteristic pathological features of the disease. Airway remodelling in asthma involves cellular hyperplasia and hypertrophy of bronchial myocytes. Smooth muscle cells from a variety of tissues have been shown to be multifunctional mesenchymal cells capable of expressing considerable phenotypic plasticity in vivo in response to injury and pathological stimuli. The growth response of vascular smooth muscle cells following arterial injury has been fairly well characterized, and it appears many of the chemical mediators responsible are common to the inflamed bronchi seen in asthmatics. Specific studies regarding the effects of phenotypic modulation of airway smooth muscle and the potential contribution of this phenomenon to the pathogenesis of chronic asthma have not been carried out. Limited evidence, some indirect, suggests that contractile properties of smooth muscle from inflamed tissues are altered; if this is the case in asthma, then considerations of the effects of airway smooth muscle hypertrophy should be broadened beyond that of only contributing to bronchial hyperresponsiveness via an increase in bronchial wall thickness. Recruitment and modulation of smooth muscle cells to functionally different phenotypes, which contribute to fibrosis by secreting extracellular matrix materials and promote cellular hyperplasia by producing growth factors, are known to occur in atherogenic blood vessels; and evidence suggests that airway smooth muscle cells might play a similar role in asthma. We report the identification of markers of differentiation for airway smooth muscle cells. These markers should be useful tools in the elucidation of phenotypic heterogeneity of smooth muscle in asthmatic airways and, thereby, allow for the definition of a clearer role for bronchial smooth muscle cells in the pathogenesis of chronic asthma.Key words: airway smooth muscle cells, asthma, phenotype, pathogenesis, proliferation.
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Pascoe, C. D., L. Wang, H. T. Syyong, and P. D. Paré. "A Brief History of Airway Smooth Muscle’s Role in Airway Hyperresponsiveness." Journal of Allergy 2012 (October 18, 2012): 1–8. http://dx.doi.org/10.1155/2012/768982.

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A link between airway smooth muscle (ASM) and airway hyperresponsiveness (AHR) in asthma was first postulated in the midnineteenth century, and the suspected link has garnered ever increasing interest over the years. AHR is characterized by excessive narrowing of airways in response to nonspecific stimuli, and it is the ASM that drives this narrowing. The stimuli that can be used to demonstrate AHR vary widely, as do the potential mechanisms by which phenotypic changes in ASM or nonmuscle factors can contribute to AHR. In this paper, we review the history of research on airway smooth muscle’s role in airway hyperresponsiveness. This research has ranged from analyzing the quantity of ASM in the airways to testing for alterations in the plastic behavior of smooth muscle, which distinguishes it from skeletal and cardiac muscles. This long history of research and the continued interest in this topic mean that the precise role of ASM in airway responsiveness remains elusive, which makes it a pertinent topic for this collection of articles.
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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.

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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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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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Chin, Leslie Yee Mann. "Airway smooth muscle in health and disease." Thesis, University of British Columbia, 2010. http://hdl.handle.net/2429/27650.

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This thesis focuses on the structure and function of airway smooth muscle (ASM) in health and disease. By employing the use of structural analysis by electron microscopy, functional analysis by mechanical measurements, and biochemical analysis, this thesis provides valuable insight into ASM pathophysiology. The first two chapters focus on the mechanisms by which the contractile apparatus is arranged within the cell. The studies examined whether the actin filament lattice acts a scaffold to facilitate myosin filament assembly within contractile units and the contractile response to potassium chloride (KCl). The muscle was treated with cytochalasin D (CD), a known actin filament disrupter, but this provided little insight on whether the actin lattice guides myosin filament assembly, since CD had a limited effect on actin filaments but a significant effect on force. KCl was found to cause contraction of similar force to acetylcholine contraction, despite the presence of fewer myosin filaments. KCl likely caused depolymerization of myosin filaments upon activation and allowed for force generation by non-filamentous myosin molecules. In the last two studies, human ASM was sourced from the tracheas of whole lungs donated for medical research. From this tissue source it was shown that, unlike in previous human ASM studies, human muscle is similar to that of other mammalian species and capable of significant isotonic shortening. This finding lends support to the use of animal ASM models as a proxy for human ASM. This also was the first study to examine human ASM in the paradigm of mechanical plasticity, using in situ muscle length as a reference length instead of the traditional Lmax, and was the first to demonstrate length adaptation in human ASM. The mechanical properties of asthmatic ASM were found to differ from those of non-asthmatic ASM at several key measurements. Asthmatic ASM was found to have an altered length-tension relationship, increased passive tension, and maintained force better in response to a mechanical perturbation than non-asthmatic ASM. This last finding provides a possible mechanism by which asthmatic airways are more resistant to the bronchodilating effects of deep inspiration. Force generating capacity, shortening extent and velocity were not different.
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Jia, 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.

