Bibliografías temáticas / Airway epithelium

Literatura académica sobre el tema "Airway epithelium"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 6 de julio de 2024

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Artículos de revistas sobre el tema "Airway epithelium"

1

Burch, L. H., C. R. Talbot, M. R. Knowles, C. M. Canessa, B. C. Rossier y R. C. Boucher. "Relative expression of the human epithelial Na+ channel subunits in normal and cystic fibrosis airways". American Journal of Physiology-Cell Physiology 269, n.º 2 (1 de agosto de 1995): C511—C518. http://dx.doi.org/10.1152/ajpcell.1995.269.2.c511.

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The availability of the newly cloned subunits (alpha, beta, gamma) of the epithelial Na+ channel (ENaC) permits molecular studies of the pathogenesis of the abnormal Na+ transport rates of cystic fibrosis (CF) airway epithelia. Northern analyses of airway epithelia showed that both normal and CF airway epithelia express ENaC subunit mRNAs in a ratio of alpha > beta > gamma. In situ hybridization studies revealed expression of all three ENaC subunits in the superficial epithelium and the alpha- and beta-subunits in the gland ductular and acinar epithelium of both normal and CF airways. Ribonuclease protection assays revealed that the steady-state levels of alpha-, beta-, and gamma-ENaC mRNAs were similar in CF and normal airway superficial epithelia. These findings indicate that 1) Na+ transport defects in CF airways disease may be expressed in glandular acinar and ductal epithelium as well as superficial epithelium, and 2) the molecular pathogenesis of Na+ hyperabsorption in CF airways does not reflect increased levels of Na+ channel mRNAs, and probably number, but reflects an absence of the normal inhibitory regulation of Na+ channels by CF transmembrane conductance regulator proteins.
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2

Inoue, Hideki, Kaho Akimoto, Tetsuya Homma, Akihiko Tanaka y Hironori Sagara. "Airway Epithelial Dysfunction in Asthma: Relevant to Epidermal Growth Factor Receptors and Airway Epithelial Cells". Journal of Clinical Medicine 9, n.º 11 (18 de noviembre de 2020): 3698. http://dx.doi.org/10.3390/jcm9113698.

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Airway epithelium plays an important role as the first barrier from external pathogens, including bacteria, viruses, chemical substances, and allergic components. Airway epithelial cells also have pivotal roles as immunological coordinators of defense mechanisms to transfer signals to immunologic cells to eliminate external pathogens from airways. Impaired airway epithelium allows the pathogens to remain in the airway epithelium, which induces aberrant immunological reactions. Dysregulated functions of asthmatic airway epithelium have been reported in terms of impaired wound repair, fragile tight junctions, and excessive proliferation, leading to airway remodeling, which contributes to aberrant airway responses caused by external pathogens. To maintain airway epithelium integrity, a family of epidermal growth factor receptors (EGFR) have pivotal roles in mechanisms of cell growth, proliferation, and differentiation. There are extensive studies focusing on the relation between EGFR and asthma pathophysiology, which describe airway remodeling, airway hypermucus secretion, as well as immunological responses of airway inflammation. Furthermore, the second EGFR family member, erythroblastosis oncogene B2 (ErbB2), has been recognized to be involved with impaired wound recovery and epithelial differentiation in asthmatic airway epithelium. In this review, the roles of the EGFR family in asthmatic airway epithelium are focused on to elucidate the pathogenesis of airway epithelial dysfunction in asthma.
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3

White, Steven R. "Apoptosis and the Airway Epithelium". Journal of Allergy 2011 (13 de diciembre de 2011): 1–21. http://dx.doi.org/10.1155/2011/948406.

