Academic literature on the topic 'Airway'

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Journal articles on the topic "Airway"

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Farrow, Catherine E., Cheryl M. Salome, Benjamin E. Harris, Dale L. Bailey, Elizabeth Bailey, Norbert Berend, Iven H. Young, and Gregory G. King. "Airway closure on imaging relates to airway hyperresponsiveness and peripheral airway disease in asthma." Journal of Applied Physiology 113, no. 6 (September 15, 2012): 958–66. http://dx.doi.org/10.1152/japplphysiol.01618.2011.

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The regional pattern and extent of airway closure measured by three-dimensional ventilation imaging may relate to airway hyperresponsiveness (AHR) and peripheral airways disease in asthmatic subjects. We hypothesized that asthmatic airways are predisposed to closure during bronchoconstriction in the presence of ventilation heterogeneity and AHR. Fourteen asthmatic subjects (6 women) underwent combined ventilation single photon emission computed tomography/computed tomography scans before and after methacholine challenge. Regional airway closure was determined by complete loss of ventilation following methacholine challenge. Peripheral airway disease was measured by multiple-breath nitrogen washout from which Scond (index of peripheral conductive airway abnormality) was derived. Relationships between airway closure and lung function were examined by multiple-linear regression. Forced expiratory volume in 1 s was 87.5 ± 15.8% predicted, and seven subjects had AHR. Methacholine challenge decreased forced expiratory volume in 1 s by 23 ± 5% and increased nonventilated volume from 16 ± 4 to 29 ± 13% of computed tomography lung volume. The increase in airway closure measured by nonventilated volume correlated independently with both Scond (partial R2 = 0.22) and with AHR (partial R2 = 0.38). The extent of airway closure induced by methacholine inhalation in asthmatic subjects is greater with increasing peripheral airways disease, as measured by ventilation heterogeneity, and with worse AHR.
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Brown, Robert H., Wayne Mitzner, Yonca Bulut, and Elizabeth M. Wagner. "Effect of lung inflation in vivo on airways with smooth muscle tone or edema." Journal of Applied Physiology 82, no. 2 (February 1, 1997): 491–99. http://dx.doi.org/10.1152/jappl.1997.82.2.491.

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Brown, Robert H., Wayne Mitzner, Yonca Bulut, and Elizabeth M. Wagner. Effect of lung inflation in vivo on airways with smooth muscle tone or edema. J. Appl. Physiol. 82(2): 491–499, 1997.—Fibrous attachments to the airway wall and a subpleural surrounding pressure can create an external load against which airway smooth muscle must contract. A decrease in this load has been proposed as a possible cause of increased airway narrowing in asthmatic individuals. To study the interaction between the airways and the surrounding lung parenchyma, we investigated the effect of lung inflation on relaxed airways, airways contracted with methacholine, and airways made edematous by infusion of bradykinin into the bronchial artery. Measurements were made in anesthetized sheep by using high-resolution computed tomography to visualize changes in individual airways. During methacholine infusion, airway area was decreased but increased minimally with increases in transpulmonary pressure. Bradykinin infusion caused a 50% increase in airway wall area and a small decrease in airway luminal area. In contrast to airways contracted with methacholine, the luminal area after bradykinin increased substantially with increases in transpulmonary pressure, reaching 99% of the relaxed area at total lung capacity. Thus airway edema by itself did not prevent full distension of the airway at lung volumes approaching total lung capacity. Therefore, we speculate that if a deep inspiration fails to relieve airway narrowing in vivo, this must be a manifestation of airway smooth muscle contraction and not airway wall edema.
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Sorkness, Ronald L., Kathryn M. Herricks, Renee J. Szakaly, Robert F. Lemanske, and Louis A. Rosenthal. "Altered allergen-induced eosinophil trafficking and physiological dysfunction in airways with preexisting virus-induced injury." American Journal of Physiology-Lung Cellular and Molecular Physiology 292, no. 1 (January 2007): L85—L91. http://dx.doi.org/10.1152/ajplung.00234.2006.

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Although both asthmatics and allergic rhinitics develop an acute inflammatory response to lower airway allergen challenge, only asthmatics experience airway obstruction resulting from chronic environmental allergen exposure. Hypothesizing that asthmatic airways have an altered response to chronic allergic inflammation, we compared the effects of repeated low-level exposures to inhaled Alternaria extract in sensitized rats with preexisting chronic postbronchiolitis airway dysfunction versus sensitized controls with normal airways. Measurements of air space (bronchoalveolar lavage) inflammatory cells, airway goblet cells, airway wall collagen, airway wall eosinophils, airway alveolar attachments, and pulmonary physiology were conducted after six weekly exposures to aerosolized saline or Alternaria extract. Postbronchiolitis rats, but not those starting with normal airways, had persistent increases in airway wall eosinophils, goblet cell hyperplasia in small airways, and loss of lung elastic recoil after repeated exposure to aerosolized Alternaria extract. Despite having elevated airway wall eosinophils, the postbronchiolitis rats had no eosinophils in bronchoalveolar lavage at 5 days after the last allergen exposure, suggesting altered egression of tissue eosinophils into the air space. In conclusion, rats with preexisting airway pathology had altered eosinophil trafficking and allergen-induced changes in airway epithelium and lung mechanics that were absent in sensitized control rats that had normal airways before the allergen exposures.
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Danek, Christopher J., Charles M. Lombard, Donald L. Dungworth, P. Gerard Cox, John D. Miller, Michael J. Biggs, Thomas M. Keast, et al. "Reduction in airway hyperresponsiveness to methacholine by the application of RF energy in dogs." Journal of Applied Physiology 97, no. 5 (November 2004): 1946–53. http://dx.doi.org/10.1152/japplphysiol.01282.2003.