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Airway hyperresponsiveness to bronchoconstrictors has been found in asthma and related to the severity of the disease. The factors which result in hyperresponsiveness are not completely understood. A possible mechanism is an imbalance between endogenous bronchoconstrictors and dilators. NO is known to relax tracheal smooth muscle by activating soluble guanylate cyclase and increasing the level of intracellular cyclic guanosine monophosphate (GMP). The first hypothesis tested was that the NO-cyclic GMP-relaxant pathway is involved in the regulation of airway responsiveness. Inhibition of endogenous nitric oxide by N$ sp{ omega}$-nitro-L-arginine (L-NNA) significantly increased airway responsiveness to inhaled methacholine in normoresponsive Lewis rats but less so in hyperresponsiveness Fisher rats. In addition, carbachol increased cyclic GMP levels in tracheal tissues from both strains; this cyclic GMP accumulation in tracheal tissues was also less in Fisher than in Lewis rats and abolished by L-NNA in both strains, indicating that it was mediated by a NO-dependent mechanism. These results suggest that endogenous NO plays a role in regulation of airway responsiveness and contributes to the strain-related difference in airway responsiveness in rats. To investigate the NO-cyclic GMP-relaxant pathway in rat airway, the effect of sodium nitroprusside (SNP, a NO donor) on airway responsiveness to a cholinergic agonist was measured in hyperresponsive Fisher rats and compared with the less responsive Lewis strain. Fisher rats were resistant to SNP as evidenced by less relaxation of carbachol contracted tracheal rings by SNP and less cyclic GMP accumulation induced by SNP in cultured airway smooth muscle cells in Fisher rats compared with Lewis rats, indicating an impaired response to SNP in Fisher airways.
NO is known to be synthesized from L-arginine in a reaction catalyzed by NO synthase (NOS). Liver cytochrome P450 also catalyzes the oxidative cleavage of C=N bonds of compounds containing a -C(NH$ 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.
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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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Lei, 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.

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Airway smooth muscle (ASM) shortening is the key event leading to broncho-constriction. The degree of airway narrowing which occurs with ASM shortening is a function both of the mechanical properties of the airway wall as well as the angle of orientation of ASM. If ASM is oriented very obliquely, ASM shortening would in part be transduced to a change in airway length rather than airway narrowing. Previous reports have suggested that the angle of ASM orientation may be as high as 30$ sp circ.$ To measure ASM orientation we have developed a technique based on en-face dissection. The lungs from 4 cats and one human were fixed with 10% buffered formalin at 25 cmH$ sb2$O for 48 hrs. The airway generations 4 to 17 were dissected out from the left lower lobes. Each airway generation was individually embedded in paraffin from which 5$ mu$m thick serial sections were cut parallel to the airway long axis ("en-face") and stained with haematoxylin-phloxine-saffron. Each block yielded 3-5 sections in which the orientation of ASM nuclei relative to the airway long axis ($ theta$) was measured as an index of ASM orientation. $ theta$ was measured clockwise and counterclockwise to the short axis by using a digitizing tablet and a light microscope (X250) equipped with a drawing tube attachment. Inspection of the sections revealed extensive ASM crisscrossing without a homogeneous orientation. Between 29 and 102 nuclei were measured per generation. Although there was considerable variation within airway generations, $ theta$ clustered between $-$20$ sp circ$ and 10$ sp circ$ in all generations and did not vary significantly between generations in any of the subjects. When $ theta$ was converted to an acute angle without regard to sign($ Theta$), the mean angle was 12-13$ sp circ$ both in cat and the human lung. (Abstract shortened by UMI.)
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Le, 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.

