In our center the prevalence of MRSA in CF patients, chronically colonized with S. aureus and over the age of 4 years, was 15.2% (12.6% chronic infection). MRSA colonization was shown to be associated with a genotype F508del, presence of bronchiectasis and hospitalization. Our spirometric data also show that a MRSA episode entails an FEV(1) decline that is almost double that predicted for CF patients who can remain unaffected by MRSA.

Since studies about clinical status after COVID-19 are scarce, we conducted a cross sectional study with assessment of residual symptoms, lung function and chest CT. Materials and Methods: During an outpatient follow-up visit, chest CT, pulmonary function and COVID-19 related symptoms were assessed approximately 10 weeks after diagnosis. Demographics, baseline (time of diagnosis) CT score and blood results were collected from patient files. Association between lung function and clinical characteristics (baseline), blood markers (baseline), chest CT (baseline and follow-up) and symptom score (followup) was analysed. Mann-Whitney U tests and Chi squared tests were used for statistical comparison between subgroups with and without restriction. Results and discussion: Two hundred-twenty subjects were evaluated at a median follow-up of 74±12 (SD) days. Median symptom and median CT score at follow-up were 1(IQR=0-2) and 2(IQR=0-6) respectively. Forty-six percent of patients had normal lung function, while TLC and TLCO below the lower limit of normal were observed in 38% and 22% of subjects respectively. This restrictive pulmonary impairment was associated with length of hospital stay (8 vs 6 days; p=0.003), admission to the intensive care unit (27% vs 13%;p=0.009), and invasive mechanical ventilation (10% vs 0.7%;p=0.001), but not with symptom score or CT score at baseline and follow-up. Conclusions: Fifty-four percent of COVID-19 survivors had abnormal lung function 10 weeks after diagnosis. Restriction was the most prevalent pulmonary function, with the more critically ill patients being more prone to this condition. Yet, restriction could not be linked with abnormal imaging results or residual symptoms.

This review is the summary of a workshop on the role of distal airways in chronic obstructive pulmonary disease (COPD), which took place in 2009 in Vence, France.The evidence showing inflammation and remodelling in distal airways and the possible involvement of these in the pathobiology, physiology, clinical manifestations and natural history of COPD were examined. The usefulness and limitations of physiological tests and imaging techniques for assessing distal airways abnormalities were evaluated.Ex vivo studies in isolated lungs and invasive measurements of airway resistance in living individuals have revealed that distal airways represent the main site of airflow limitation in COPD. Structural changes in small conducting airways, including increased wall thickness and obstruction by muco-inflammatory exudates, and emphysema (resulting in premature airway closure), were important determinants of airflow limitation. Infiltration of small conducting airways by phagocytes (macrophages and neutrophils), dendritic cells and T and B lymphocytes increased with airflow limitation. Distal airways abnormalities were associated with patient-related outcomes (e.g. dyspnoea and reduced health-related quality of life) and with the natural history of the disease, as reflected by lung function decline and mortality.These data provide a clear rationale for targeting distal airways in COPD.

BackgroundTomoBreast is a unicenter, non-blinded randomized trial comparing conventional radiotherapy (CR) vs. hypofractionated Tomotherapy (TT) for post-operative treatment of breast cancer. The purpose of the trial is to compare whether TT can reduce heart and pulmonary toxicity. We evaluate early toxicities.MethodsThe trial started inclusion in May 2007 and reached its recruitment in August 2011. Women with stage T1-3N0M0 or T1-2N1M0 breast cancer completely resected by tumorectomy (BCS) or by mastectomy (MA) who consented to participate were randomized, according to a prescribed computer-generated randomization schedule, between control arm of CR 25x2 Gy/5 weeks by tangential fields on breast/chest wall, plus supraclavicular-axillary field if node-positive, and sequential boost 8x2 Gy/2 weeks if BCS (cumulative dose 66 Gy/7 weeks), versus experimental TT arm of 15x2.8 Gy/3 weeks, including nodal areas if node-positive and simultaneous integrated boost of 0.6 Gy if BCS (cumulative dose 51 Gy/3 weeks). Outcomes evaluated were the pulmonary and heart function. Comparison of proportions used one-sided Fisher's exact test.ResultsBy May 2010, 70 patients were randomized and had more than 1 year of follow-up. Out of 69 evaluable cases, 32 were assigned to CR (21 BCS, 11 MA), 37 to TT (20 BCS, 17 MA). Skin toxicity of grade ≥1 at 2 years was 60% in CR, vs. 30% in TT arm. Heart function showed no significant difference for left ventricular ejection fraction at 2 years, CR 4.8% vs. TT 4.6%. Pulmonary function tests at 2 years showed grade ≥1 decline of FEV1 in 21% of CR, vs. 15% of TT and decline of DLco in 29% of CR, vs. 7% of TT (P = 0.05).ConclusionsThere were no unexpected severe toxicities. Short course radiotherapy of the breast with simultaneous integrated boost over 3 weeks proved feasible without excess toxicities. Pulmonary tests showed a slight trend in favor of Tomotherapy, which will need confirmation with longer follow-up of patients.Trail registrationClinicalTrials.gov NCT00459628