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We delivered controlled radio frequency energy to the airways of anesthetized, ventilated dogs to examine the effect of this treatment on reducing airway narrowing caused by a known airway constrictor. The airways of 11 dogs were treated with a specially designed bronchial catheter in three of four lung regions. Treatments in each of the three treated lung regions were controlled to a different temperature (55, 65, and 75°C); the untreated lung region served as a control. We measured airway responsiveness to local methacholine chloride (MCh) challenge before and after treatment and examined posttreatment histology to 3 yr. Treatments controlled to 65°C as well as 75°C persistently and significantly reduced airway responsiveness to local MCh challenge ( P ≤ 0.022). Airway responsiveness (mean percent decrease in airway diameter after MCh challenge) averaged from 6 mo to 3 yr posttreatment was 79 ± 2.2% in control airways vs. 39 ± 2.6% ( P ≤ 0.001) for airways treated at 65°C, and 26 ± 2.7% ( P ≤ 0.001) for airways treated at 75°C. Treatment effects were confined to the airway wall and the immediate peribronchial region on histological examination. Airway responsiveness to local MCh challenge was inversely correlated to the extent of altered airway smooth muscle observed in histology ( r = −0.54, P < 0.001). We conclude that the temperature-controlled application of radio frequency energy to the airways can reduce airway responsiveness to MCh for at least 3 yr in dogs by reducing airway smooth muscle contractility.
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Noble, P. B., D. J. Turner, and H. W. Mitchell. "Relationship of airway narrowing, compliance, and cartilage in isolated bronchial segments." Journal of Applied Physiology 92, no. 3 (March 1, 2002): 1119–24. http://dx.doi.org/10.1152/japplphysiol.00662.2001.

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Structural components of the airway wall may act to load airway smooth muscle and restrict airway narrowing. In this study, the effect of load on airway narrowing was investigated in pig isolated bronchial segments. In some bronchi, pieces of cartilage were removed by careful dissection. Airway narrowing was produced by maximum electrical field stimulation. An endoscope was used to record lumen narrowing. The compliance of the bronchial segments was determined from the cross-sectional area of the lumen and the transmural pressure. Airway narrowing and the velocity of airway narrowing were increased in cartilage-removed airways compared with intact control bronchi. Morphometric assessment of smooth muscle length showed greater muscle shortening to acetylcholine in cartilage-removed airways than in controls. Airway narrowing was positively correlated with airway compliance. Compliance and area of cartilage were negatively correlated. These results show that airway narrowing is increased in compliant airways and that cartilage significantly loads airway smooth muscle in whole bronchi.
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Naureckas, E. T., C. A. Dawson, B. S. Gerber, D. P. Gaver, H. L. Gerber, J. H. Linehan, J. Solway, and R. W. Samsel. "Airway reopening pressure in isolated rat lungs." Journal of Applied Physiology 76, no. 3 (March 1, 1994): 1372–77. http://dx.doi.org/10.1152/jappl.1994.76.3.1372.

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In a previous modeling study, we predicted that the yield pressure for airway reopening (Pyield) should depend on airway fluid surface tension (gamma) and airway radius (R), according to the relationship Pyield = 8.3 gamma/R. To test this prediction, we studied tantalum bronchograms of isolated perfused rat lungs from three rats by using microfocal X-ray imaging. Thirty-two airways with diameters ranging from 300 to 2,400 microns were recorded as the airways were collapsed and reinflated. Airway pressure was reduced transiently to -40 cmH2O to produce airway closure. Airway pressure was then slowly increased from 0 to 25 cmH2O. In each airway, the observed diameter remained constant until a Pyield was reached; at this pressure, airways were seen to “pop” open, allowing clear identification of airway reopening pressure. When Pyield was plotted against diameter at maximum inflation, the experimental data were in approximate agreement with predictions of Pyield made assuming a gamma of 35 dyn/cm. The close correspondence of the measured values with these predictions suggests that surfactant is present in these airways and facilitates airway reopening.
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Brown, R. H., and W. Mitzner. "Effect of lung inflation and airway muscle tone on airway diameter in vivo." Journal of Applied Physiology 80, no. 5 (May 1, 1996): 1581–88. http://dx.doi.org/10.1152/jappl.1996.80.5.1581.

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How normal airway dimensions change with lung volume is of great importance in determining flow limitation during the normal forced vital capacity maneuver as well as in the manifestation of obstructive lung disease. The literature presents a confusing picture, with some results suggesting that airway diameter increases linearly with the cube root of lung volume and others showing a highly nonlinear relation. The effect of smooth muscle contraction on lung-airway interdependence is even less well understood. Recent morphological work explicitly assumes that airway basement membrane is nondistensible, although the lung volume at which this maximal airway size is reached is unknown. With smooth muscle contraction, folding of the epithelium and basement membrane accounts for the changes in luminal area. In this study, we measured the effect of lung inflation on relaxed and contracted airway areas by using high-resolution computed tomography at different transpulmonary pressures, each held for 2 min. We found that fully relaxed airways are quite distensible up to a pressure of 5-7 cmH2O (P < 0.001), where they reach a maximal size with no further distension up to an airway pressure of 30 cmH2O (P = 0.49). Thus relaxed airways clearly do not expand isotropically with the lung. With smooth muscle tone, the airways in different animals responded differently to lung inflation, with some animals showing minimal airway dilation up to an airway pressure of 20 cmH2O and others showing airways that were more easily dilated with lung expansion. However, maximal diameter of these moderately constricted airways was not usually achieved even up to an airway pressure of 30 cmH2O. Thus a transient deep inspiration in vivo would be expected to have only a small effect on contracted airways.
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Fasano, Mary Beth. "Combined airways: impact of upper airway on lower airway." Current Opinion in Otolaryngology & Head and Neck Surgery 18, no. 1 (February 2010): 15–20. http://dx.doi.org/10.1097/moo.0b013e328334aa0e.

