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This article advocates for better nurse training and their active involvement in asthma care in Great Britain. Asthma care in Great Britain varies, with poor outcomes including preventable attacks, hospital admissions, and deaths. Nurses play a crucial role in asthma management but often lack adequate training. Emphasizing post-attack reviews and quality control, the article proposes a 7-step plan for primary care practices to improve asthma management and reduce attacks.

Purpose: Sensorimotor cough skill training (CST) has been shown to improve cough strength, as well as facilitate changes during training (i.e., motor performance) and generalization to untrained tasks (i.e., motor learning). However, there is a gap in our understanding of the effects of voluntary CST (without sensory stimuli) on motor performance and learning. Furthermore, the contribution of physiologic factors, such as lung volume, a driver of cough strength in healthy adults, and treatment-specific factors, such as biofeedback, remains unexamined. Method: Twenty individuals with Parkinson’s disease (PD) completed pre- and post-CST single voluntary, sequential voluntary, and reflex cough testing. Participants were randomized to biofeedback or no biofeedback groups. They completed one CST session involving 25 trials of voluntary coughs, with the treatment target set 25% above baseline peak flow. Participants were instructed to “cough hard” to exceed the target. In the biofeedback group, participants received direct visualization of the target line in real time. Results: Cough peak flow showed positive improvements in motor performance (β = .02; 95% credible interval [CI]: 0.01, 0.03) and learning (β = .26; 95% CI: 0.03, 0.47). Changes in lung volume from pre- to post-CST did not predict treatment response. No differences in treatment response were detected between the biofeedback groups. Conclusions: A single session of voluntary CST improved voluntary cough motor performance and learning. Although lung volume increased during CST, changes to lung volume did not predict treatment response. These findings demonstrate the potential of voluntary CST to improve motor performance and motor learning among individuals with PD and cough dysfunction. [ABSTRACT FROM AUTHOR]

• Life-course risk for incident dementia was modulated by lung function. • Immunity, oxygen-carrying indices and specific metabolites are critical mediators. • Brain structures were substantially changed with poor lung function. • Monitoring lung function is of great significance for cognitive brain health. Whether lung function prospectively affects cognitive brain health independent of their overlapping factors remains largely unknown. This study aimed to investigate the longitudinal association between decreased lung function and cognitive brain health and to explore underlying biological and brain structural mechanisms. This population-based cohort included 43,1834 non-demented participants with spirometry from the UK Biobank. Cox proportional hazard models were fitted to estimate the risk of incident dementia for individuals with low lung function. Mediation models were regressed to explore the underlying mechanisms driven by inflammatory markers, oxygen-carrying indices, metabolites, and brain structures. During a follow-up of 3,736,181 person-years (mean follow-up 8.65 years), 5,622 participants (1.30 %) developed all-cause dementia, which consisted of 2,511 Alzheimer's dementia (AD) and 1,308 Vascular Dementia (VD) cases. Per unit decrease in lung function measure was each associated with increased risk for all-cause dementia (forced expiratory volume in 1 s [liter]: hazard ratio [HR, 95 %CI], 1.24 [1.14–1.34], P = 1.10 × 10-07; forced vital capacity [liter]: 1.16 [1.08–1.24], P = 2.04 × 10-05; peak expiratory flow [liter/min]: 1.0013 [1.0010–1.0017], P = 2.73 × 10-13). Low lung function generated similar hazard estimates for AD and VD risks. As underlying biological mechanisms, systematic inflammatory markers, oxygen-carrying indices, and specific metabolites mediated the effects of lung function on dementia risks. Besides, brain grey and white matter patterns mostly affected in dementia were substantially changed with lung function. Life-course risk for incident dementia was modulated by individual lung function. Maintaining optimal lung function is useful for healthy aging and dementia prevention. [ABSTRACT FROM AUTHOR]

