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Purpose: Obstructive sleep apnea (OSA) is a chronic disease that affects 1%–6% of children. Our study aims to explore the effectiveness and clinical characteristics of integrative Traditional Chinese Medicine (ITCM) for pediatric OSA. Materials and methods: In this retrospective cohort study, we assessed differences of polysomnography (PSG) parameters and clinical characteristics between 2009 and 2020. Children

Background: Persistent sinonasal symptoms are common in children with chronic rhinosinusitis. The Sinus and Nasal Quality of Life (QoL) Survey (SN-5) was the first validated questionnaire measuring sinonasal-related QoL in populations aged 2–12 years. No norm has been established for Chinese-speaking countries. We translated the SN-5 into traditional Chinese and evaluated validity and reliability. Methods: From December 2016 to December 2017, healthy volunteers and children with persistent sinonasal symptoms were enrolled. Guardians of the participants completed the SN-5, a visual analog scale (VAS) of nasal symptoms, and the Obstructive Sleep Apnea-18 (OSA-18); the responses were used to assess internal consistency, discriminant validity, and treatment responsiveness. A nontreatment group was administered the SN-5 1 week later to assess test–retest reliability. Results: We recruited 31 healthy volunteers and 85 children with rhinosinusitis, 50 and 35 in the treatment and nontreatment groups, respectively. The SN-5 demonstrated good internal consistency (Cronbach's α = 0.86) and test–retest reliability (0.74, p

Abstract Background To date, there is insufficient knowledge about the association of air pollution and childhood nephrotic syndrome in the real world. This study aimed to evaluate the effects of the three common gaseous air pollutants, including sulfur dioxide, total hydrocarbon, and methane, on the risk of idiopathic nephrotic syndrome (INS) in children. Methods We collected data from the Taiwan National Health Insurance Research Database and Taiwan Air Quality-Monitoring Database. Children younger than 18 years old, identified from January 1, 2000, were followed up until the first diagnosis of INS was established or until December 31, 2012. We measured the incidence rates and hazard ratios for INS stratified based on the quartiles (Q1–Q4) of air pollutant concentration. Multivariate Cox proportional hazards models were also applied by adjusting age, sex, monthly income, and urbanization. Results Compared with participants exposed to Q1 concentrations, the adjusted hazard ratios (aHRs) for INS increased progressively along the four quartiles of sulfur dioxide, total hydrocarbon, and methane, from 1 (Q1) to 1.78 (Q4), 1 (Q1) to 3.49 (Q4), 1 (Q1) to 7.83 (Q4), respectively. Conclusions Our study revealed that children with exposure to higher concentrations of sulfur dioxide, total hydrocarbon, and methane was associated with an increased risk of INS.

Abstract Background There is growing evidence suggesting that air pollution may act as an important environmental risk factor in the development and aggravation of childhood atopic dermatitis (AD). Methods We collected data from the Taiwan National Health Insurance (NHI) research database and linked the data to the Taiwan Air Quality-Monitoring Database. From January 1, 2000 to December 31, 2012; children aged below 18 years were selected from the database and followed longitudinally until the diagnosis of AD, withdrawal from the NHI, or December 31, 2012. Children with missing data or those diagnosed with AD before enrolment in this study were excluded. We measured the incidence rate and hazard ratios (HRs) for AD and stratified them by quartiles (Q1–Q4) of air pollutant concentration. Multivariable Cox proportional hazards models were also applied by adjusting for age, sex, monthly income, and level of urbanization. Results When compared with the concentrations of pollutants in the Q1 quartile, the adjusted HR for AD increased with an increase in the exposure concentrations of total hydrocarbons (THCs), non-methane hydrocarbons (NMHCs), and methane (CH4) from 1.65 (95% confidence interval [CI]: 1.47–1.84) to 10.6 (95% CI: 5.85–7.07), from 1.14 (95% CI: 1.06–1.24) to 2.47 (95% CI: 2.29–2.66), and from 1.70 (95% CI: 1.52–1.89) to 11.9 (95% CI: 10.8–13.1), respectively. Patients exposed to higher levels of THCs, NMHCs, and CH4 exhibited greater incidence rates of childhood AD. Conclusions The present study demonstrated that exposure to higher concentrations of THCs, NMHCs, and CH4 were associated with an increased risk of childhood AD.

