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Traditionally, single‐beam echo sounder (SBES) data are used to determine the position of emission structures in the form of a two‐dimensional profile, which may not be straightforward enough to correlate the data of adjacent profiles and determine the exact discharge area. In this study, we develop semiautomatic software to remove noise and select possible flare signals to enhance the speed and precision of the data processing. The program also allows for the transformation of the data into a three‐dimensional point cloud distribution by computing the receiving angle of the data. By applying this method to investigate the distribution and mechanism of gas emission structures in the South Okinawa Trough (SOT), we determine four high flux areas and 22 isolated plumes with roots. Widespread gas flares usually occur in areas with large‐scale volcanic activity or gas‐enriched structures. Isolated gas plumes could be found for a single knoll outcrop and normal faulting structures. The energy of the flares around the knoll area is generally stronger than that observed along the normal faults. Compared with other geophysical data, we find that the widespread distribution of gas flares generally implies a larger hydrothermal potential, which may not be revealed by single‐profile acoustic image observations. We also find that the direction of flares is strongly influenced by tides, and the height of the flare represents the thermocline as a strong boundary for bubbles composited by carbon dioxide. Plain Language Summary: This study introduces a new method using SBES data to analyze gas emission structures in the South Okinawa Trough. By developing specialized software, the researchers enhance the speed and precision of data processing, allowing for the identification of high flux areas and isolated plumes. The study reveals that widespread gas flares indicate significant hydrothermal potential, influenced by tides and thermocline height. This research expands our understanding of gas emissions in the region. Key Points: The precise range and magnitude of gas discharges in the southern Okinawa Trough are determined by processing the SBES dataThe magnitude and intensity of gas discharges can be attributed to volcanic fluid activity or structural faultsThe three‐dimensional flares observed in the water column illustrate the impact of tides on the upward movement of gas plumes [ABSTRACT FROM AUTHOR]

BACKGROUND: Perfluorinated compounds (PFCs) are ubiquitous pollutants. Experimental data suggest that they may be associated with adverse health outcomes, including asthma. However, there is little supporting epidemiological evidence. METHODS: A [...]

Abstract Background Although studies show that maternal smoking during pregnancy increases the risks of respiratory outcomes in childhood, evidence concerning the effects of household environmental tobacco smoke (ETS) exposure remains inconsistent. Methods We conducted a population-based study comprised of 5,019 seventh and eighth-grade children in 14 Taiwanese communities. Questionnaire responses by parents were used to ascertain children's exposure and disease status. Logistic regression models were fitted to estimate the effects of ETS exposures on the prevalence of asthma, wheeze, and bronchitic symptoms. Results The lifetime prevalence of wheeze was 11.6% and physician-diagnosed asthma was 7.5% in our population. After adjustment for potential confounders, in utero exposure showed the strongest effect on all respiratory outcomes. Current household ETS exposure was significantly associated with increased prevalence of active asthma, ever wheeze, wheeze with nighttime awakening, and bronchitis. Maternal smoking was associated with the increased prevalence of a wide range of wheeze subcategories, serious asthma, and chronic cough, but paternal smoking had no significant effects. Although maternal smoking alone and paternal smoking alone were not independently associated with respiratory outcomes, joint exposure appeared to increase the effects. Furthermore, joint exposure to parental smoking showed a significant effect on early-onset asthma (OR, 2.01; 95% CI, 1.00-4.02), but did not show a significant effect on late-onset asthma (OR, 1.17; 95% CI, 0.36-3.87). Conclusion We concluded that prenatal and household ETS exposure had significant adverse effects on respiratory health in Taiwanese children.

