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In these cases, calculating the PaCO2 and ETCO2 gradient [P a-ETCO2)] might be useful as an indicator of dead sP a-ETCO2ilation and the changes in airway physiology.
Inflammatory responses and changes in airway physiology elicited by rCARDS toxin are similar to those observed during M. pneumoniae infection suggesting that the CARDS toxin plays a major role in the pathogenesis of M. pneumoniae-mediated disease.
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The underlying mechanism(s) of in utero SHS-induced alterations in airway physiology is yet to be studied and may involve proteostasis-mediated modulation of surfactant proteins, NFκB and growth factors.
Thus, it is well recognized that oxidative stress-induced changes in airway epithelial cells physiology plays a central role in innate and adaptive immune responses as well as mucosal inflammation [34].
This might be due to changes in airway mechanics in the presence of inflammation or structural changes within the airways.
Changes in airway measurements were assessed using lateral cephalometric radiographs.
These changes in airway structure result from chronic inflammation and airway remodeling (Woolcock and Permutt 2011).
In chronic airway inflammatory lung diseases, airway remodeling is correlated with marked changes in airway mechanics and symptoms related to airway obstruction [ 14].
Minimal changes in airway eosinophils are predicted in this phase.
Airway diameter with changes in lung volume, or so-called airway distensibility is reflected by reactance, and changes in airway pressure with lung volume by resistance.
Changes in airway pressure and TV were not quantitatively related to cardiac index changes.
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