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Zimmermann, Nives, Marc Rothenberg, and Leah Kottyan. "IL-13 is required and sufficient for airway acidification in allergic airway inflammation (141.16)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 141.16. http://dx.doi.org/10.4049/jimmunol.184.supp.141.16.

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Abstract Clinical studies have shown acidification of airways in asthma. Importantly, studies have suggested that acidification contributes to the pathophysiological process. However, the mechanism of acidification is unclear. We developed a novel method for measuring the acidity of mouse airways and demonstrated that mouse airways are acidified during models of allergic airway inflammation. Our studies determined that airway acidification does not develop in IL-13-deficient mice and that IL-13 delivery alone is sufficient to induce airway acidification. There are multiple ways IL-13 could lead to acidification, including direct effects on epithelial cells or through recruitment of inflammatory cells. We demonstrated a partial role for eosinophils in airway acidification as CCR3 and IL-5-deficient mice had decreased extent of airway acidification in allergen-challenged mice. Furthermore, using dimethyl amiloride, a specific inhibitor of the Na+/H+ exchanger, we demonstrated significant inhibition of airway acidification in allergic airway inflammation, suggesting a role for ion (proton) channels. In summary, our studies demonstrate that mouse airways are acidified during allergic airway inflammation. We also showed that the mechanism of airway acidification in asthma involves IL-13-mediated pathways including eosinophils and proton channels. These results have considerable implications for the development of therapies that target airway acidification.
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Brown, Robert H., and Wayne Mitzner. "Airway closure with high PEEP in vivo." Journal of Applied Physiology 89, no. 3 (September 1, 2000): 956–60. http://dx.doi.org/10.1152/jappl.2000.89.3.956.

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When airway smooth muscle is contracted in vitro, the airway lumen continues to narrow with increasing concentrations of agonist until complete airway closure occurs. Although there remains some controversy regarding whether airways can close in vivo, recent work has clearly demonstrated that, if the airway is sufficiently stimulated with contractile agonists, complete closure of even large cartilaginous conducting airways can readily occur with the lung at functional residual capacity (Brown RH and Mitzner W. J Appl Physiol 85: 2012–2017, 1998). This result suggests that the tethering of airways in situ by parenchymal attachments is small at functional residual capacity. However, at lung volumes above functional residual capacity, the outward tethering of airways should increase, because both the parenchymal shear modulus and tethering forces increase in proportion to the transpulmonary pressure. In the present study, we tested whether we could prevent airway closure in vivo by increasing lung volume with positive end-expiratory pressure (PEEP). Airway smooth muscle was stimulated with increasing methacholine doses delivered directly to airway smooth muscle at three levels of PEEP (0, 6, and 10 cmH2O). Our results show that increased lung volume shifted the airway methacholine dose-response curve to the right, but, in many airways in most animals, airway closure still occurred even at the highest levels of PEEP.
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Dissertations / Theses on the topic "Airway"

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Williams, Adele. "Polymeric airway mucins in equine recurrent airway obstruction." Thesis, University of Manchester, 2014. https://www.research.manchester.ac.uk/portal/en/theses/polymeric-airway-mucins-in-equine-recurrent-airway-obstruction(14c6bee5-5406-4b7a-a9b5-495443c7c635).html.

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In healthy airways, mucus forms part of the innate immune response protecting the respiratory epithelium from damage by pathogens and environmental debris (Rose and Voynow, 2006). Conversely, in many respiratory diseases, mucus becomes part of the airway disease pathology. Mucus hypersecretion along with reduced clearance can cause blockage of the small airways, impairing gas exchange, promoting inflammation and becoming a culture medium for bacterial colonisation (Thornton et al., 2008). Recurrent airway obstruction (RAO) is a common yet poorly understood equine chronic respiratory disease where such altered mucus properties and clearance have been identified as major factors in the disease pathology (Davis and Rush, 2002; Gerber et al., 2000; Kaup et al., 1990; Robinson, 2001). The gel-forming mucins are largely responsible for the transport properties of mucus. The major equine airway gel-forming mucin in health is Muc5b and to a lesser extent Muc5ac; produced in specialised respiratory epithelial goblet cells and sub-mucosal glands (Rousseau et al., 2011b). Changes in mucin relative and net amounts and their macromolecular properties and interactions have been attributed to the altered physical properties of airway mucus in airways disease (Groneberg et al., 2002a; Jefcoat et al., 2001; Kirkham et al., 2002; Robinson et al., 2003; Sheehan et al., 1995).The project investigates the biochemical properties of mucins present in mucus from healthy horses and horses with RAO. This project identifies the anatomical presence of mucin-producing goblet cells and glands in fixed tissues from the respiratory tracts of healthy horses and subsequently examines mucin-production sites in respiratory tracts from horses with RAO. Finally the project investigates a methodology for the study of mucin production in airway cells harvested from live horses suffering from RAO.Our investigations confirmed that horses with RAO have more endotracheal mucus than healthy controls, and that Muc5b is the predominant mucin with Muc5ac also present in RAO horse mucus, both during symptomatic disease and when horses are asymptomatic. Mucins are produced in epithelial goblet cells and sub-mucosal glands dispersed throughout the length and circumference of the equine trachea and bronchi. Goblet cell hyperplasia occurs in symptomatic exposed RAO horse airways, although goblet cells are smaller than in asymptomatic RAO horse airways. Exposure to a dusty stable environment is associated with more goblet cells per length of bronchial compared to tracheal epithelium in all horses. RAO horses have larger sub-mucosal glands containing more mucin than control horses. Primary epithelial cell cultures grown at an air liquid interface are an alternative approach to study equine airway mucus, although the use of this culture system is in its early stages. We have developed novel ways to harvest equine airway epithelial cells (tracheal brushing) and shown it is possible to freeze cells collected via tracheal epithelial brushing in 20 % FBS and then culture to ALI at a later date.
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Zhao, Jingyue. "Th17 responses in airway inflammation and airway remodelling." Thesis, King's College London (University of London), 2011. http://kclpure.kcl.ac.uk/portal/en/theses/th17-responses-in-airway-inflammation-and-airway-remodelling(94ca2e63-6304-4694-998e-b40747ca0f9a).html.

