Pediatric obstructive sleep apnea (OSA) is closely linked to the growth and interaction of upper airway soft tissues. The relevance of Scammon's classical growth curves to site-specific oropharyngeal development has been called into question, despite the fact that they have long provided a fundamental framework for comprehending lymphoid tissue maturation.

This narrative review synthesizes current imaging-based and morphometric evidence on the age-related growth of the adenoids, palatine tonsils, lingual tonsils, and tongue, within the context of craniofacial development. Adenoidal tissue undergoes rapid early growth, peaking between 6 and 8 years - earlier than predicted by Scammon's lymphoid curve. Palatine tonsils reach maximum dimensions between 8 and 10 years before gradual involution. Lingual tonsils lack normative developmental data in healthy children and appear largely absent on MRI in asymptomatic subjects, with hypertrophy representing a compensatory or condition-dependent response rather than normal development. The tongue follows a general-type growth trajectory with marked regional differences: the anterior two-thirds attains near-adult size by 8-10 years, while the posterior third continues enlarging into adolescence. These structure-specific trajectories interact with the differential maturation of craniofacial structures - the cranium, maxilla, and mandible - creating a transient "window of vulnerability" between approximately 5 and 10 years of age, during which soft tissue volume disproportionately narrows the upper airway.

Oropharyngeal soft tissue growth is structure-specific and does not conform to a single generalized growth curve. A conceptual, site-specific clinical framework integrating the distinct growth trajectories of each tissue and their proportional relationship to craniofacial development is essential for orthodontic assessment, airway risk stratification, and timely intervention in children with or at risk for sleep-disordered breathing.

Acute respiratory distress syndrome (ARDS) is a life-threatening form of acute respiratory failure characterized by diffuse alveolar injury, severe hypoxemia, and high mortality. Despite advances in supportive care, effective pharmacological interventions remain limited owing to the complex pathophysiology of ARDS, poor pulmonary drug accumulation, systemic adverse effects, and substantial disease heterogeneity. Increasing evidence indicates that distinct clinical and biological subphenotypes of ARDS exhibit differential inflammatory responses, molecular signatures, and therapeutic susceptibilities, underscoring the need for precision medicine approaches. Nanomedicine has emerged as a promising strategy to address these challenges. Through tunable physicochemical properties, surface functionalization, and microenvironment-responsive designs, nanomaterials can enhance drug stability, improve pulmonary targeting, and enable controlled drug release within injured lung tissues. Moreover, nanotherapeutic platforms can exert anti-inflammatory, antioxidant, immunomodulatory, barrier-protective, anticoagulant, and antifibrotic effects through passive and active targeting, biomimetic delivery systems, and stimuli-responsive mechanisms. In this review, we summarize the current understanding of ARDS heterogeneity and its underlying pathophysiological mechanisms, discuss the limitations of existing therapeutic approaches, and comprehensively examine recent advances in nanomaterial-based therapies and targeted drug delivery systems for ARDS. We further highlight key challenges associated with biosafety, large-scale manufacturing, regulatory approval, and clinical translation. Collectively, this review provides a framework for the rational development of precision nanomedicines and outlines future directions for improving therapeutic outcomes in patients with ARDS.

The COVID-19 pandemic exposed profound weaknesses in global infectious disease surveillance yet, in its aftermath, pandemic-prone threats have intensified rather than receded. This narrative review synthesizes contemporary evidence on three converging drivers of pandemic risk zoonotic emergence, antimicrobial resistance, and climate-sensitive disease expansion and examines how structural failures in surveillance and global health governance amplify their impact. Drawing on recent epidemiological analyses, policy reports, and One Health evaluations, the review maps post-COVID surges in zoonotic outbreaks, drug-resistant infections, and vector and water-borne diseases, and links these trends to fragmented laboratory networks, inequitable genomic capacity, and weak integration across human, animal, and environmental systems. It further interrogates the geopolitical and socioeconomic determinants of vulnerability, including conflict-related surveillance collapse, vaccine inequity, and the political economy of pandemic financing. Emerging digital tools from AI-enabled forecasting to wastewater and social media surveillance are assessed not only for their technical promise but also for risks related to data bias, extractives, and governance gaps. The review argues that without redistributive investment in One Health integration, regional genomic platforms, community-based surveillance, and enforceable IHR-based accountability, the world will continue to detect converging threats late and respond inequitably, leaving pandemic preparedness structurally fragile in the post-COVID era.

Lungs are highly affected by brain death, with females showing a higher inflammatory response, linked sex hormones acute reduction. With the aging of world population, the number of older donors is increasing. So, the study of menopause associated changes gain importance. Here we investigated menopause's effects in female brain death rats, previously subjected to transitional follicular depletion and aging. Female Wistar rats were divided in young and menopause groups. After follicular depletion, rats aged for 10 weeks. The animals were submitted to brain death and Sham operated rats served as controls. White blood cell counts, bronchoalveolar lavage were analyzed and inflammatory mediators were quantified. Lung tissue was evaluated for myeloperoxidase, intercellular adhesion molecules, miRNA expression, and protein and gene expression of estradiol receptors. In menopause group, there was increase in systemic and tissue leukocyte infiltration, myeloperoxidase expression, inducible nitric oxide synthase, intercellular adhesion molecule-1, lung edema, and loss of IL-10 regulation. Additionally, we found alterations in estradiol receptors along with changes in the expression of miRNAs associated to inflammation, vascular function and senescence. Menopause increases lung inflammation after brain death, by higher leukocyte infiltration and reduction of IL-10 and may impact the outcome of lung transplantation.