This study evaluated the risks of childhood acute bronchitis and bronchiolitis (CABs) for children with asthma or allergic rhinitis (AR). Using insurance claims data of Taiwan, we identified, from children of ≤12 years old in 2000–2016, cohorts with and without asthma (N = 192,126, each) and cohorts with and without AR (N = 1,062,903, each) matched by sex and age. By the end of 2016, the asthma cohort had the highest bronchitis incidence, AR and non-asthma cohorts followed, and the lowest in the non-AR cohort (525.1, 322.4, 236.0 and 169.9 per 1000 person-years, respectively). The Cox method estimated adjusted hazard ratios (aHRs) of bronchitis were 1.82 (95% confidence interval (CI), 1.80–1.83) for the asthma cohort and 1.68 (95% CI, 1.68–1.69) for the AR cohort, relative to the respective comparisons. The bronchiolitis incidence rates for these cohorts were 42.7, 29.5, 28.5 and 20.1 per 1000 person-years, respectively. The aHRs of bronchiolitis were 1.50 (95% CI, 1.48–1.52) for the asthma cohort and 1.46 (95% CI, 1.45–1.47) for the AR cohort relative to their comparisons. The CABs incidence rates decreased substantially with increasing age, but were relatively similar for boys and girls. In conclusion, children with asthma are more likely to develop CABs than are children with AR.

Studies have associated the human respiratory syncytial virus which causes seasonal childhood acute bronchitis and bronchiolitis (CABs) with climate change and air pollution. We investigated this association using the insurance claims data of 3,965,560 children aged ≤ 12 years from Taiwan from 2006–2016. The monthly average incident CABs increased with increasing PM2.5 levels and exhibited an inverse association with temperature. The incidence was 1.6-fold greater in January than in July (13.7/100 versus 8.81/100), declined during winter breaks (February) and summer breaks (June–August). The highest incidence was 698 cases/day at 2.5 > 37.0 μg/m3, with an adjusted relative risk (aRR) of 1.01 (95% confidence interval [CI] = 0.97–1.04) compared to 568 cases/day at 2.5 < 15.0 μg/m3 (reference). The incidence at ≥30 °C decreased to 536 cases/day (aRR = 0.95, 95% CI = 0.85–1.06) with PM2.5 > 37.0 μg/m3 and decreased further to 392 cases/day (aRR = 0.61, 95% CI = 0.58–0.65) when PM2.5 was 3. In conclusion, CABs infections in children were associated with lowered ambient temperatures and elevated PM2.5 concentrations, and the high PM2.5 levels coincided with low temperature levels. The role of temperature should be considered in the studies of association between PM2.5 and CABs.

BackgroundThe use of antibiotics for treating infection in childhood and their association with increased risk of asthma remain controversial. Infants diagnosed with vesicoureteral reflux (VUR) belong to a unique population who are administered antibiotics for a long time and are susceptible to recurrent UTI. It is interesting to study the risk of asthma in these infants with or without VUR.MethodsTaiwanese children born between 2000 and 2007 were enrolled in population-based birth cohort study. Participants diagnosed with VUR and UTI within first year were classified into four groups (VUR, UTI, VUR and UTI, and control). We calculated follow-up person-years for each participant from the index date until the asthma diagnosis, their withdrawal from the insurance system (because of death or loss to follow-up), or till the end of 2008. The risk of asthma was compared between the 4 cohorts by using Cox proportional hazards model analysis, adjusted hazard ratio (aHR), and 95% confidence interval (95% CI).ResultsChildren diagnosed with VUR (n = 350), UTI (n = 15542), VUR and UTI (n = 1696), and randomly selected controls (n = 17588) were enrolled. The overall rate of incidence of asthma was found to be 1.64-fold, 1.45-fold, and 1.17-fold higher in the UTI, VUR/UTI, and VUR cohorts than in the controls (5.60, 5.07, and 4.10 vs. 3.17 per 100 person-years), respectively. After adjusting the potential factors, the overall risk of asthma remained the highest in UTI (aHR: 1.74, 95% CI : 1.65 to 1.80) followed by VUR/UTI (aHR: 1.56, 95% CI : 1.40 to 1.75) and VUR cohorts (aHR: 1.25, 95% CI: 0.96 to 1.62). The incidence of asthma was higher in boys than in girls.ConclusionThe nationwide retrospective cohort study demonstrated that short-term therapeutic dose of antibiotics for UTI in infants with or without VUR has a positive correlation with the prevalence of childhood asthma. Significant risk of childhood asthma was not observed when VUR cohort was exposed to long-term low-dose of prophylactic antibiotics.