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The airway epithelium functions as a barrier and front line of host defense in the lung. Apoptosis or programmed cell death can be elicited in the epithelium as a response to viral infection, exposure to allergen or to environmental toxins, or to drugs. While apoptosis can be induced via activation of death receptors on the cell surface or by disruption of mitochondrial polarity, epithelial cells compared to inflammatory cells are more resistant to apoptotic stimuli. This paper focuses on the response of airway epithelium to apoptosis in the normal state, apoptosis as a potential regulator of the number and types of epithelial cells in the airway, and the contribution of epithelial cell apoptosis in important airways diseases.
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Sparrow, M. P., H. W. Mitchell y T. I. Omari. "The epithelial barrier and airway responsiveness". Canadian Journal of Physiology and Pharmacology 73, n.º 2 (1 de febrero de 1995): 180–90. http://dx.doi.org/10.1139/y95-027.

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Epithelial injury and bronchial hyperresponsiveness are commonly associated with airway disease, and are widely considered to occur as the result of inflammatory changes in the airway wall. Mechanistically, the airway epithelium may influence the sensitivity of the airways to provocative stimuli through its primary function as a cellular barrier between the air and the interstitium, or by liberating a variety of bronchoactive mediators, e.g., lipoxygenase and cyclooxygenase products, nitric oxide, and an epithelium-derived relaxing factor (EpDIF). Much attention has focused on the latter function of the epithelium, particularly the putative EpDIF, which has an action considered to be analogous to that of endothelium-derived relaxing factor in blood vessels. The modulation of airway calibre by the epithelium has recently been investigated in vitro using tubular preparations of bronchi, where removal of, or damage to, the epithelium increases the sensitivity to agonists by several orders of magnitude. This contrasts with the effect of removing the epithelium on strips or rings of airway wall, where the increase in sensitivity is small and rather variable, but this has been the primary observation for proposing a putative EpDIF. This review evaluates the barrier or protective function of the airway epithelium and the major role it plays in the modulation of airway responsiveness. A role of a putative EpDIF seems, at best, to be of minor functional significance.Key words: epithelial barrier, bronchial hyprresponsiveness, airway smooth muscle, epithelial permeability, epithelium-derived inhibitory factor.
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5

Gallos, George, Elizabeth Townsend, Peter Yim, Laszlo Virag, Yi Zhang, Dingbang Xu, Matthew Bacchetta y 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, n.º 3 (1 de febrero de 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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6

Vanoni, Simone, Giada Scantamburlo, Silvia Dossena, Markus Paulmichl y Charity Nofziger. "Interleukin-Mediated Pendrin Transcriptional Regulation in Airway and Esophageal Epithelia". International Journal of Molecular Sciences 20, n.º 3 (9 de febrero de 2019): 731. http://dx.doi.org/10.3390/ijms20030731.

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Pendrin (SLC26A4), a Cl−/anion exchanger, is expressed at high levels in kidney, thyroid, and inner ear epithelia, where it has an essential role in bicarbonate secretion/chloride reabsorption, iodide accumulation, and endolymph ion balance, respectively. Pendrin is expressed at lower levels in other tissues, such as airways and esophageal epithelia, where it is transcriptionally regulated by the inflammatory cytokines interleukin (IL)-4 and IL-13 through a signal transducer and activator of transcription 6 (STAT6)-mediated pathway. In the airway epithelium, increased pendrin expression during inflammatory diseases leads to imbalances in airway surface liquid thickness and mucin release, while, in the esophageal epithelium, dysregulated pendrin expression is supposed to impact the intracellular pH regulation system. In this review, we discuss some of the recent findings on interleukin-mediated transcriptional regulation of pendrin and how this dysregulation impacts airway and esophagus epithelial homeostasis during inflammatory diseases.
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7

Hyde, Dallas M., David J. Magliano y Charles G. Plopper. "Morphometric Assessment of Pulmonary Toxicity in the Rodent Lung". Toxicologic Pathology 19, n.º 4_part_1 (noviembre de 1991): 428–46. http://dx.doi.org/10.1177/0192623391019004-112.