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Shebani, Eyman. "Ultrastructural Studies of the Airway Epithelium in Airway Diseases." Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-6632.

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Hamilton, Nicholas J. I. "Tissue-engineering airway mucosa for airway reconstruction and transplantation." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/1572383/.

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Conventional therapies are unable to treat a subset of patients with upper airway stenosis. To overcome this, tissue-engineered tracheas have been trialled as a means of replacing the damaged section of airway. All examples have suffered from poor mucosalisation following implantation which results in infection, mucostasis and airway obstruction. The aim of this thesis was to investigate methods of regenerating a respiratory mucosal graft that could be used as part of a tracheal transplant. The relationship of the extracellular matrix to human respiratory epithelial cells (HBECs) was examined to establish the optimal protein composition of the mucosal scaffold. Collagen IV was demonstrated to be the leading adhesive protein acting via the integrin α2β1 and a Src and FAK mediated intracellular pathway. Laminin was shown to play a key role in promoting HBEC proliferation and was dependent on an integrin pathway containing the subunit β1. This study compared biological, biomimetic and synthetic scaffolds for their ability to support and differentiate a respiratory epithelial layer. Decellularised dermis was shown to be the optimal scaffold and a differentiated respiratory layer with mucocilary function was achieved in-vitro. The implantation of this engineered respiratory mucosa proved more challenging with loss of differentiation markers following grafting in rabbits and mice. An alternative strategy was developed whereby basal epithelial cells were encased in collagen and successfully grafted onto the surface of decellularised trachea. This represents the most effective method for re-epithelising an allogenic trachea before or after transplantation and could also be used to reline other parts of the upper airway.
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Korpela, Antti. "Healing of airway anastomoses and stenting of airway stenosis." Helsinki : University of Helsinki, 2000. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/korpela/.

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Tao, Florence C. Y. "Mechanisms of altered airway smooth muscle calcium signalling in airway hyperresponsiveness." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape9/PQDD_0022/NQ50267.pdf.

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Tao, Florence C. Y. 1968. "Mechanisms of altered airway smooth muscle calcium signalling in airway hyperresponsiveness." Thesis, McGill University, 1998. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=35949.

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The pathophysiological origins of airway hyperresponsiveness (AHR) in asthma are unknown. The objectives of this thesis were to establish an association between AHR in an animal model of asthma and altered contractility of airway smooth muscle (ASM) and to elucidate changes in contractile signalling that could account for any observed differences in ASM contractility. The Fisher strain of rat is spontaneously hyperresponsive to methacholine inhalation challenge relative to Lewis rats. These inbred rat strains provide a model with which to study genetically-determined variations in airway smooth muscle that may underlie AHR. Fisher rats were found to be also hyperresponsive to serotonin (5-HT) in vivo compared to Lewis rats, indicating that their AHR is not agonist specific the narrowing capacity and velocity of contraction of Fisher intraparenchymal airways in cultured explants were also greater than explanted. Lewis intraparenchymal airways in response to 5-HT. In addition, 5-HT stimulated higher Ca2+ transients in Fisher than Lewis ASM, in parallel with their rank order of intraparenchymal airway responsiveness. These results suggest that ASM contractility may be determined by the extent of Ca2+ mobilization in airway myocytes. To examine the mechanism of enhanced intracellular Ca2+ mobilization in Fisher ASM, the role of the inositol (1,4,5)trisphospbate (Ins (1,4,5)P 3) pathway in determining interstrain differences in ASM Ca2+ was studied. 5-HT produced higher levels of Ins (1,4,5)P3 in Fisher than Lewis ASM. This appeared to be caused by a lower expression and activity in Fisher ASM of the type I and II 5-phosphatases which inactivate Ins (1,4,5)P3. Inhibition of 5-phosphatase activity increased Ins (1,4,5)P3-mediated Ca2+ release in ASM from both strains of rat, equalizing Ca2+ signals between Lewis and Fisher ASM. Since Ins (1,4,5)P3 receptor sensitivity to Ins (1,4,5)P 3 was found to be similar between the two rat strains, the differences in 5-phosphatas
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Kölbeck, Karl-Gustav. "Nasal and bronchial airway reactivity in allergic and non allergic airway inflammation /." Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-428-3/.

