The European respiratory journal : official journal of the European Society for Clinical Respiratory Physiology
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Cigarette smoke (CS), the primary risk factor of chronic obstructive pulmonary disease (COPD), leads to pulmonary inflammation through interleukin-1 receptor (IL-1R)I signalling, as determined using COPD mouse models. It is unclear whether interleukin (IL)-1α or IL-1β, activated by the Nlrp3/caspase-1 axis, is the predominant ligand for IL-1RI in CS-induced responses. We exposed wild-type mice (treated with anti-IL-1α or anti-IL-1β antibodies), and IL-1RI knockout (KO), Nlrp3 KO and caspase-1 KO mice to CS for 3 days or 4 weeks and evaluated pulmonary inflammation. ⋯ Interestingly, CS-induced inflammation occurred independently of IL-1β activation by the Nlrp3/caspase-1 axis. In human subjects, IL-1α and IL-1β were significantly increased in total lung tissue and induced sputum of patients with COPD, respectively, compared with never-smokers. These results suggest that not only IL-1β but also IL-1α should be considered as an important mediator in CS-induced inflammation and COPD.
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Multicenter Study
Obstructive sleep apnoea and metabolic impairment in severe obesity.
Obstructive sleep apnoea (OSA) seems to worsen metabolism. This effect has not been evaluated in morbid obesity (MO). We hypothesised that the metabolic profile is more impaired in MO patients with OSA than in those without, and investigated whether any specific metabolic dysfunction is related to OSA in MO. ⋯ AHI was independently associated with systolic and diastolic BP, triglycerides and the percentage of glycosylated haemoglobin (HbA1c) in the total sample, and with systolic BP, high-density lipoprotein cholesterol and HbA1c in those samples without DM2. OSA increased the adjusted odds ratio of having MetS by 2.8 (95% CI 1.3-6.2; p=0.009). In MO, OSA is associated with major metabolic impairment caused by higher BP and poorer lipid and glucose control, independent of central obesity or DM2.
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Randomized Controlled Trial
Effect of a nicotine-free inhalator as part of a smoking-cessation programme.
Smoking-cessation drugs are inadequate at addressing the behavioural component of tobacco dependence. Nicotine-free inhalators are plastic devices that may provide a coping mechanism for conditioned smoking by replacing some of the rituals associated with smoking gestures. This study assessed the effect of using a nicotine-free inhalator to improve success in a cessation programme. ⋯ However, the quit rate in the PAIPO group (66.7%) was more than three-fold higher than the reference group (19.2%) for those individuals with high Glover-Nilsson Smoking Behavioural Questionnaire (GN-SBQ) scores at baseline. The results of the logistic model analysis indicate that a high GN-SBQ score is a strong independent predictor for successful quitting at 24 weeks (OR 8.88; 95% CI 2.08-37.94) in the PAIPO group. Nicotine-free inhalators may be beneficial when used in the context of smoking-cessation interventions, particularly for those smokers for whom handling and manipulation of their cigarettes plays an important part in the ritual of smoking.
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Randomized Controlled Trial Multicenter Study
Inhaled dry powder mannitol in cystic fibrosis: an efficacy and safety study.
This international phase III study of inhaled dry powder mannitol was a randomised, double-blind, 26-week study, followed by a further 26-week, open-label (OL) extension. 324 cystic fibrosis (CF) patients were randomised, in a 3:2 ratio, to mannitol (400 mg b.i.d.) and control groups. The primary efficacy end-point was to determine the change in forced expiratory volume in 1 s (FEV₁) over the double-blind phase. Secondary end-points included changes in forced vital capacity and pulmonary exacerbations. ⋯ The most common mannitol-related AEs were cough, haemoptysis and pharyngolaryngeal pain. Mannitol showed sustained, clinically meaningful benefit in airway function in CF, irrespective of concomitant rhDNase use. Mannitol appears to have an acceptable safety profile for patients with CF.
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A decreased transfer coefficient of the lung for carbon monoxide (K(CO)) is associated with emphysema. We evaluated whether in heavy smokers, baseline K(CO) was associated with the progression of computed tomography (CT)-detected emphysema, and the progression of airflow limitation. Heavy smokers, mean ± sd 41.3 ± 18.7 pack-yrs, participating in a lung cancer screening trial underwent diffusion testing and CT scanning of the lungs. ⋯ Mean ± sd 15th percentile was -938 ± 19, absolute FEV₁/FVC was 71.6 ± 9% and K(CO) was 1.23 ± 0.25, which is 81.8 ± 16.5% of predicted. By interpolation, a one sd (0.25) lower K(CO) value at baseline predicted a 1.6 HU lower 15th percentile and a 0.78% lower FEV₁/FVC after follow-up (p < 0.001). A lower baseline K(CO) value is independently associated with a more rapid progression of emphysema and airflow limitation in heavy smokers.