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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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Lau, Justine Y. "Novel genes associated with airway smooth muscle proliferation in asthma." Connect to full text, 2008. http://hdl.handle.net/2123/5134.

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Thesis (Ph. D.)--University of Sydney, 2009.
Title 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.
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Books on the topic "Airway smooth muscle"

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Coburn, Ronald F. Airway Smooth Muscle in Health and Disease. Boston, MA: Springer US, 1989.

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Chung, Kian Fan, ed. Airway Smooth Muscle in Asthma and COPD. Chichester, UK: John Wiley & Sons, Ltd, 2008. http://dx.doi.org/10.1002/9780470754221.

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Coburn, Ronald F., ed. Airway Smooth Muscle in Health and Disease. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0779-2.

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Wang, Yong-Xiao, ed. Calcium Signaling In Airway Smooth Muscle Cells. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-01312-1.

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Workshop on Airway Smooth Muscle (1983 Bethesda, Md.). Report of Workshop on Airway Smooth Muscle, September 25-27, 1983. [Bethesda, Md.?]: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, 1985.

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National Institutes of Health (U.S.), ed. Report of Workshop on Airway Smooth Muscle, September 25-27, 1983. [Bethesda, Md.?]: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, 1985.

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Cook, Stephen John. Studies of agonists at b-adrenoreceptors acting on airway smooth muscle. Manchester: University of Manchester, 1993.

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Raeburn, David, and Mark A. Giembycz, eds. Airways Smooth Muscle. Basel: Birkhäuser Basel, 1994. http://dx.doi.org/10.1007/978-3-0348-7558-5.

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Raeburn, David, and Mark A. Giembycz, eds. Airways Smooth Muscle: Development, and Regulation of Contractility. Basel: Birkhäuser Basel, 1994. http://dx.doi.org/10.1007/978-3-0348-7408-3.

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Raeburn, David, and Mark A. Giembycz, eds. Airways Smooth Muscle: Modelling the Asthmatic Response In Vivo. Basel: Birkhäuser Basel, 1996. http://dx.doi.org/10.1007/978-3-0348-9000-7.

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Book chapters on the topic "Airway smooth muscle"

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Knox, A. J., and A. E. Tattersfield. "Airway Smooth Muscle." In Handbook of Experimental Pharmacology, 405–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-642-78920-5_11.

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Stewart, Alastair G., Darren J. Fernandes, Valentina Koutsoubos, Aurora Messina, Claire E. Ravenhall, Ross Vlahos, and Kai-Feng Xu. "Airway smooth muscle cells." In Cellular Mechanisms in Airways Inflammation, 263–302. Basel: Birkhäuser Basel, 2000. http://dx.doi.org/10.1007/978-3-0348-8476-1_10.

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Halayko, Andrew J., and Pawan Sharma. "Airway Smooth Muscle Cells." In Inflammation and Allergy Drug Design, 163–71. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444346688.ch12.

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Hogg, James C. "Airway Hyperreactivity." In Airway Smooth Muscle in Health and Disease, 267–76. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0779-2_13.

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Rodger, I. W., and R. C. Small. "Pharmacology of Airway Smooth Muscle." In Pharmacology of Asthma, 107–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-75855-3_4.

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Jacoby, David B., and Jay A. Nadel. "Airway Epithelial Metabolism and Airway Smooth Muscle Hyperresponsiveness." In Airway Smooth Muscle in Health and Disease, 237–66. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0779-2_12.

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Coburn, Ronald F., and Kenji Baba. "Coupling Mechanisms in Airway Smooth Muscle." In Airway Smooth Muscle in Health and Disease, 183–97. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0779-2_10.