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An overview of the epithelial and interstitial composition of rat respiratory airways shows complexity and variability. Airway epithelium varies in 1) different airway levels; 2) the types and ultrastructure of cells present; and 3) the abundance, type, and composition of stored secretory product. Unbiased sampling of airways is done using airway microdissection with a specific binary numbering system for airway generation. Vertical sections of selected airways are used to sample epithelium and interstitium. We determine the ratios of the volume of epithelial or interstitial cells to the total epithelial or interstitial volume (Vv). The surface of the epithelial basal lamina to the total epithelial or interstitial volume (Sv) is determined using point and intersection counting with a cycloid grid. Using the selector method on serial plastic sections, we determine the number of epithelial or interstitial cells per volume (Nv) of total epithelium or interstitium. We calculate the number of epithelial or interstitial cells per surface of epithelial basal lamina (Ns) by dividing Nv by Sv where the volumes are the same compartment. We calculate average cell volumes (v̄) for specific epithelial and interstitial cells by dividing the absolute nuclear volume by the ratio of the nucleus to cell volume (Vv). By multiplying the average cell volume (v̄) by the ratio of organellar volume to cell volume (Vv), we calculate the average organellar volume per cell. These unbiased stereological approaches are critical in a quantitative evaluation of toxicological injury of rat tracheobronchial airways.
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8

Dey, R. D., J. B. Altemus, I. Zervos y J. Hoffpauir. "Origin and colocalization of CGRP- and SP-reactive nerves in cat airway epithelium". Journal of Applied Physiology 68, n.º 2 (1 de febrero de 1990): 770–78. http://dx.doi.org/10.1152/jappl.1990.68.2.770.

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A combination of neuroanatomic techniques was used to examine the origin and neuropeptide content of nerve fibers in the airway epithelium of adult cats. By the use of immunocytochemical methods, the peptides substance P (SP) and calcitonin gene-related peptide (CGRP) were colocalized in airway epithelial nerve fibers. Two days after wheat germ agglutinin (WGA) was injected into the nodose ganglion, fibers containing WGA immunoreactivity (IR) were detected in the airway epithelium. SP-like immunoreactivity (LI) and CGRP-LI were demonstrated separately in the WGA-IR fibers, establishing their origin from nerve cell bodies of nodose ganglion. Vagal transection inferior to the nodose ganglion reduced the number of SP- and CGRP-IR fibers by greater than 90% in ipsilateral airways. In contralateral airways, SP-IR fibers were substantially reduced, whereas the effect on CGRP-IR fibers was not statistically significant. Vagotomy superior to the nodose ganglion did not alter the density of peptide-IR fibers. The results prove that SP- and CGRP-IR nerve fibers of cat airway epithelium originate from nerve cell bodies in the nodose ganglion and that SP- and CGRP-like peptides may be stored together in some nerve fibers of the airway epithelium.
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9

Flodby, Per, Janice M. Liebler, Mitsuhiro Sunohara, Dan R. Castillo, Alicia M. McConnell, Manda S. Krishnaveni, Agnes Banfalvi et al. "Region-specific role for Pten in maintenance of epithelial phenotype and integrity". American Journal of Physiology-Lung Cellular and Molecular Physiology 312, n.º 1 (1 de enero de 2017): L131—L142. http://dx.doi.org/10.1152/ajplung.00005.2015.

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Previous studies have demonstrated resistance to naphthalene-induced injury in proximal airways of mice with lung epithelial-specific deletion of the tumor-suppressor gene Pten, attributed to increased proliferation of airway progenitors. We tested effects of Pten loss following bleomycin injury, a model typically used to study distal lung epithelial injury, in conditional PtenSFTPC-cre knockout mice. Pten-deficient airway epithelium exhibited marked hyperplasia, particularly in small bronchioles and at bronchoalveolar duct junctions, with reduced E-cadherin and β-catenin expression between cells toward the luminal aspect of the hyperplastic epithelium. Bronchiolar epithelial and alveolar epithelial type II (AT2) cells in PtenSFTPC-cre mice showed decreased expression of epithelial markers and increased expression of mesenchymal markers, suggesting at least partial epithelial-mesenchymal transition at baseline. Surprisingly, and in contrast to previous studies, mutant mice were exquisitely sensitive to bleomycin, manifesting rapid weight loss, respiratory distress, increased early mortality (by day 5), and reduced dynamic lung compliance. This was accompanied by sloughing of the hyperplastic airway epithelium with occlusion of small bronchioles by cellular debris, without evidence of increased parenchymal lung injury. Increased airway epithelial cell apoptosis due to loss of antioxidant defenses, reflected by decreased expression of superoxide dismutase 3, in combination with deficient intercellular adhesion, likely predisposed to airway sloughing in knockout mice. These findings demonstrate an important role for Pten in maintenance of airway epithelial phenotype integrity and indicate that responses to Pten deletion in respiratory epithelium following acute lung injury are highly context-dependent and region-specific.
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10