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Opazo, Saez Anabelle M. (Anabelle Marjorie). "Airway responsiveness to methacholine and airway smooth muscle in the guinea pig." Thesis, McGill University, 1991. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=60629.

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The purpose of this study was two-fold: (1) to examine the relationship between the amount of airway smooth muscle and the airway responsiveness to inhaled aerosolized methacholine (MCh) in guinea pigs, and (2) to characterize the distribution of airway narrowing following MCh.
In summary: (1) the quantity of airway smooth muscle (ASM) does not appear to determine differences in maximal bronchoconstriction among normal guinea pigs; the lack of a correlation between responsiveness and amount of ASM may be explained by the heterogenous distribution of bronchoconstriction among the airways studied or the modality of challenge; (2) the sensitivity to MCh appears to be related to differences in the amount of ASM in intraparenchymal cartilaginous airways; (3) variability in the EC$ sb{50}$ may also reflect differences in airway cross-sectional area; (4) lung resistance appears to be a good measure of constriction since the morphometric measure of airway narrowing correlated well with resistance; (5) the heterogeneity of airway narrowing does not appear to be determined by differences in ASM.
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Wang, Jiahua. "The role of airway epithelium in airway inflammation and effect of corticosteroids." Thesis, Queen Mary, University of London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300175.

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Books on the topic "Airway"

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Pacific airway. Roberts Creek, B.C: Creekside Publications, 2005.

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Khan, Zahid Hussain, ed. Airway Management. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-08578-4.

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1952-, Howarth Peter, ed. Airway remodeling. New York: Marcel Dekker, 2001.

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Popat, Mansukh T. Difficult airway management. Oxford: Oxford University Press, 2009.

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Pediatric airway surgery. Basel: Karger, 2012.

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Difficult airway management. Oxford: Oxford University Press, 2009.

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Rogers, Duncan F., and Louise E. Donnelly. Human Airway Inflammation. New Jersey: Humana Press, 2001. http://dx.doi.org/10.1385/1592591515.

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Kovacs, George. Emergency airway management. New York, NY: McGraw-Hill, 2008.

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Klemm, Eckart, and Andreas Nowak, eds. Tracheotomy and Airway. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-44314-6.

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Benger, Jonathan, Jerry Nolan, and Mike Clancy, eds. Emergency Airway Management. Cambridge: Cambridge University Press, 2008. http://dx.doi.org/10.1017/cbo9780511544491.

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Book chapters on the topic "Airway"

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Jankovic, Danilo, and Peter Cheng. "Airway." In Regional Nerve Blocks in Anesthesia and Pain Therapy, 105–25. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-05131-4_8.

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Kristensen, Michael Seltz, Wendy H. Teoh, and Danilo Jankovic. "Airway." In Regional Nerve Blocks in Anesthesia and Pain Therapy, 105–20. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-88727-8_7.

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Banhidy, Norbert, and David Zhang. "Airway." In Pocket Essential Medical Equipment, 2–17. Boca Raton: CRC Press, 2021. http://dx.doi.org/10.1201/9781003159179-2.

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Rayees, Sheikh, and Inshah Din. "Airway Inflammation and Airway Hyperresponsiveness." In SpringerBriefs in Immunology, 7. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-70270-0_3.

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Ubaradka, Raveendra Shankaranarayana, Abhishek Kumar, and Nishkarsh Gupta. "Airway Management in Airway Emergency." In The Airway Manual, 603–16. Singapore: Springer Nature Singapore, 2023. http://dx.doi.org/10.1007/978-981-19-4747-6_34.

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Zhang, Jinbin, and Orlando Hung. "Surgical Airway." In Airway Management, 203–21. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-08578-4_13.

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Chan, Yoo Kuen. "Physiology of the Airway." In Airway Management, 1–14. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-08578-4_1.

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Sridhar, Srikanth, and Carin A. Hagberg. "Airway Management in Cervical Spine Injured Patients." In Airway Management, 157–75. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-08578-4_10.

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Arya, Virendra K. "Indigenous Devices in Difficult Airway Management." In Airway Management, 177–88. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-08578-4_11.

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Arya, Virendra K. "Cricothyrotomy." In Airway Management, 189–201. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-08578-4_12.

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Conference papers on the topic "Airway"

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Krumpe, Peter E. "Evolutionary Biology of Airway Clearance." In ASME 1999 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1999. http://dx.doi.org/10.1115/imece1999-0372.

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Abstract The survival of air breathers depends upon maintaining clear airways. The primary defense of the airways under normal conditions is the mucociliary escalator. Only under conditions of airway inflammation does cough clearance mechanisms become predominant. In order to facilitate the expectoration of mucous and retained particulates, cells, and debris, coupling between the air stream and the mucous layer must occur. High linear velocity of the airstream and unstable flow regimes (vortices, eddies) facilitates development of waves in the mucous layer. Expectoration requires a catastrophic separation of mucous from underlying airway structures. The response of airways is initially to secrete a deeper mucous layer, and to remodel airway glands to produce a mucous blend having a higher elastic modulus. Mucous rheologic properties seem to be tailored by the presence of inflammation to become more easily cleared, even at lower air flow rates which are characteristic of lung disease. Airway oscillations (wheezes and rhonchi) which are physical findings associated with airway inflammation may further enhance mucous clearance by adding additional energy to the mucous layer, aiding catastrophic separation. Thus airway clearance is a highly evolved and coordinated example of evolutionary biology.
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Krumpe, Peter, and Cahit A. Evrensel. "Potential Benefits of Adhesive Airway Mucus." In ASME 2001 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2001. http://dx.doi.org/10.1115/imece2001/bed-23108.