Clinical trials with mepolizumab, a humanised monoclonal antibody against interleukin-5, show a 50% reduction in severe asthma exacerbations in people with severe eosinophilic asthma. Exacerbations in patients treated with mepolizumab seem to be different to exacerbations in those given placebo, as patients treated with mepolizumab report fewer symptoms, have a lower sputum eosinophil count, and smaller fall in peak expiratory flow. We aimed to investigate the inflammatory phenotype and physiological characteristics of exacerbation events in patients with severe eosinophilic asthma who were treated with mepolizumab. This multicentre, prospective, observational cohort study was carried out at four UK specialist severe asthma centres. Participants were aged 18–80 years, with severe eosinophilic asthma (Global Initiative for Asthma steps 4 and 5), and were eligible for mepolizumab therapy. All participants received mepolizumab 100 mg subcutaneously every 4 weeks, had a scheduled study visit when stable on mepolizumab (≥3 months on treatment), and measured daily peak flow and completed symptoms diaries throughout the course of the study. Participants attended their study centre for unscheduled exacerbation assessment when symptoms worsened outside of their normal daily variation and before commencing rescue treatment. If a participant was unable to attend their study centre for exacerbation or had initiated rescue treatment before the study visit, clinical details of the missed exacerbation were collected by clinical staff. In this exploratory study, the endpoint was 100 clinical assessments at exacerbation completed across all sites for participants on mepolizumab before initiation of rescue treatment. Characteristics of those who had exacerbations on mepolizumab were compared with those who did not, peak flow and symptoms diaries were compared for assessed versus missed exacerbations, and exacerbation phenotypes defined by sputum eosinophil cell count were compared. The utility of fractional exhaled nitric oxide (FeNO) and C-reactive protein in determining exacerbation phenotype on mepolizumab treatment were also assessed. This study is registered with ClinicalTrials.gov , NCT03324230. Between Nov 30, 2017, and May 29, 2019, 145 participants were enrolled and treated with mepolizumab, five were excluded from the analysis. 172 exacerbations occurred, with 96 (56%) assessed before commencing rescue treatment. Compared with patients who did not exacerbate, patients who exacerbated had a higher exacerbation rate and more emergency department attendances in the year before commencing mepolizumab. The change in peak expiratory flow at nadir in the assessed exacerbation group was mean −40·5 L/min (SD 76·3) versus mean −37·0 L/min (93·0; p=0·84) in the missed exacerbation group, and there was no difference in reported symptom burden. When comparing exacerbations with a high sputum eosinophil count (≥2%; SEHIGH) with exacerbations with a low sputum eosinophil count (<2%; SELOW), the SEHIGH exacerbations were FeNO high (median difference 33 parts per billion [ppb; 95% CI 8 to 87]; p=0·0004), with lower FEV 1 percent predicted (mean difference −15·9% [–27·0 to −4·8]; p=0·0075), lower FEV 1 to forced vital capacity ratio (mean difference −10·3 [–17·0 to −3·6]; p=0·0043), and higher blood eosinophil counts (median difference 40 cells per μL [20 to 70]; p=0·0009). By contrast, SELOW exacerbations had higher C-reactive protein concentrations (median difference 12·7 mg/L [3·5 to 18·5]; p<0·0001), higher sputum neutrophil counts (median difference 52·7% [34·5 to 59·2]; p<0·0001), and were more likely to be treated with antibiotics (p=0·031). FeNO (≤20 or ≥50 ppb) was the most useful discriminator of inflammatory phenotype at exacerbation. The most common adverse event was hospital admission due to asthma exacerbation (17 [50%] of 34 events), none of the adverse events were study procedure related. Exacerbations on mepolizumab are two distinct entities, which can largely be differentiated using FeNO: non-eosinophilic events are driven by infection with a low FeNO and high C-reactive protein concentration, whereas eosinophilic exacerbations are FeNO high. The results of the MEX study challenge the routine use of oral corticosteroids for the treatment of all asthma exacerbation events on mepolizumab, as well as the switching of biological therapies for treatment failure without profiling the inflammatory phenotype of ongoing asthma exacerbations. The results highlight clinically available tools to enable profiling of these residual exacerbations in patients treated with mepolizumab. UK Medical Research council. [ABSTRACT FROM AUTHOR]

• Asthma or atopic dermatitis were associated with increased risk of depression and anxiety. The association was stronger among participants on current therapy. • Participants reporting both asthma and atopic dermatitis presented the highest risk of depression and anxiety. • A dose-response association was observed between neutrophil-to-lymphocyte ratio with depression and anxiety. • A dose-response relationship was observed between Peak Expiratory Flow rate with depression and anxiety in asthma. • Middle-age onset asthma or atopic dermatitis presented the strongest associations with depression and anxiety. The present study investigated the association of depression and anxiety symptomatology (DAS) with asthma and atopic dermatitis (AD) diagnosis during mid-adult years. The study employed data from 502,641 participants in the UK Biobank. Neutrophils to Lymphocytes Ratios (NLRs) of patients with asthma and AD were calculated and evaluated in relation to DAS, measured via the Patient Health Questionnaire-4 (PHQ-4). Age of asthma or AD onset association with DAS were also estimated. Multivariable regression analyses were implemented among participants with asthma or AD, compared to those without these disorders. Out of 58,833 participants with asthma and 13,462 with AD, the prevalence of DAS was 11.7% and 2.7%, respectively. DAS increased among participants with either asthma or AD, being highest within patients having both (β = 0.41, 95% confidence interval (95%CI), 0.34,0.49). NLR showed a linear increase with PHQ scores in asthma patients, (tertile 1, β = 0.30, 95% CI, 0.27,0.34; tertile 2, β = 0.36, 95%CI, 0.32,0.39, and tertile 3, β = 0.43, 95%CI, 0.39,0.46). An inverted U-shaped association was seen between age of asthma onset and PHQ, with the 40–59 age group (β = 0.54, 95%CI, 0.48,0.59) showing the highest risk followed by the 60+ (β = 0.43, 95%CI, 0.34,0.51 and 20–39 groups (β = 0.32, 95%CI, 0.27,0.38). Similar patterns emerged within AD. Asthma and AD were associated with increased DAS during mid-adult years, being strongest among participants reporting both disorders. A dose–response relationship between NLR and DAS was observed. Asthma or AD onset during mid-adult years (40–59) were associated with the highest increment in DAS. [ABSTRACT FROM AUTHOR]