Soleas, John P., Ana Paz, Paula Marcus, Alison McGuigan y Thomas K. Waddell. "Engineering Airway Epithelium". Journal of Biomedicine and Biotechnology 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/982971.

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Airway epithelium is constantly presented with injurious signals, yet under healthy circumstances, the epithelium maintains its innate immune barrier and mucociliary elevator function. This suggests that airway epithelium has regenerative potential (I. R. Telford and C. F. Bridgman, 1990). In practice, however, airway regeneration is problematic because of slow turnover and dedifferentiation of epithelium thereby hindering regeneration and increasing time necessary for full maturation and function. Based on the anatomy and biology of the airway epithelium, a variety of tissue engineering tools available could be utilized to overcome the barriers currently seen in airway epithelial generation. This paper describes the structure, function, and repair mechanisms in native epithelium and highlights specific and manipulatable tissue engineering signals that could be of great use in the creation of artificial airway epithelium.
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Tesis sobre el tema "Airway epithelium"

1

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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Stevens, Paul. "Intrinsic differences of the airway epithelium in childhood allergic asthma". University of Western Australia. School of Paediatrics and Child Health, 2009. http://theses.library.uwa.edu.au/adt-WU2010.0022.

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[Truncated abstract] Asthma affects millions of people worldwide and places a substantial burden on the healthcare system. Despite advances in our understanding of disease mechanisms and the role of respiratory viruses in asthma exacerbations, there is little known regarding the role of the epithelium in commonly observed structural changes in the airway wall. The epithelium of the airways provides an essential protective barrier between the environment and underlying structures and is responsible for the secretion of diverse compounds. Since it is likely that dysregulated epithelial characteristics and function in childhood asthma are critical determinants of disease progression in adults, it is pertinent to investigate the cellular mechanisms involved in paediatric asthma. However, full comprehension of paediatric respiratory diseases and the childhood antecedents of adult respiratory disease are currently hampered by the difficulty in obtaining relevant target organ tissue and most of the data to date have been generated from studies involving adults or commercially derived cell lines. This laboratory has successfully developed methodologies of obtaining and studying samples of paediatric primary airway epithelial cells (pAECs) and has identified significant biochemical and functional differences between healthy non-atopic (pAECHNA) and atopic asthmatic (pAECAA) airway cells, which have assisted in the identification of potential mechanisms responsible for abnormal epithelial function. Stevens 2009 ... Exposure of pAECs with RV resulted in elevated PAI-1 mRNA expression and reduced MMP-9 release in both pAECAA and pAECHNA samples. Collectively, the data presented indicate that RV exposure induces a pronounced antiproliferative and retardative repair effect in pAECAA and that the presence of virus may have a role in the PAI-1 and MMP expression witnessed in these cells. In conclusion, this investigation has further characterised the essential role the airway epithelium plays in childhood asthma by demonstrating for the first time that pAECs from asthmatic children lack the ability to successfully repair mechanically induced wounds. This investigation also showed that PAI-1 is elevated in pAECAA and has a functional role in the pAEC proliferative and regenerative processes. It was demonstrated that MMP-2 and MMP-9 activities and the MMP-9/TIMP-1 as well as MMP2/TIMP2 ratios were significantly reduced in pAECAA thereby providing additional evidence that there is a dysregulation in the mechanisms that monitor the turnover of the ECM in childhood asthma. Furthermore, this study has shown for the first time that pAECs from untreated mild atopic-asthmatic children are more sensitive to the pathogenic effects of RV than healthy control cells and that RV exposure delays cellular proliferation and repair. Ultimately, these findings support the hypothesis postulated and provide evidence that indeed the dysregulated epithelial functional characteristics seen in childhood mild asthma may be a critical determinant of disease progression in adults.
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3

Scull, Margaret Adele Pickles Raymond J. "Myxovirus interaction with the human airway epithelium". Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2009. http://dc.lib.unc.edu/u?/etd,2848.