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Abstract What possible benefit could there be to sticky respiratory mucus? Most of the clinical efforts of respiratory therapy are aimed at thinning thick mucus and decreasing its adhesivity to the airway walls. Yet evidence has accumulated that thinning airway mucus may contribute to dependent atelectasis and may worsen respiratory failure in ventilated patients. We speculate that mucus adhesivity benefits cough clearance by keeping mucus in central airways where cough velocity can clear it, rather than allowing backsliding of mucus due to gravity that would result in distal plugging. It follows that mucus in central airways would benefit from increased adhesivity while mucus in distal airways would not.
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Glumac, Daniel, Koji Kadowaki, Roy Cho, Gregory Peterson, Ryan Hunter, Leslie Kent, Robroy MacIver, Vidhu Pandey, and Kazuhiro Tanahashi. "An Anti-Fouling Airway Stent." In 2022 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2022. http://dx.doi.org/10.1115/dmd2022-1031.

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Abstract Airway stents are used to keep airways open for those patients symptomatic from tracheobronchial disease. Tracheobronchial disease or central airway obstruction (CAO) can occur with benign or malignant disease, or complications from lung transplantation. Although stents can offer symptomatic relief for CAO, complications such as granulation tissue formation, stent fracture, and infection commonly occur after stent placement. Currently, all airway stents promote mucus buildup which can lead to stent failure and airway complications. In this paper, we demonstrate the use of special anti-fouling coatings to prevent mucus buildup. The coatings have been tested: 1) for wettability, 2) using XPS and TOF-SIMS to characterize surface properties, and 3) in the laboratory (in vitro) to study effects of mucin incubation. Findings include significant improvement in limiting mucus adhesion in a lab model.
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Bian, Shiyao, Ying Zheng, Shuichi Takayama, and James B. Grotberg. "Micro-PIV Measurements of an Airway Closure Model." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206831.

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A thin liquid layer coating the airway can be unstable and forms a plug. Airway closure usually happens at the small airways near the end of expiration, often accompanied with hypersecretion or/and surfactant deficiency in the airway in a variety of lung diseases, such as chronic obstructive pulmonary disease (COPD) and acute respiratory distress syndrome (ARDS). Modeling work by Halpern and Grotberg [1] has shown that several forces could contribute to airway closure, such as the surface tension instability and the wall compliance. Experiments in a capillary tube were conducted by Cassidy et al. [2] who found that adding surfactant increased the airway closure time and the critical film thickness. In vitro studies [3] [4] illustrated that exposure of primary human airway epithelial cells to plug propagation and rupture led to significant cell injury. Experimental studies [5] [6] on excised lungs or in vivo animal models have shown that severe tissue damage was found in surfactant-deficient lungs due to the repetitive airway reopening. However, mechanical forces induced by airway closure have not been experimentally evaluated.
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Al-Jumaily, A. M., S. Ashaat, B. A. Martin, R. Heinzer, J. Haba Rubio, and N. Stergiopulos. "Uvula Dynamic Characteristics." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14019.

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The airway binary fluid layer and the structural characteristics of the upper airways have significant influence on the activity of the airway muscles by changing airway compliance and collapsibility during obstructive sleep apnea trauma. The uvula plays an important role in the collapse process. Using MRI scans, this paper develops a structural model for the uvula and determines its dynamic characteristics in terms of natural frequencies and mode shapes as a preliminary process to determine optimum conditions to therapeutically relieve upper airway obstruction. The effect of the variation of tissue elasticity due to water content is elaborated on.
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Cheong, S. H., S. H. Ro, and A. M. Al-Jumaily. "How the Input Impedance Relates to Airway Characteristics." In ASME 2007 International Mechanical Engineering Congress and Exposition. ASMEDC, 2007. http://dx.doi.org/10.1115/imece2007-43283.

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To understand how the input impedance determined at the throat correlates with changes in the dynamic characteristics of the airways, a simplified 5-lobe model is developed and simulated. The model takes into account some realistic conditions such as varying cross-sectional areas, flexible wall properties and branching. The lobe terminal impedances are implemented in the model to predict the input impedance at the throat. The effects of airway constrictions and wall eleatance variations on this impedance are determined for a range of frequencies. It is concluded that the developed model is capable of predicting various physiological changes in the airway passages.
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Wang, Xiao, Keith Walters, Greg W. Burgreen, and David S. Thompson. "Cyclic Breathing Simulations: Pressure Outlet Boundary Conditions Coupled With Resistance and Compliance." In ASME/JSME/KSME 2015 Joint Fluids Engineering Conference. American Society of Mechanical Engineers, 2015. http://dx.doi.org/10.1115/ajkfluids2015-26569.

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A patient-specific non-uniform pressure outlet boundary condition was developed and used in unsteady simulations of cyclic breathing in a large-scale model of the lung airway from the oronasal opening to the terminal bronchioles. The computational domain is a reduced-geometry model, in which some airway branches in each generation were truncated, and only selected paths were retained to the terminal generation. To characterize pressure change through airway tree extending from the truncated outlets to pulmonary zone, virtual airways represented by extended volume mesh zones were constructed in order to apply a zero-dimensional airway resistance model. The airway resistances were prescribed based on a precursor steady simulation under constant ventilation condition. The virtual airways accommodate the use of patient-specific alveolar pressure conditions. Furthermore, the time-dependent alveolar pressure profile was composed with the physiologically accurate pleural pressure predicted by the whole-body simulation software HumMod, and the transpulmonary pressure evaluated based on lung compliance and local air volume change. To investigate airway flow patterns of healthy and diseased lungs, unsteady breathing simulations were conducted with varying lung compliances accounting for healthy lungs, and lungs with emphysema or interstitial fibrosis. Results show that the simulations using this patient-specific pressure boundary condition are capable of reproducing physiologically realistic flow patterns corresponding to abnormal pulmonary compliance in diseased lungs, such as the hyperventilation in lungs with emphysema, and the demand of more mechanic work for breathing in lungs with fibrosis.
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Vaughan, Benjamin L., and James B. Grotberg. "Propagation of an Air Finger Into a Fluid Filled Bifurcation." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19079.

