Results 131 to 140 of about 783,276 (359)
Differentiation Between Localized and Generalized Airway Obstruction [PDF]
Bo Simonsson, R Malmberg
openalex +1 more source
ABSTRACT Background Elexacaftor/tezacaftor/ivacaftor (ETI) is a Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) therapy that improves pulmonary function and chronic rhinosinusitis (CRS) in cystic fibrosis (CF) adults with at least one copy of the F508del CFTR mutation.
Margaux Petitjean+16 more
wiley +1 more source
Trial of Bronchodilator Drugs Given by Metered Aerosol with a Comparison of Two Bedside Methods of Estimating Airway Resistance [PDF]
B I Hoffbrand+3 more
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MiR‐221‐3p Attenuates IL‐33‐Induced Mast Cell Cytokine Expression by Targeting KIT
ABSTRACT Background Mast cells (MCs) are involved in type 2 inflammation in chronic rhinosinusitis with nasal polyps (CRSwNP), which depends on interleukin (IL)‐33 stimulation. MiR‐221 is reported to be an important regulator of MCs, and miR‐221‐3p can be expressed in CRSwNP. However, the role of miR‐221‐3p in CRSwNP is unclear. Methods Ethmoid tissues
Ruowu Liu+11 more
wiley +1 more source
Bronchodilator response patterns in patients with chronic airways obstruction: use of peak inspiratory flow rate. [PDF]
K.B. Saunders
openalex +1 more source
ABSTRACT Background Chronic rhinosinusitis with nasal polyps (CRSwNP) significantly impacts patients’ quality of life (QoL). Standard treatments include nasal irrigations, nasal steroids, systemic corticosteroids, and functional endoscopic sinus surgery (FESS).
Anne‐Sophie Homøe+7 more
wiley +1 more source
ABSTRACT Background The pathogenesis of inflammation in eosinophilic chronic rhinosinusitis (ECRS) and non‐eosinophilic chronic rhinosinusitis (NECRS) remains poorly understood. This study aimed to assess immune cell infiltration within the sinonasal microenvironment in these conditions.
Katarzyna Czerwaty+5 more
wiley +1 more source
ABSTRACT Background Particulate matter ⩽2.5 µm in diameter (PM2.5) and its role in chronic rhinosinusitis (CRS) pathogenesis have gained heightened attention. We previously demonstrated that PM2.5 exposure may bias the nasal mucosa in CRS toward a Type 2 inflammatory pathway.
Rory J. Lubner+5 more
wiley +1 more source