Wave Inundation on the Coral Coast of Fiji

The roaring winds of the Southern Ocean and the Tasman Sea can generate some large swells, big enough to cause inundation on the Coral Coast in the south west of Viti Levu in Fiji, some 3000 km to the north. These inundation events are sometimes associated with tsunami-like long waves that hit the shore and inundate the coast with brute force. These are locally known as loka waves. To understand the origin of the loka waves and how they become so destructive in a fringing reef environment, this research monitored the waves and water levels, for 2 years, at 4 locations across the reef at a pilot site in Maui Bay on the Coral Coast of Fiji. In order to test the size of waves necessary to cause coastal inundation, a validated numerical model, XBeach, was used to simulate the development, propagation and dissipation of these infragravity waves using different water level scenarios. The result of this analysis is intended as a predictive tool to evaluate the risk of coastal inundation from ocean surface waves that can be used to support an early warning system and coastal management tool for both the tourism industry and coastal communities on the Coral Coast

Epidemiology, genetics, and subtyping of preserved ratio impaired spirometry (PRISm) in COPDGene.

BackgroundPreserved Ratio Impaired Spirometry (PRISm), defined as a reduced FEV1 in the setting of a preserved FEV1/FVC ratio, is highly prevalent and is associated with increased respiratory symptoms, systemic inflammation, and mortality. Studies investigating quantitative chest tomographic features, genetic associations, and subtypes in PRISm subjects have not been reported.MethodsData from current and former smokers enrolled in COPDGene (n = 10,192), an observational, cross-sectional study which recruited subjects aged 45-80 with ≥10 pack years of smoking, were analyzed. To identify epidemiological and radiographic predictors of PRISm, we performed univariate and multivariate analyses comparing PRISm subjects both to control subjects with normal spirometry and to subjects with COPD. To investigate common genetic predictors of PRISm, we performed a genome-wide association study (GWAS). To explore potential subgroups within PRISm, we performed unsupervised k-means clustering.ResultsThe prevalence of PRISm in COPDGene is 12.3%. Increased dyspnea, reduced 6-minute walk distance, increased percent emphysema and decreased total lung capacity, as well as increased segmental bronchial wall area percentage were significant predictors (p-value <0.05) of PRISm status when compared to control subjects in multivariate models. Although no common genetic variants were identified on GWAS testing, a significant association with Klinefelter's syndrome (47XXY) was observed (p-value < 0.001). Subgroups identified through k-means clustering include a putative "COPD-subtype", "Restrictive-subtype", and a highly symptomatic "Metabolic-subtype".ConclusionsPRISm subjects are clinically and genetically heterogeneous. Future investigations into the pathophysiological mechanisms behind and potential treatment options for subgroups within PRISm are warranted.Trial registrationClinicaltrials.gov Identifier: NCT000608764

Relationship between diffusion capacity and small airway abnormality in COPDGene.

Impaired single breath carbon monoxide diffusing capacity (DLCO) is associated with emphysema. Small airways disease (SAD) may be a precursor lesion to emphysema, but the relationship between SAD and DLCO is undescribed. We hypothesized that in mild COPD, functional SAD (fSAD) defined by computed tomography (CT) and Parametric Response Mapping methodology would correlate with impaired DLCO. Using data from ever-smokers in the COPDGene cohort, we established that fSAD correlated significantly with lower DLCO among both non-obstructed and GOLD 1-2 subjects. The relationship between DLCO with CT-defined emphysema was present in all GOLD stages, but most prominent in severe disease. TRIAL REGISTRATION: NCT00608764. Registry: COPDGene. Registered 06 February 2008, retrospectively registered

Chronic Airways Assessment Test : Psychometric properties in patients with asthma and/or COPD

Acknowledgements The authors would like to thank the patients who participated in this study and wish to acknowledge the work of the NOVELTY Scientific Community and the NOVELTY study investigators, who are listed in full below, and Sharon MacLachlan (Evidera, London, UK), who participated in the analysis of sections of the data. Medical writing support, under the direction of the authors, was provided by Niall Tyrer, MBiolSci, CMC Connect, a division of IPG Health Medical Communications, funded by AstraZeneca, Cambridge, UK, in accordance with Good Publication Practice (GPP 2022) guidelines (Ann Intern Med 2022; 175(9):1298–1304). Funding The NOVELTY study was funded by AstraZeneca.Peer reviewedPublisher PD

Validation of a diagnosis-agnostic symptom questionnaire for asthma and/or COPD

ACKNOWLEDGEMENTS The authors wish to acknowledge the work of the NOVELTY study investigators, who are listed in full in the supplementary material, and Sharon MacLachlan (Evidera, London, UK), who participated in the analysis of sections of the data. Medical writing support, under the direction of the authors, was provided by Lauren McNally, MSci, CMC Connect, McCann Health Medical Communications, and was funded by AstraZeneca, Cambridge, UK, in accordance with Good Publication Practice (GPP3) guidelines (Ann Intern Med 2015; 163: 461–464). Support statement: The NOVELTY study is funded by AstraZenecaPeer reviewedPublisher PD

Validation of the Chronic Airways Assessment Test in the NOVELTY Study

Peer reviewedPostprin