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Thesis (Ph. D.)--University of North Carolina at Chapel Hill, 2009.
Title from electronic title page (viewed Jun. 4, 2010). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Department of Microbiology and Immunology." Discipline: Microbiology and Immunology; Department/School: Medicine.
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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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Rowley, Jessica. "The interaction of Aspergillus fumigatus with the respiratory epithelium". Thesis, University of Manchester, 2014. https://www.research.manchester.ac.uk/portal/en/theses/the-interaction-of-aspergillus-fumigatus-with-the-respiratory-epithelium(0fc10449-977d-4f14-a169-172e8204fee4).html.

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Aspergillus fumigatus is a filamentous fungus and the main pathogen responsible for the often fatal respiratory condition, aspergillosis. Airway epithelial cells (AECs) are likely to be the first line of host defence that come into contact with the inhaled conidia of A. fumigatus. Recent evidence strongly suggests that the response of the airway epithelium to inhaled pathogens is pivotal in orchestrating immune responses by inducing phagocytic-like reactions and the secretion of inflammatory cytokines and antimicrobial peptides. However, the majority of previous work investigating A. fumigatus-host interactions has been performed using macrophages and neutrophils, thereby neglecting the epithelium. AECs have been shown to secrete inflammatory cytokines in response to A. fumigatus although these studies predominantly used transformed AEC lines that lack tight junctions and do not fully differentiate. Furthermore, most studies used culture filtrate or extract of A. fumigatus rather than live, whole organism and as a result, the direct interaction of the germinating fungus and the airway epithelium has been overlooked. During the early germination and growth period, the cell wall composition of A. fumigatus is dynamic, with various antigens exposed at different morphological stages. The aim of this thesis was to determine whether AECsare able to alter the germination and growth rate of A. fumigatus, and, conversely, if A. fumigatus affects AECs in terms of the secretion of inflammatory mediators. These studies used live, germinating A. fumigatus, and human primary differentiated AECs to obtain a more realistic in vitro model than those used in previous studies. Data showed that AECs are able to significantly inhibit the germination and growth of A. fumigatus, although this effect was less pronounced in differentiated primary AEC than in transformed AEC lines. A. fumigatus also significantly inducedthe expression and secretion of the inflammatory cytokines, IL-6 and IL-8, probably via the interaction of fungal cell wall β-glucans, and as of yet unidentified AEC receptor. The A1160pyrG+ strain of A. fumigatus secreted factors capable of inducing cytokine secretion whereas Af293 strain did not, highlighting diverse mechanisms of action for different strains. Upregulation of both cytokines was dependent on the stage of A. fumigatus growth with induction synchronous with germination. Despite being associated with fungal sensitisation in asthmatics, AEC-derived cytokines associated with this disease, namely TSLP, IL33 and IL25,did not appear to be upregulated by transformed AECs in response to A. fumigatus. Similarly, A. fumigatus did not seem to induce synthesis and secretion of the acute phase response protein, fibrinogen above baseline levels. The data presented in this thesis confirms the importance of the airway epithelium in directing anti-A. fumigatus immunity and the involvement of complex ligand-receptor interactions.
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Fox, Emma. "Systemic delivery of DNA to the airway epithelium". Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.409742.

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Leahy, Rachel A. "Signal Transduction and Cellular Differentiation in Airway Epithelium". Kent State University / OhioLINK, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=kent1352673026.

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FORTNER, CHRISTOPHER NEIL. "EPITHELIUM-DEPENDENT RELAXATION OF AIRWAY SMOOTH MUSCLE IS LINKED TO EPITHELIAL CHLORIDE CURRENTS". University of Cincinnati / OhioLINK, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=ucin983467525.