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Tomita, Tadao. "Electrical Properties of Airway Smooth Muscle." In Airway Smooth Muscle in Health and Disease, 151–67. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0779-2_8.

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Kotlikoff, Michael I. "Ion Channels in Airway Smooth Muscle." In Airway Smooth Muscle in Health and Disease, 169–82. Boston, MA: Springer US, 1989. http://dx.doi.org/10.1007/978-1-4613-0779-2_9.

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Su, Yunchao. "Airway Smooth Muscle Malfunction in COPD." In Calcium Signaling In Airway Smooth Muscle Cells, 441–57. Cham: Springer International Publishing, 2013. http://dx.doi.org/10.1007/978-3-319-01312-1_25.

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Conference papers on the topic "Airway smooth muscle"

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Jansen, Sepp R., Marieke van Ziel, Hoeke A. Baarsma, and Reinoud Gosens. "²-catenin Regulates Airway Smooth Muscle Contraction." 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.a5292.

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Ijpma, G., A. M. Al-Jumaily, and G. C. Sieck. "Logarithmic Superposition in Airway Smooth Muscle Dynamics." In ASME 2010 International Mechanical Engineering Congress and Exposition. ASMEDC, 2010. http://dx.doi.org/10.1115/imece2010-38214.

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Abstract:
Airway smooth muscle contraction is the main driving mechanism in asthma. However, in the dynamic environment of the ASM passive dynamics play an important role. The main aim of this research is to investigate the relative contribution of passive dynamics to ASM tissue dynamics and to characterize this behavior. The major finding of this study is the ability of the principle of logarithmic superposition to describe a wide range of dynamic behavior in relaxed (unstimulated) ASM and to a lesser extend in contracted ASM. The ability of this model to describe the force response to length oscillations in contracted muscle shows that cross-bridge cycling in ASM when fully contracted is not affected by oscillations. We hypothesize that this could be caused either by a very slow cross-bridge cycling rate, or by a large degree of non-contractile cross-linking which results in a greatly increased passive force.
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Chin, LY, Y. Bosse, PD Pare, and CY Seow. "Myosin Filament Assembly in Airway Smooth Muscle." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2063.

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Matusovsky, Oleg S., Emily Nakada, Linda Kachmar, Elizabeth D. Fixman, and Anne-Marie Lauzon. "Sensitized Splenocytes Promote Airway Smooth Muscle Contractility." 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.a3578.

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Bos, Isabella Sophie T., Hoeke A. Baarsma, Andrew J. Halayko, and Reinoud Gosens. "Functional Wnt Signaling In Airway Smooth Muscle." 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.a2126.

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Pascoe, Chris, Leslie Chin, Ynuk Bossé, Tillie-Louise Hackett, Peter Pare, and Chun Seow Seow. "Mechanical Properties Of Asthmatic Airway Smooth Muscle." 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.a1253.

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Zavaletta, Vanessa, philippe F. delmotte, Michael A. Thompson, Christina M. Pabelick, Y. S. Prakash, and Gary Sieck. "Mitochondrial Kinetics In Human Airway Smooth Muscle." 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.a2535.

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Béland, Marianne, Yuki Sumi, Saleh Al Muhsen, Hamdan Al Jahdali, Qutayba Hamid, and Rabih Halwani. "Eosinophils Enhance Airway Smooth Muscle Cell Proliferation." 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.a2581.

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Zeki, A. A., R. A. Lu, X. Ai, K. Chmiel, R. Krishnan, and C. Ghosh. "Inhaled Pitavastatin Reduces Airway Smooth Muscle Contraction." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2840.

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Chen, Chun, Xiaozhu Huang, Makoto Kudo, Hiromi Takano, and Dean Sheppard. "Integrin Alpha9beta1 Ligation Inhibits Airway Smooth Muscle Contraction And In Vivo Airway Responsiveness By Modulating Local Polyamine Catabolism In Airway Smooth Muscle." 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.a1276.

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