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The occlusion of pulmonary airways can be caused by many respiratory diseases such as respiratory distress syndrome. It is believed that these occluded airways are reopened by the propagation of an air finger. The mechanics of airway reopening have been studied in-depth for an individual airway [1,2] without considering the frequent branching of pulmonary airways. The presence of a bifurcation leads to the question of whether the propagating air finger will clear both branches of the airway or will propagate through a single branch, leaving the other branch occluded. The propagation of a finite length liquid plug through a fixed bifurcation has been studied experimentally [3, 4]. We wish to develop a numerical model for the propagation of an air finger through bifurcating channel filled with a viscous fluid. In this model, the air finger is driven by a pressure difference between the parent channel and the two daughter branches. The presence of an additional pressure difference between the two branches can cause unsymmetrical splitting of the air finger and, above a critical pressure difference, prevent the clearance of both branches.
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Waters, Sarah L., Peter D. Howell, and James B. Grotberg. "The Influence of Wall Flexibility and Surfactant on Liquid Bolus Propagation Along a Liquid-Lined Tube." In ASME 1998 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1998. http://dx.doi.org/10.1115/imece1998-0048.

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Abstract The thin liquid lining that coats the airways is susceptible to a Rayleigh instability driven by capillarity at its free surface. If a sufficiently large volume of fluid is present, the instability results in the formation of a liquid bridge or lens that blocks the flow of air along the airway. This phenomena is known as airway closure.
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Al-Jumaily, A. M., and Y. Al-Fakhri. "Asymmetrically Respiratory System Simulation for Identifying Airway Occlusion." In ASME 2001 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2001. http://dx.doi.org/10.1115/imece2001/de-23233.

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Abstract A theoretical model is developed to investigate the dynamic characteristic of a healthy and an occluded asymmetric respiratory system. The model takes the elastance and inertance of the airway walls into consideration. Frequency spectra of the input impedance determined at the throat are generated and examined for two regimes of airway terminations and for occlusion at each generation from the end terminal (alveolar sacs) up to the proximal end of the trachea. In the asymmetric arrangement the impact of merging dissimilar flows due to different airways geometry from the adjacent regions is considered. Further, the effect of the nature of the terminal impedance (ie. rigid termination or compliant termination) on the acoustic response is also investigated.
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Reports on the topic "Airway"

1

Schwartz, Richard B. Deployment Ready Airway Management System (DRAMS). Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada612919.

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Carney, Nancy, Tamara Cheney, Annette M. Totten, Rebecca Jungbauer, Matthew R. Neth, Chandler Weeks, Cynthia Davis-O'Reilly, et al. Prehospital Airway Management: A Systematic Review. Agency for Healthcare Research and Quality (AHRQ), June 2021. http://dx.doi.org/10.23970/ahrqepccer243.

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Objective. To assess the comparative benefits and harms across three airway management approaches (bag valve mask [BVM], supraglottic airway [SGA], and endotracheal intubation [ETI]) by emergency medical services in the prehospital setting, and how the benefits and harms differ based on patient characteristics, techniques, and devices. Data sources. We searched electronic citation databases (Ovid® MEDLINE®, CINAHL®, the Cochrane Central Register of Controlled Trials, the Cochrane Database of Systematic Reviews, and Scopus®) from 1990 to September 2020 and reference lists, and posted a Federal Register notice request for data. Review methods. Review methods followed Agency for Healthcare Research and Quality Evidence-based Practice Center Program methods guidance. Using pre-established criteria, studies were selected and dual reviewed, data were abstracted, and studies were evaluated for risk of bias. Meta-analyses using profile-likelihood random effects models were conducted when data were available from studies reporting on similar outcomes, with analyses stratified by study design, emergency type, and age. We qualitatively synthesized results when meta-analysis was not indicated. Strength of evidence (SOE) was assessed for primary outcomes (survival, neurological function, return of spontaneous circulation [ROSC], and successful advanced airway insertion [for SGA and ETI only]). Results. We included 99 studies (22 randomized controlled trials and 77 observational studies) involving 630,397 patients. Overall, we found few differences in primary outcomes when airway management approaches were compared. • For survival, there was moderate SOE for findings of no difference for BVM versus ETI in adult and mixed-age cardiac arrest patients. There was low SOE for no difference in these patients for BVM versus SGA and SGA versus ETI. There was low SOE for all three comparisons in pediatric cardiac arrest patients, and low SOE in adult trauma patients when BVM was compared with ETI. • For neurological function, there was moderate SOE for no difference for BVM compared with ETI in adults with cardiac arrest. There was low SOE for no difference in pediatric cardiac arrest for BVM versus ETI and SGA versus ETI. In adults with cardiac arrest, neurological function was better for BVM and ETI compared with SGA (both low SOE). • ROSC was applicable only in cardiac arrest. For adults, there was low SOE that ROSC was more frequent with SGA compared with ETI, and no difference for BVM versus SGA or BVM versus ETI. In pediatric patients there was low SOE of no difference for BVM versus ETI and SGA versus ETI. • For successful advanced airway insertion, low SOE supported better first-pass success with SGA in adult and pediatric cardiac arrest patients and adult patients in studies that mixed emergency types. Low SOE also supported no difference for first-pass success in adult medical patients. For overall success, there was moderate SOE of no difference for adults with cardiac arrest, medical, and mixed emergency types. • While harms were not always measured or reported, moderate SOE supported all available findings. There were no differences in harms for BVM versus SGA or ETI. When SGA was compared with ETI, there were no differences for aspiration, oral/airway trauma, and regurgitation; SGA was better for multiple insertion attempts; and ETI was better for inadequate ventilation. Conclusions. The most common findings, across emergency types and age groups, were of no differences in primary outcomes when prehospital airway management approaches were compared. As most of the included studies were observational, these findings may reflect study design and methodological limitations. Due to the dynamic nature of the prehospital environment, the results are susceptible to indication and survival biases as well as confounding; however, the current evidence does not favor more invasive airway approaches. No conclusion was supported by high SOE for any comparison and patient group. This supports the need for high-quality randomized controlled trials designed to account for the variability and dynamic nature of prehospital airway management to advance and inform clinical practice as well as emergency medical services education and policy, and to improve patient-centered outcomes.
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Skinner, Joseph C., Gilmer Jr., Molloy William D., Wells Brian A., Austin Gary A., and Paul N. Imposed Work of Breathing of Airway Adjuncts. Fort Belvoir, VA: Defense Technical Information Center, December 2004. http://dx.doi.org/10.21236/ada428809.