Background: Respiratory syncytial virus (RSV) is associated with childhood asthma. Nevertheless, not all children exposed to RSV develop asthma symptoms, possibly because genes modulate the effects of RSV on asthma exacerbations.Objective: The purpose of this study was to identify genes that modulate the effect of RSV latent infection on asthma exacerbations.Methods: We performed a meta-analysis to investigate differentially expressed genes (DEGs) of RSV infection from Gene Expression Omnibus datasets. Expression quantitative trait loci (eQTL) methods were applied to select single nucleotide polymorphisms (SNPs) that were associated with DEGs. Gene-based analysis was used to identify SNPs that were significantly associated with asthma exacerbations in the Taiwanese Consortium of Childhood Asthma Study (TCCAS), and validation was attempted in an independent cohort, the Childhood Asthma Management Program (CAMP). Gene-RSV interaction analyses were performed to investigate the association between the interaction of SNPs and RSV latent infection on asthma exacerbations.Results: A total of 352 significant DEGs were found by meta-analysis of RSV-related genes. We used 38 123 SNPs related to DEGs to investigate the genetic main effects on asthma exacerbations. We found that eight RSV-related genes (GADD45A, GYPB, MS4A3, NFE2, RNASE3, EPB41L3, CEACAM6 and CEACAM3) were significantly associated with asthma exacerbations in TCCAS and also validated in CAMP. In TCCAS, rs7251960 (CEACAM3) significantly modulated the effect of RSV latent infection on asthma exacerbations (false-discovery rate <0.05). The rs7251960 variant was associated with CEACAM3 mRNA expression in lung tissue (p for trend=1.2×10-7). CEACAM3 mRNA was reduced in nasal mucosa from subjects with asthma exacerbations in two independent datasets.Conclusions: rs7251960 is an eQTL for CEACAM3, and CEACAM3 mRNA expression is reduced in subjects experiencing asthma exacerbations. CEACAM3 may be a modulator of RSV latent infection on asthma exacerbations. [ABSTRACT FROM AUTHOR]

Background: Respiratory syncytial virus (RSV) infection is epidemiologically linked to asthma. During RSV infection, IL‐33 is elevated and promotes immune cell activation, leading to the development of asthma. However, which immune cells are responsible for triggering airway hyperreactivity (AHR), inflammation and eosinophilia remained to be clarified. We aimed to elucidate the individual roles of IL‐33‐activated innate immune cells, including ILC2s and ST2+ myeloid cells, in RSV infection‐triggered pathophysiology. Methods: The role of IL‐33/ILC2 axis in RSV‐induced AHR inflammation and eosinophilia were evaluated in the IL‐33‐deficient and YetCre‐13 Rosa‐DTA mice. Myeloid‐specific, IL‐33‐deficient or ST2‐deficient mice were employed to examine the role of IL‐33 and ST2 signaling in myeloid cells. Results: We found that IL‐33‐activated ILC2s were crucial for the development of AHR and airway inflammation, during RSV infection. ILC2‐derived IL‐13 was sufficient for RSV‐driven AHR, since reconstitution of wild‐type ILC2 rescued RSV‐driven AHR in IL‐13‐deficient mice. Meanwhile, myeloid cell‐derived IL‐33 was required for airway inflammation, ST2+ myeloid cells contributed to exacerbation of airway inflammation, suggesting the importance of IL‐33 signaling in these cells. Local and peripheral eosinophilia is linked to both ILC2 and myeloid IL‐33 signaling. Conclusions: This study highlights the importance of IL‐33‐activated ILC2s in mediating RSV‐triggered AHR and eosinophilia. In addition, IL‐33 signaling in myeloid cells is crucial for airway inflammation. [ABSTRACT FROM AUTHOR]

Background: Inhaled corticosteroids are recommended as the first-line controller medication for childhood asthma owing to their multiple clinical benefits. However, heterogeneity in the response towards these drugs remains a significant clinical problem.Methods: Children aged 5 to 18 years with mild to moderate persistent asthma were recruited into the Taiwanese Consortium of Childhood Asthma Study. Their responses to inhaled corticosteroids were assessed based on their improvements in the asthma control test and peak expiratory flow. The predictors of responsiveness were demographic and clinical features that were available in primary care settings. We have developed a prediction model using logistic regression and have simplified it to formulate a practical tool. We assessed its predictive performance using the area under the receiver operating characteristic curve.Results: Of the 73 asthmatic children with baseline and follow-up outcome measurements for inhaled corticosteroids treatment, 24 (33%) were defined as non-responders. The tool we have developed consisted of three predictors yielding a total score between 0 and 5, which are comprised of the following parameters: the age at physician-diagnosis of asthma, sex, and exhaled nitric oxide. Sensitivity and specificity of the tool for prediction of inhaled corticosteroids non-responsiveness, for a score of 3, were 0.75 and 0.69, respectively. The areas under the receiver operating characteristic curve for the prediction tool was 0.763.Conclusions: Our prediction tool represents a simple and low-cost method for predicting the response of inhaled corticosteroids treatment in asthmatic children. [ABSTRACT FROM AUTHOR]