Monitoring of chronic lung disease requires reference values of lung function indices, including putative markers of small airway function, spanning a wide age range.We measured spirometry, transfer factor of the lung for carbon monoxide (TLCO), static lung volume, resistance and ventilation distribution in a healthy population, studying at least 20 subjects per sex and per decade between the ages of 20 and 80 years.With respect to the Global Lung Function Initiative reference data, our subjects had average z-scores for forced expiratory volume in 1 s (FEV1), forced vital capacity (FVC) and FEV1/FVC of −0.12, 0.04 and −0.32, respectively. Reference equations were obtained which could account for a potential dependence of index variability on age and height. This was done for (but not limited to) indices that are pertinent to asthma and chronic obstructive pulmonary disease studies: forced expired volume in 6 s, forced expiratory flow, TLCO, specific airway conductance, residual volume (RV)/total lung capacity (TLC), and ventilation heterogeneity in acinar and conductive lung zones.Deterioration in acinar ventilation heterogeneity and lung clearance index with age were more marked beyond 60 years, and conductive ventilation heterogeneity showed the greatest increase in variability with age. The most clinically relevant deviation from published reference values concerned RV/TLC values, which were considerably smaller than American Thoracic Society/European Respiratory Society-endorsed reference values. @ERSpublications We present reference equations for median and variability of most lung function indices, in the age range 20-80 years http://ow.ly/SsZFW

Rationale Positive pressure ventilation exposes the lung to mechanical stresses that can exacerbate injury. The exact mechanism of this pathological process remains elusive. Objectives Describe Recruitment/Derecruitment (R/D) at acinar length scales over short time frames and test the hypothesis that mechanical interdependence between neighboring lung units determines the spatial and temporal distributions of R/D, using a computational model. Methods Experiments were performed in anaesthetized rabbits ventilated in Pressure Controlled mode (PCV). The lung was consecutively imaged at ~1.5 min intervals, at each Positive End-Expiratory Pressure (PEEP) of 12, 9, 6, 3 and 0 cmH2O before and after injury. The extent and spatial distribution of R/D was analyzed by subtracting subsequent images. In a realistic lung structure we implemented a mechanistic model in which each unit has individual pressures and speeds of opening and closing. Derecruited and Recruited lung fractions (Fderecruited, Frecruited) were computed based on the comparison of the aerated volumes at successive time points. Results Alternative R/D occurred in neighboring alveoli over short time scales in all tested PEEP levels and despite stable PCV. The computational model reproduced this behavior only when parenchymal interdependence between neighboring acini was accounted for. Simulations closely mimicked the experimental magnitude of Fderecruited and Frecruited when mechanical interdependence was included, while its exclusion gave Frecruited values of zero at PEEP ≥ 3 cmH2O. Conclusions These findings give further insight into the microscopic behavior of the injured lung and provide a means of testing protective-ventilation strategies to prevent R/D and subsequent lung damage.

This study investigated the effect of cigarette smoke exposure and the potential protection N-acetylcysteine (NAC) in rat lungs.Forty-eight rats were exposed to cigarette smoke (CS) for 10 weeks, without (CS group) or with (CS+NAC group) oral intake of NAC 200 mg . rat -1 . day -1 , or to fresh air (Control). All rat lungs were assessed in terms of lung function, ventilation distribution (nitrogen, helium and sulphur hexafluoride phase III slopes), and morphometry (airway wall thickening of small, medium and large bronchi).The small bronchi, defined as the airways with an internal perimeter <1,000 mm showed significantly thicker airway walls in the CS than in the Control group. By contrast, no airway wall thickening was observed in the CS+NAC group with respect to Control. Except for decreased lung volumes and compliance in CS and CS+NAC groups, which were entirely attributable to smaller body weight gain, lung function was indistinguishable from Control. Phase III slopes were significantly increased only in the CS group.In conclusion, smoke-induced alterations in the rat lungs were reflected in wall thickening of the small bronchi and increased ventilation maldistribution. These smoke-induced morphometric and ventilation distribution alterations were prevented by N-acetylcysteine. Eur Respir J 2000; 15: 505±511. In humans, a major site of inflammatory action of cigarette smoke has been attributed to the so-called small airways, stimulating a number of studies aimed at characterizing and detecting structural change in the lung periphery [1,2]. The phase III slope of the N 2 single breath washout (SBW) test became a popular index of small airways alteration since the work by COSIO et al. [3] showed its correlation with morphological scores of small airways abnormalities in smokers with normal spirometry. A later SBW study by VAN MUYLEM et al. [4], which included helium and sulphur hexafluoride tracer concentrations, also revealed distinct correlations between indices derived from He and SF 6 slopes and airway pathology scores. Due to the fact that the diffusion front is located more peripherally for SF 6 than for He, the respective phase III slopes are indicative of the site where ventilation inhomogeneities occur.Although animal studies are well-suited for the study of lung function in the diseased lung, the difficulty often resides in reproducing a lesion which is comparable to that encountered in the human lung [5]. Previous studies in rats have led to conflicting results as to whether the cigarette smoke induces emphysematous lesions [6,7] or not [8,9] and not all studies provide any information about the extent to which the nonalveolated airways are affected [10]. Despite these difficulties, rat lungs have been used to investigate the possible protective role of N-acetylcysteine (NAC) over cigarette smoke induced lesions. NAC is an antioxidant and can therefore be expected to change lung oxidant-antioxidant imbalance induced by cigarette smoke which is a source of oxidants. Previous histopathology...

We showed combined imaging experiments and CFD simulations to systematically study aerosol deposition patterns in human airways down to generation 5, where particle deposition could be spatially linked to the airway geometry. As particles are negotiating an increasing number of airways in subsequent branching generations, CFD predicts marked deviations of aerosol distribution with respect to ventilation distribution, even in the normal human lung.