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Williams, M. T. S. "Impact of different CFTR Mutations on Airway Epithelium Function". Thesis, Queen's University Belfast, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.527902.

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Jing, Yi. "Epithelial mechanisms in airway responses induced by hyperosmolarity". Morgantown, W. Va. : [West Virginia University Libraries], 2007. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=5054.

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Thesis (Ph. D.)--West Virginia University, 2007.
Title from document title page. Document formatted into pages; contains xiv, 155 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references.
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Libros sobre el tema "Airway epithelium"

1

1954-, Farmer Stephen G. y Hay, Douglas W. P., 1956-, eds. The airway epithelium: Physiology, pathophysiology, and pharmacology. New York: Marcel Dekker, 1991.

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1954-, Farmer Stephen G. y Hay, Douglas W. P., 1956-, eds. The Airway epithelium: Physiology, pathophysiology, and pharmacology. New York: M. Dekker, 1991.

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Houghton, Shelagh Anne. The effect of vasoactive intestinal peptide on chloride conductance in airway epithelial cells. [New Haven, Conn: s.n.], 1997.

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Widdicombe, Jonathan. Airway Epithelium. Morgan & Claypool Life Science Publishers, 2012.

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Widdicombe, Jonathan. Airway Epithelium. Morgan & Claypool Life Science Publishers, 2012.

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6

Pintelon, Isabel, Jean-Pierre Timmermans, Inge Brouns, Line Verckist y Dirk Adriaensen. Pulmonary Neuroepithelial Body Microenvironment: A Multifunctional Unit in the Airway Epithelium. Springer International Publishing AG, 2021.

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Li Bassi, Gianluigi y J. D. Marti. Chest physiotherapy and tracheobronchial suction in the ICU. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0121.

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The airway lining fluid is a biphasic layer covering the respiratory tract epithelium. It has antimicrobial and immunomodulatory properties, and it is formed by a gel-phase (mucus), and a low-viscosity inner layer (sol-phase) that provides lubrication for ciliary beating. Mucus is continuously cleared from the airways through the ciliated epithelium and via the two-phase gas–liquid flow mechanism (i.e. coughing). Mucus production in healthy subjects is approximately 10–100 mL/day. Whereas, mucociliary clearance rates range between 4 and 20 mm/min. Critically-ill, mechanically-ventilated patients often retain mucus. Several chest physiotherapy techniques are applied to promote mucus clearance in these patients. The role of chest physiotherapy in mechanically-ventilated patients is debated, due to the lack of evidence from well-designed clinical trials. Retained mucus is aspirated through tracheobronchial suctioning. Closed suctioning is beneficial in patients with severe lung failure and at risk of alveolar collapse upon ventilator disconnection.
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Harrison, Mark. Respiratory physiology. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198765875.003.0033.

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This chapter describes respiratory physiology as it applies to Emergency Medicine, and in particular the Primary FRCEM examination. The chapter outlines the key details of lung volumes and pressures, lung epithelium, lung compliance, surfactant, airway resistance, gas transfer, gas transport within circulation, control of respiration, and ventilation–perfusion relationship. This chapter is laid out exactly following the RCEM syllabus, to allow easy reference and consolidation of learning.
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Relova, Anne-Jacqueline. Mechanisms for & Effects of Airway Epithelial Damage in Ashthma. Uppsala Universitet, 2002.

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Burn, Mellisa. The regulation of airway epithelial function by adenosine and related nucleotides. 2005.

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Capítulos de libros sobre el tema "Airway epithelium"

1

Braga, P. C., L. Allegra y G. Piatti. "Damage to Airway Epithelium". En Lungscapes, 77–92. Milano: Springer Milan, 1992. http://dx.doi.org/10.1007/978-88-470-2255-3_7.

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Mullol, Joaquim, James N. Baraniuk, Cesar Picado y James H. Shelhamer. "Endothelin and the Airway Epithelium". En Pulmonary Actions of the Endothelins, 155–76. Basel: Birkhäuser Basel, 1999. http://dx.doi.org/10.1007/978-3-0348-8821-9_9.