Myopia is a highly prevalent eye disease. There is limited information suggesting a relationship between myopia and inflammation. We found children with allergic conjunctivitis (AC) had the highest adjusted odds ratio (1.75, 95% confidence interval [CI], 1.72–1.77) for myopia among the four allergic diseases. A cohort study was conducted and confirmed that children with AC had a higher incidence and subsequent risk of myopia (hazard ratio 2.35, 95%CI 2.29–2.40) compared to those without AC. Lower refractive error and longer axial length were observed in an AC animal model. Myopia progression was enhanced by tumor necrosis factor (TNF)-α or interleukin (IL)-6 administration, two cytokines secreted by mast cell degranulation. The TNF-α or IL-6 weakened the tight junction formed by corneal epithelial (CEP) cells and inflammatory cytokines across the layer of CEP cells, which increased the levels of TNF-α, IL-6, and IL-8 secreted by retinal pigment epithelial cells. The expression levels of TNF-α, IL-6, IL-8, monocyte chemoattractant protein-1, and nuclear factor kappa B were up-regulated in eyes with AC, whereas IL-10 and the inhibitor of kappa B were down-regulated. In conclusion, the experimental findings in mice corroborate the epidemiological data showing that allergic inflammation influences the development of myopia.

[This corrects the article DOI: 10.1371/journal.pone.0128461.].

Prevention and treatment of myopia is an important public problem worldwide. We found a higher incidence of myopia among patients with inflammatory diseases such as type 1 diabetes mellitus (7.9%), uveitis (3.7%), or systemic lupus erythematosus (3.5%) compared to those without inflammatory diseases (p

BACKGROUND:There is a demonstrated association between asthma and irritable bowel syndrome (IBS). In this study, we examined the bidirectional association between asthma and IBS using a nationwide database. METHODS:We conducted two retrospective cohort studies using data obtained from the National Health Insurance of Taiwan. Study 1 included 29,648 asthma patients newly diagnosed between 2000 and 2010. Study 2 included 29,875 IBS patient newly diagnosed between 2000 and 2010. For each study, four subjects without asthma and IBS were selected, respectively, frequency-matched by sex, age, and the diagnosis date. All four cohorts were followed up until the end of 2011 to estimate incident IBS for Study 1 and incident asthma for study 2. Adjusted hazard ratios (aHRs) were estimated using the Cox proportional hazards model after controlling for sex, age and comorbidities. RESULTS:The incidence of IBS was 1.89 times higher in the asthma cohort than in the comparison cohort (8.26 vs. 4.36 per 1,000 person-years), with an aHR of 1.57 [95% confidence interval (CI) = 1.47-1.68]. The aHRs remained significant in all subgroups measured by sex, age and the presence of comorbidities. In contrast, the incidence of asthma was 1.76 times higher in the IBS cohort than the comparison cohort (7.09 vs. 4.03 per 1,000 person-years), with an aHR of 1.54 (95% CI = 1.44-1.64). Similarly, aHRs remained significant in all subgroups measured by sex, age and the presence of comorbidities. CONCLUSION:The present study suggests a bidirectional association between asthma and IBS. Atopy could be a shared pathophysiology underlying this association, deserving a further investigation.

The relationship between asthma and ankylosing spondylitis (AS) is controversial. We examined the risk of asthma among AS patients in a nationwide population.We conducted a retrospective cohort study using data from the National Health Insurance (NHI) system of Taiwan. The cohort included 5,974 patients newly diagnosed with AS from 2000 to 2010. The date of diagnosis was defined as the index date. A 4-fold of general population without AS was randomly selected frequency matched by age, gender and the index year. The occurrence and hazard ratio (HR) of asthma were estimated by the end of 2011.The overall incidence of asthma was 1.74 folds greater in the AS cohort than in the non-AS cohort (8.26 versus 4.74 per 1000 person-years) with a multivariable Cox method measured adjusted HR of 1.54 (95% confidence interval (CI), 1.34-1.76). The adjusted HR of asthma associated with AS was higher in women (1.59; 95% CI, 1.33-1.90), those aged 50-64 years (1.66; 95% CI, 1.31-2.09), or those without comorbidities (1.82; 95% CI, 1.54-2.13).Patients with AS are at a higher risk of developing asthma than the general population, regardless of gender and age. The pathophysiology needs further investigation.

