Objective: Studying smokers with normal spirometry requires monitoring tools of the peripheral lung. A validated multiple breath washout technique was used to assess possible recovery of smoking-induced small airway malfunction in acinar and conductive lung zones.
Methods: Eighty-seven smokers with a smoking history of at least 10 pack-years but absence of spirometric airflow obstruction were invited for assessment of lung function and small airway function at baseline and after 1 wk, 3 mo, 6 mo, and 12 mo of smoking cessation. A control group of 16 persistent smokers was studied at the same time intervals.
Measurements And Main Results: Of the 87 smokers, 66, 32, 28, and 21% successfully ceased smoking for 1 wk, 3 mo, 6 mo, and 12 mo, respectively. Lung function parameters remained essentially unaffected by smoking cessation. Ventilation heterogeneity showed transient improvements after 1 wk in the acinar lung compartment with a return to baseline afterwards. By contrast, there were persistent improvements in the conductive airway compartment; for example, smokers who successfully quit smoking for 12 mo (n=18) showed a 30 and 42% reduction of conductive airways abnormality after 1 wk and 1 yr, respectively.
Conclusions: Smokers with early signs of small airway malfunction who successfully quit smoking show sustained improvements of conductive airway malfunction. In contrast, acinar airway malfunction quickly returns to baseline after a transient improvement.
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http://dx.doi.org/10.1164/rccm.200603-422OC | DOI Listing |
Ann Plast Surg
January 2025
Division of Plastic Surgery, Northwestern University Feinberg School of Medicine, Chicago, IL.
Background: Nasal septal defects cause considerable morbidity and represent a challenging reconstructive problem. Traditional repair techniques have employed local intranasal tissues and allograft adjuncts. For large septal defects (>4-5 cm2), less than half are successfully resolved.
View Article and Find Full Text PDFEMBO Mol Med
January 2025
Sabri Ülker Center for Metabolic Research, Department of Molecular Metabolism, Harvard T.H. Chan School of Public Health, Boston, MA, USA.
Host metabolic fitness is a critical determinant of infectious disease outcomes. Obesity, aging, and other related metabolic disorders are recognized as high-risk disease modifiers for respiratory infections, including coronavirus infections, though the underlying mechanisms remain unknown. Our study highlights fatty acid-binding protein 4 (FABP4), a key regulator of metabolic dysfunction and inflammation, as a modulator of SARS-CoV-2 pathogenesis, correlating strongly with disease severity in COVID-19 patients.
View Article and Find Full Text PDFHosp Pediatr
January 2025
Paediatric Intensive Care Unit Service, Hospital Sant Joan de Déu, University of Barcelona, Esplugues de Llobregat, Barcelona, Spain.
Purpose: There is limited evidence to guide the treatment of enteral nutrition (EN) for children with bronchiolitis who receive biphasic positive airway pressure (BiPAP) support.
Methods: This quality improvement project included patients with bronchiolitis who were supported by BiPAP ventilation. An algorithm to increase EN treatment in those patients was created by stakeholders.
J Am Vet Med Assoc
January 2025
1Department of Small Animal Medicine and Surgery, College of Veterinary Medicine, University of Georgia, Athens, GA.
Objective: To determine whether folded-flap palatoplasty (FFP) results in improved respiratory outcomes compared to standard staphylectomy (SS).
Methods: English Bulldogs were randomized to receive FFP or SS in a parallel, equal-allocation, prospective study design at a single institution. Exercise-tolerance testing (ETT), arterial blood gas, head CT, and an owner survey were completed preoperatively and at recheck (approx 30 days postoperatively).
Am J Respir Cell Mol Biol
January 2025
National Heart & Lung Institute, Imperial College London, Airway Disease Section, London, United Kingdom of Great Britain and Northern Ireland.
Chronic obstructive pulmonary disease (COPD) is associated with the acceleration of lung aging, and the accumulation of senescent cells in lung tissue. MicroRNA (miR)-34a induces senescence by suppressing the anti-aging molecule, sirtuin-1 (SIRT1). Senescent cells spread senescence to neighbouring and distant cells, favouring COPD progression and its comorbidities.
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