Maximal expiratory airflow peaks early in the third decade of life, then gradually declines with age. The pattern of airflow through adulthood for individuals born very preterm (at <32 weeks' gestation) or with very low birthweight (<1501 g) is unknown. We aimed to compare maximal expiratory airflow in these individuals during late adolescence and early adulthood with that of control individuals born with normal birthweight (>2499 g) or at term. We did a meta-analysis of individual participant data from cohort studies, mostly from the pre-surfactant era. Studies were identified through the Adults born Preterm International Collaboration and by searching PubMed and Embase (search date May 25, 2016). Studies were eligible if they reported on expiratory flow rates beyond 16 years of age in individuals born very preterm or with very low birthweight, as well as controls born at term or with normal birthweight. Studies with highly selected cohorts (eg, only participants with bronchopulmonary dysplasia) or in which few participants were born very preterm or with very low birthweight were excluded. De-identified individual participant data from each cohort were provided by the holders of the original data to a central site, where all the data were pooled into one data file. Any data inconsistencies were resolved by discussion with the individual sites concerned. Individual participant data on expiratory flow variables (FEV 1 , forced vital capacity [FVC], FEV 1 /FVC ratio, and forced expiratory flow at 25–75% of FVC [FEF 25–75% ]) were converted to Z scores and analysed with use of generalised linear mixed models in a one-step approach. Of the 381 studies identified, 11 studies, comprising a total of 935 participants born very preterm or with very low birthweight and 722 controls, were eligible and included in the analysis. Mean age at testing was 21 years (SD 3·4; range 16–33). Mean Z scores were close to zero (as expected) in the control group, but were reduced in the very preterm or very low birthweight group for FEV 1 (−0·06 [SD 1·03] vs −0·81 [1·33], mean difference −0·78 [95% CI −0·96 to −0·61], p<0·0001), FVC (−0·15 [0·98] vs −0·38 [1·18], −0·25 [–0·40 to −0·10], p=0·0012), FEV 1 /FVC ratio (0·14 [1·10] vs −0·64 [1·35], −0·74 [–0·85 to −0·64], p<0·0001), and FEF 25–75% (−0·04 [1·10] vs −0·95 [1·47], −0·88 [–1·12 to −0·65], p<0·0001). Similar patterns were observed when we compared the proportions of individuals with values below the fifth percentile. Individuals born very preterm or with very low birthweight are at risk of not reaching their full airway growth potential in adolescence and early adulthood, suggesting an increased risk of chronic obstructive pulmonary disease in later adulthood. National Health and Medical Research Council (Australia), University of Bergen, Western Norway Regional Authority, National Institute for Health Research (UK), Stichting Astmabestrijding, St Olav's Hospital's Research Fund, Academy of Finland, European Commission, National Institute of Child Health and Human Development (USA), Victorian Government's Operational Infrastructure Support Program. [ABSTRACT FROM AUTHOR]

NRXN1 deletions are a confirmed risk factor for schizophrenia and ASD. The full phenotypic spectrum of consequences of these deletions has not been established. We tested 140,187 white British or Irish participants in the UK Biobank (aged 40–70) for the presence of deletions that intersect at least one exon of the NRXN1 gene 48 people (30 women and 18 men) carried such deletions (0.03%). Carriers had subtle cognitive deficits: on seven tests they showed differences of between 0 and 1 SD (Z-scores, corrected for age and gender), with only two of these reaching significance: Digit Symbol and Reaction Time tests. Carriers did not differ on their educational qualifications (e.g., 15 carriers went to college or university), their occupational attainment, income or subjective happiness and satisfaction with their health and financial situation. We tested over 30 health outcomes, such as heart attacks, diabetes, cancer or number of hospital admissions. There was no increase in any adverse health outcomes. There was no increase in major psychiatric disorders, and no carrier had developed schizophrenia or mania. There were slight reductions of some measures of physical fitness: carriers had slight increases in hip and waist circumference, and lower peak expiratory volume. Despite the only subtle differences and the lack of adverse health outcomes, NRXN1 deletion carriers had on average 0.7 fewer children than the rest of the participants (on average women in the Biobank had 1.82 children and men had 1.78 children). Nine of the 18 men and 13 of the 30 women had no children. The differences in both men and women were significant, confirming previous suggestions that carriers have reduced fecundity (Rees et al., 2011; Stefansson et al., 2014). Reduced fecundity appears to be present even among overall healthy middle-aged people who have escaped early neurodevelopmental disorders. [ABSTRACT FROM AUTHOR]