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Steegman, Ralph, Anne-Marie Renkema, Herman Verbeek, Adriaan Schoeman, Anne Marie Kuijpers-Jagtman, and Yijin Ren. Upper Airway Volumetric Changes on CBCT after Orthodontic Interventions: protocol for a systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0017.

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Review question / Objective: Does the volume of the upper airway change after an orthodontic intervention? P: growing subjects, adults; I: orthodontic treatment, dentofacial orthopedics, extractions; C: untreated subjects and/or non-extractions; O: volumetric changes of the upper airway measured on CBCT scans. Condition being studied: The primary objective of orthodontic treatment is to establish optimal dental and/or skeletal relationship in harmony with the soft tissue morphology and functioning. In addition, un-impeding or facilitating airway growth and development is an important objective, especially in patients susceptible for airway obstruction or sleep apnea. It is therefore important to look into the effect of various orthodontic treatments on the 3D volumetric changes of the upper airway. Compared with the use of traditional 2D lateral cephalograms, CBCT scans provide the opportunity to perform measurements in more dimensions on the airway with demonstrated reliability. This systematic review therefore includes studies using CBCT scans for evaluation of the airway.
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Dong, Wei, Wei Zhang, Jianxu Er, Jiapeng Liu, and Jiange Han. Lesser complications of laryngeal mask airway than endotracheal tubes in pediatric airway management: A review of literature and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2022. http://dx.doi.org/10.37766/inplasy2022.5.0066.

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Review question / Objective: The relevant expert consensus has not pointed out which ventilation device is better during general anesthesia in the pediatric airway management for elective surgery. Condition being studied: We carried out a keyword search using the terms “layngeal mask, LMA, endotracheal tube, tracheal tube, children, pediatric, anesthesia, RCT, randomized controlled trials, randomized, elective surgery.” In general, searches are developed in MEDLINE in Ovid; Embase.com; the Cochrane Central Register of Controlled Trials (CENTRAL) via the Wiley Interface; Web of Science Core Collection; PubMed restricting to records in the subset “as supplied by publisher” to find references that not yet indexed in MEDLINE; and Google Scholar. When available, these databases were searched using a combination of subject headings (such as MeSH) and filters (such as RCT). We reviewed references of included studies to identify relevant studies. We imposed no language or time restriction. The exact date of the database search is September 1, 2021.We carried out a keyword search using terms “layngeal mask, LMA, endotracheal tube, tracheal tube, children, pediatric, anesthesia, RCT, randomized controlled trials, randomized, elective surgery.”
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Collie, D. D., J. A. Wilder, and D. E. Bice. Nonspecific airway reactivity in a mouse model of asthma. Office of Scientific and Technical Information (OSTI), December 1995. http://dx.doi.org/10.2172/381396.

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Raju, Dr Dinesh, Dr Chinnamuthu Murugesan, Dr Sanjaya Kumar Bnakal, and Dr N. Chennakeshava. Melanotic neuroectodermal tumour- difficult airway management in an infant. The Association of Anaesthetists of Great Britain and Ireland, February 2014. http://dx.doi.org/10.21466/ac.odaapnb.2014.

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Lee, Lu-Yuan. Pulmonary Stress Induced by Hyperthermia: Role of Airway Sensory Nerves. Fort Belvoir, VA: Defense Technical Information Center, October 2012. http://dx.doi.org/10.21236/ada612760.

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Lee, Lu-Yuan. Pulmonary Stress Induced by Hyperthermia: Role of Airway Sensory Nerves. Fort Belvoir, VA: Defense Technical Information Center, October 2011. http://dx.doi.org/10.21236/ada612762.

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Lee, Lu-Yuan. Pulmonary Stress Induced by Hyperthermia: Role of Airway Sensory Nerves. Fort Belvoir, VA: Defense Technical Information Center, October 2013. http://dx.doi.org/10.21236/ada612769.

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