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Idris, Tahir, Marc Chanson y Mehdi Badaoui. "Biology of the CF Airway Epithelium". En Hodson and Geddes' Cystic Fibrosis, 48–58. 5a ed. Boca Raton: CRC Press, 2023. http://dx.doi.org/10.1201/9781003262763-6.

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Henricks, Paul A. J., Ferdi Engels, Betty van Esch, Henk J. van der Linde, Moira J. Oosthuizen y Frans P. Nijkamp. "Epithelium-Derived Linoleic Acid Metabolites Modulate Airway Smooth Muscle Function". En Mediators in Airway Hyperreactivity, 283–86. Basel: Birkhäuser Basel, 1990. http://dx.doi.org/10.1007/978-3-0348-7379-6_39.

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Bartlett, Jennifer A., Anthony J. Fischer y Paul B. Jr McCray. "Innate Immune Functions of the Airway Epithelium". En Contributions to Microbiology, 147–63. Basel: KARGER, 2008. http://dx.doi.org/10.1159/000136349.

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Skerrett, Shawn J. "Toll-Like Receptors in the Airway Epithelium". En Mucosal Immunology of Acute Bacterial Pneumonia, 125–38. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4614-5326-0_5.

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Mitchell, H. W., K. E. Willet y M. P. Sparrow. "The Role of Epithelium in the Responsiveness of the Bronchi to Stimuli". En Mediators in Airway Hyperreactivity, 275–78. Basel: Birkhäuser Basel, 1990. http://dx.doi.org/10.1007/978-3-0348-7379-6_37.

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Puchelle, Edith, Jean-Marie Zahm, Sophie de Bentzmann y Dominique Gaillard. "Mucus and Airway Epithelium Alterations in Cystic Fibrosis". En Airway Mucus: Basic Mechanisms and Clinical Perspectives, 301–26. Basel: Birkhäuser Basel, 1997. http://dx.doi.org/10.1007/978-3-0348-8874-5_12.

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Jones, Rosemary. "The Glycoproteins of Secretory Cells in Airway Epithelium". En Novartis Foundation Symposia, 175–201. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470720356.ch9.

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Reynolds, Susan D., Moumita Ghosh, Heather M. Brechbuhl, Shama Ahmad y Carl W. White. "Stem and Progenitor Cells of the Airway Epithelium". En Stem Cells in the Respiratory System, 1–23. Totowa, NJ: Humana Press, 2010. http://dx.doi.org/10.1007/978-1-60761-775-4_1.

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Actas de conferencias sobre el tema "Airway epithelium"

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Koo, J., C. Kim, J. Lee, K. Kim y J. Yoon. "Regeneration of Airway Epithelium Using Autologous Epithelial Cells." En 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.a2012.

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De, Bishnu P., Lindsay Lief, Michelle R. Staudt, Jennifer Fuller, Neil R. Hackett, Timothy Wilson, Maryna Elnasher, Matthew S. Walters y Ronald G. Crystal. "Smoking Accelerates Airway Epithelial Aging: Smoking-Dependent Decrease In Small Airway Epithelium Telomere Length". En 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.a4123.

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Cohn, Lauren E., Karin Provost, Robert J. Homer, Naiqian Niu y Charlotte Andreasen. "IFN-³ Acts On The Airway Epithelium To Regulate Allergic Airway Inflammation". En 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.a2485.

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Gallos, George, Sarah Zaidi, Peter Yim, Yi Zhang, Lazlo Virag, Robert Whittington y Charles Emala. "Airway Epithelium Is The Predominant Cellular Source Of Endogenous Airway GABA". En 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.a6455.

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Kotnala, S., J. A. Gimenes, H. Reddy Vari, N. Owuor, N. Xander, W. Li y U. Sajjan. "FOXO3A Regulates Antiviral Responses in Airway Epithelium". En 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.a5753.