BACKGROUND:There are several publications reported that obstructive sleep apnea (OSA) was associated with asthma. However, large-scaled, population-based cohort study has been limited. We aimed to examine the risk of OSA among adult patients with asthma in an Asian population. METHODS:We conducted a retrospective cohort study using data from the National Health Insurance (NHI) of Taiwan. The asthma cohort included 38,840 newly diagnosed patients between 2000 and 2010. The date of diagnosis was defined as the index date. Each patient was randomly matched with four people without asthma according to gender, age, and the index year as the comparison cohort. The occurrence of OSA was followed up until the end of 2011. The risk of OSA was estimated using the Cox proportional hazard model after adjusting for gender, age, and comorbidities. RESULTS:The overall incidence of OSA was 2.51-fold greater in the asthma cohort than in the comparison cohort (12.1 versus 4.84 per 1000 person-years). Compared to non-asthma subjects, the adjusted hazard ratio (aHR) of OSA increased to 1.78 for asthma patients with one or less annual emergency room (ER) visit, and 23.8 for those who visited ER more than once per year. In addition, aHR in patients with inhaled steroid treatment compared to those without steroid treatment was 1.33 (95% CI = 1.01-1.76). CONCLUSION:Patients with asthma have a significantly higher risk of developing OSA than the general population. The results suggest that the risk of OSA is proportional to asthma control and patients with inhaled steroid treatment have a higher risk for OSA than those without steroid treatment.

BACKGROUND: Previous studies have suggested that chronic obstructive pulmonary disease (COPD) is an independent risk factor for lung cancer. There are some evidence that people with diabetes are at a risk of developing many forms of cancer, but inconclusive with regard to lung cancer. The aim of this study was to evaluate whether COPD with or without type 2 diabetes mellitus (T2DM) influences the risk of developing lung cancer. METHODS: This is a retrospective cohort study consisting of 20,730 subjects newly diagnosed with COPD ("cases"). Their data was collected from the National Health Insurance system of Taiwan from 1998 to 2010. Among these patients, 5,820 patients had T2DM and 14,910 patients did not have T2DM. The retrospective matched control group consisted of 20,729 subjects without either COPD or T2DM. The control group was matched with the cases for sex, age, and index year (the year that the patient was diagnosed with COPD). The subjects were followed until the end of 2011. RESULTS: The findings of our study showed that the risk of lung cancer was higher in the COPD group than in the non-COPD group, with adjusted hazard ratio (HR) of 5.02 [95% confidence interval (CI) = 4.23-5.94] among total case group, adjusted HR was 5.38 (95% CI = 4.52-6.40) in the cohort without T2DM and adjusted HR was 4.05 (95% CI = 3.26-5.03) in the cohort with T2DM. We observed a significantly protective effect from lung cancer (adjusted HR = 0.75, 95% CI = 0.63-0.90) of diabetic cohort than non-diabetic cohort among patients with COPD. CONCLUSION: Patients with COPD had a significantly higher risk of developing lung cancer than healthy people. However, there was a protective effect of T2DM for lung cancer among patients with COPD. Further investigation may be needed to corroborate the mechanism or bring up reliable reasons.

While is widely acknowledged that nonmuscle myosin II (NMMII) enables stress fibers (SFs) to generate traction forces against the extracellular matrix, little is known about how specific NMMII isoforms and functional domains contribute to SF mechanics. Here we combine biophotonic and genetic approaches to address these open questions. First, we suppress the NMMII isoforms MIIA and MIIB and apply femtosecond laser nanosurgery to ablate and investigate the viscoelastic retraction of individual SFs. SF retraction dynamics associated with MIIA and MIIB suppression qualitatively phenocopy our earlier measurements in the setting of Rho kinase (ROCK) and myosin light chain kinase (MLCK) inhibition, respectively. Furthermore, fluorescence imaging and photobleaching recovery reveal that MIIA and MIIB are enriched in and more stably localize to ROCK- and MLCK-controlled central and peripheral SFs, respectively. Additional domain-mapping studies surprisingly reveal that deletion of the head domain speeds SF retraction, which we ascribe to reduced drag from actomyosin crosslinking and frictional losses. We propose a model in which ROCK/MIIA and MLCK/MIIB functionally regulate common pools of SFs, with MIIA crosslinking and motor functions jointly contributing to SF retraction dynamics and cellular traction forces.