Obstructive sleep apnea (OSA) is a global health concern and is typically diagnosed using in-laboratory polysomnography (PSG). However, PSG is highly time-consuming and labor-intensive. We, therefore, developed machine learning models based on easily accessed anthropometric features to screen for the risk of moderate to severe and severe OSA. We enrolled 3503 patients from Taiwan and determined their PSG parameters and anthropometric features. Subsequently, we compared the mean values among patients with different OSA severity and considered correlations among all participants. We developed models based on the following machine learning approaches: logistic regression, k-nearest neighbors, naïve Bayes, random forest (RF), support vector machine, and XGBoost. Collected data were first independently split into two data sets (training and validation: 80%; testing: 20%). Thereafter, we adopted the model with the highest accuracy in the training and validation stage to predict the testing set. We explored the importance of each feature in the OSA risk screening by calculating the Shapley values of each input variable. The RF model achieved the highest accuracy for moderate to severe (84.74%) and severe (72.61%) OSA. The level of visceral fat was found to be a predominant feature in the risk screening models of OSA with the aforementioned levels of severity. Our machine learning models can be employed to screen for OSA risk in the populations in Taiwan and in those with similar craniofacial structures.

Obstructive sleep apnea (OSA) is a risk factor for neurodegenerative diseases. This study determined whether continuous positive airway pressure (CPAP), which can alleviate OSA symptoms, can reduce neurochemical biomarker levels. Thirty patients with OSA and normal cognitive function were recruited and divided into the control (n = 10) and CPAP (n = 20) groups. Next, we examined their in-lab sleep data (polysomnography and CPAP titration), sleep-related questionnaire outcomes, and neurochemical biomarker levels at baseline and the 3-month follow-up. The paired t-test and Wilcoxon signed-rank test were used to examine changes. Analysis of covariance (ANCOVA) was performed to increase the robustness of outcomes. The Epworth Sleepiness Scale and Pittsburgh Sleep Quality Index scores were significantly decreased in the CPAP group. The mean levels of total tau (T−Tau), amyloid-beta-42 (Aβ42), and the product of the two (Aβ42 × T−Tau) increased considerably in the control group (ΔT−Tau: 2.31 pg/mL; ΔAβ42: 0.58 pg/mL; ΔAβ42 × T−Tau: 48.73 pg2/mL2), whereas the mean levels of T−Tau and the product of T−Tau and Aβ42 decreased considerably in the CPAP group (ΔT−Tau: −2.22 pg/mL; ΔAβ42 × T−Tau: −44.35 pg2/mL2). The results of ANCOVA with adjustment for age, sex, body mass index, baseline measurements, and apnea–hypopnea index demonstrated significant differences in neurochemical biomarker levels between the CPAP and control groups. The findings indicate that CPAP may reduce neurochemical biomarker levels by alleviating OSA symptoms.

BackgroundExposure to air pollution may be a risk factor for obstructive sleep apnea (OSA) because air pollution may alter body water distribution and aggravate OSA manifestations.ObjectivesThis study aimed to investigate the mediating effects of air pollution on the exacerbation of OSA severity through body water distribution.MethodsThis retrospective study analyzed body composition and polysomnographic data collected from a sleep center in Northern Taiwan. Air pollution exposure was estimated using an adjusted nearest method, registered residential addresses, and data from the databases of government air quality motioning stations. Next, regression models were employed to determine the associations between estimated air pollution exposure levels (exposure for 1, 3, 6, and 12 months), OSA manifestations (sleep-disordered breathing indices and respiratory event duration), and body fluid parameters (total body water and body water distribution). The association between air pollution and OSA risk was determined.ResultsSignificant associations between OSA manifestations and short-term (1 month) exposure to PM2.5 and PM10 were identified. Similarly, significant associations were identified among total body water and body water distribution (intracellular-to-extracellular body water distribution), short-term (1 month) exposure to PM2.5 and PM10, and medium-term (3 months) exposure to PM10. Body water distribution might be a mediator that aggravates OSA manifestations, and short-term exposure to PM2.5 and PM10 may be a risk factor for OSA.ConclusionBecause exposure to PM2.5 and PM10 may be a risk factor for OSA that exacerbates OSA manifestations and exposure to particulate pollutants may affect OSA manifestations or alter body water distribution to affect OSA manifestations, mitigating exposure to particulate pollutants may improve OSA manifestations and reduce the risk of OSA. Furthermore, this study elucidated the potential mechanisms underlying the relationship between air pollution, body fluid parameters, and OSA severity.

(1) Purpose: We analysed overall survival (OS) rates following radiotherapy (RT) and chemo-RT of locally-advanced non-small cell lung cancer (LA-NSCLC) to investigate whether tumour repopulation varies with treatment-type, and to further characterise the low α/β ratio found in a previous study. (2) Materials and methods: Our dataset comprised 2-year OS rates for 4866 NSCLC patients (90.5% stage IIIA/B) belonging to 51 cohorts treated with definitive RT, sequential chemo-RT (sCRT) or concurrent chemo-RT (cCRT) given in doses-per-fraction ≤3 Gy over 16–60 days. Progressively more detailed dose-response models were fitted, beginning with a probit model, adding chemotherapy effects and survival-limiting toxicity, and allowing tumour repopulation and α/β to vary with treatment-type and stage. Models were fitted using the maximum-likelihood technique, then assessed via the Akaike information criterion and cross-validation. (3) Results: The most detailed model performed best, with repopulation offsetting 1.47 Gy/day (95% confidence interval, CI: 0.36, 2.57 Gy/day) for cCRT but only 0.30 Gy/day (95% CI: 0.18, 0.47 Gy/day) for RT/sCRT. The overall fitted tumour α/β ratio was 3.0 Gy (95% CI: 1.6, 5.6 Gy). (4) Conclusion: The fitted repopulation rates indicate that cCRT schedule durations should be shortened to the minimum in which prescribed doses can be tolerated. The low α/β ratio suggests hypofractionation should be efficacious.