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Hansi, R. K., G. K. Singhera, T. Shaipanich, D. D. Sin, D. R. Dorscheid y J. M. Leung. "Respiratory Syncytial Virus Induces Epithelial Permeability in COPD and HIV Airway Epithelium". En American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a3650.

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Meuchel, Lucas W., Elizabeth A. Townsend, Michael A. Thompson, Stephen D. Cassivi y Y. S. Prakash. "Neurotrophins Produce Nitric Oxide In Human Airway Epithelium". En 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.a5550.

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Legebeke, Jelmer, Katie Horton, Gabrielle Wheway, Htoo Wai, Claire Jackson, Janice Coles, John Holloway, Jane Lucas y Diana Baralle. "Transcriptome analysis of ciliary differentiation in airway epithelium". En ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa2398.

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Koliana, Marianne, Ernie Wong, David J. Jackson, Tatiana Kebadze, Carine Blanchard, Sebastian L. Johnston, Elaine Holmes y Gary Frost. "Presence of airway SCFAs in asthma and response of airway epithelium to SCFAs". En ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa2379.

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Schamberger, Andrea, Fien Verhamme, Michael Lindner, Jürgen Behr y Oliver Eickelberg. "Transcriptome analysis of the human airway epithelium duringin vitrodifferentiation". En ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa3993.

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Informes sobre el tema "Airway epithelium"

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Tierney, L. A., C. Bloomfield y N. F. Johnson. Expression of a TGF-{beta} regulated cyclin-dependent kinase inhibitor in normal and immortalized airway epithelial cells. Office of Scientific and Technical Information (OSTI), diciembre de 1995. http://dx.doi.org/10.2172/381389.

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Zuraw, Bruce L. Epithelial Cell TRPV1-Mediated Airway Sensitivity as a Mechanism for Respiratory Symptoms Associated with Gulf War Illness?". Fort Belvoir, VA: Defense Technical Information Center, junio de 2010. http://dx.doi.org/10.21236/ada536752.

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Pacheco-Ojeda, Luis, Carolina Sáenz-Gómez, Stalin Cañizares-Quisiguiña, Tatiana Borja-Herrera, Juan Carlos Vallejo-Garzón y Sergio Poveda. Function Sparing Conservative Approach of a Low-Grade Chondrosarcoma of the Larynx: Case Report and Literature Review. Science Repository, marzo de 2024. http://dx.doi.org/10.31487/j.scr.2024.01.04.

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Background: Laryngeal cancer is relatively uncommon in Ecuador. Usually epithelial in origin, the most frequent histological type is squamous cell carcinoma. The most common mesenchymal tumor is chondrosarcoma. Most laryngeal chondrosarcomas are treated with total laryngectomy, but a conservative function sparing resection is recommended in low-grade limited tumors. Case Report: In a 68-year-old female nonsmoker patient, a small tumor was found in the posterior left aspect of the cricoid cartilage in a computed tomography (CT) performed immediately after an unexpected difficulty to pass the endotracheal tube for a thoracoscopic biopsy of 4 cm tumor of the left lung, in another hospital. The patient underwent, then, an initial tracheostomy, a total thyroidectomy for a goiter and a biopsy of the tumor of the cricoid cartilage whose pathological study was inconclusive. One month later, a low-grade neuroendocrine pulmonary tumor was completed resected. Two years later, a CT scan showed the cricoid lesion with the same characteristics. At endoscopic video laryngoscopy, two subglottic masses that narrowed the airway in approximately 60% of the normal caliber, were observed located at the posterior and left walls. An intraluminal resection was performed through a transcricoid anterior approach. The pathological diagnosis was a low-grade chondrosarcoma. Tracheal decannulation was performed one month later. At an endoscopic video laryngoscopy performed six months post-operatively, the tracheal caliber and mucosa were normal. The patient remained with normal voice and breathing. Conclusion: We report the second case of chondrosarcoma of the larynx in our country, treated by a conservative approach.
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High-fat Western diet alters silica-induced airway epithelium ion exchange but not airway smooth muscle reactivity (dataset). U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, mayo de 2023. http://dx.doi.org/10.26616/nioshrd-1068-2023-0.

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