Exposure to fine particulate matter (PM_2.5) is harmful to people, leading to respiratory disease and even death. The association between PM_2.5 pollution and health outcomes has become a key foundation for public health policy development. This study aims to quantify the effects of PM_2.5 on health outcomes (mortality, morbidity) and estimate the benefits of reducing PM_2.5 levels in South Korea.

This study uses an instrumental variable (IV) analysis to estimate the effects of PM_2.5 on health outcomes in South Korea, using mortality data for 2015-2022 and morbidity data for 2016-2019. Local air pollution in South Korea is instrumented using a wind-direction indicator with air pollution levels measured at upwind Chinese monitors to address potential endogeneity concerns. Estimates of PM_2.5-related death and the life-year loss are used to calculate the economic benefits of preventing PM_2.5-related deaths.

The results indicate that a 1 µg/m³ increase in local PM_2.5 levels is associated with a 0.17% rise in older (65+) adult mortality rate and a 5.1% increase in respiratory hospitalizations. Significant rises in mortality and morbidity were observed for disease categories directly associated with PM_2.5 pollution. Considering only the avoided life years lost, the 5.58 µg/m³ reduction in PM_2.5 levels achieved in South Korea from 2015 to 2022 corresponds to an estimated economic benefit of USD 14.14 billion. The study also found that a 1 µg/m³ increase in PM_2.5 raised hospital visits by 1.2% for acute upper respiratory infections and 2.6% for lower respiratory infections.

These findings highlight the magnitude and cost of the health risks posed by air pollution, underscoring the importance of effective policies to manage air quality. This study provides clear evidence of the harmful effects of air pollution on human health, particularly on vulnerable groups and related diseases.

Objective: To determine the threshold for influenza epidemic intensity during the 2024-2025 season in Tianjin using the moving epidemic method (MEM). Methods: Collect weekly data on the percentage of influenza-like illness cases (ILI%), positive detection rate of influenza virus (PR), and PR×ILI% from sentinel hospitals in Tianjin for 2017-2025. Establish an influenza early warning model using MEM, select the optimal value of parameter δ, compare model fitting performance, evaluate the reliability of the three types of data, and determine the threshold for influenza epidemic intensity in Tianjin for 2024-2025. Model selection employs cross-validation, with evaluation metrics including sensitivity, specificity, positive predictive value, negative predictive value, positive likelihood ratio, negative likelihood ratio, Matthews correlation coefficient, and Youden index. Results: The models based on PR and PR×ILI% showed better fitting effect than those based on ILI% alone, with the PR×ILI%-based model demonstrating the best performance. The MEM model constructed by using PR indicated that with δ set at 3.0, the epidemic start threshold for Tianjin in the 2024-2025 season was 16.05%, the end threshold was 19.68%, and the thresholds for medium, high, and very high epidemic intensity were 51.61%, 66.98%, and 75.16%, respectively. The model based on PR×ILI% showed that with δ set at 3.2, the epidemic start threshold was 105.23%, the end threshold was 128.08%, and the thresholds for medium, high, and very high epidemic intensity were 377.55%, 560.61%, and 667.64%, respectively. Conclusions: The moving epidemic method can be used to determine the influenza epidemic intensity thresholds in Tianjin. The influenza early warning model established based on PR×ILI% data better reflects changes in influenza activity intensity, providing a reliable basis for early warning.

Soft robotic devices may be a useful adjunct for stroke rehabilitation by providing higher intensity training, while allowing comfort and portability compared to rigid exoskeletons. We evaluated the efficacy of a sensor-assisted soft robotic glove (SSR) during inpatient stroke rehabilitation.

This assessor-blinded, randomised controlled trial was conducted in 2 inpatient rehabilitation units. Adults aged 21-90 years old, with ischaemic or haemorrhagic stroke and unilateral upper-limb impairment were recruited between July 2023 and May 2025. Participants were randomised to either [1] SSR or [2] supervised Graded Repetitive Arm Supplementary Programme (GRASP) training for up to 15 sessions, 30-45 min/session; 5 days/week for up to 3 weeks. The primary outcome was Fugl-Meyer Assessment of Upper Extremity (FMA-UE). Secondary outcomes included Stroke Upper Limb Capacity Scale, the DuruÖz Hand Index, and Stroke Impact Scale-16 (SIS-16). Outcomes were assessed at baseline (T1), post-intervention (T2) and follow-up at 3 months (T3).

Recruitment ceased before the planned sample size was reached due to funding constraints. Therefore, the trial was underpowered to detect the prespecified between-group difference. Of 323 screened individuals, 61 were randomised. 3 participants did not complete T2 assessment resulting in a modified intention-to-treat population of 58 (SSR n = 28, control n = 30). Both groups showed improvement across primary and secondary outcomes, with no statistically significant differences observed between them. In a post-hoc exploratory subgroup analysis with baseline FMA-UE < 35 and ≥ 10 sessions (n = 38), a statistically significant difference in FMA-UE distal sub-score at T2 was observed, favouring the SSR group (mean difference 3.06, 95% confidence interval [CI] 0.02 to 6.09, p = 0.049) but not at T3. A numerically higher proportion of participants in the SSR group achieved minimal clinically important difference value for SIS-16 (77.8% vs. 55.0%, adjusted odds ratio 6.52 (95% CI 1.00 to 42.58, absolute risk difference 22.8% [95% CI -7.2% to 47.4%], p = 0.050) at T2, but did not reach statistical significance.

Sensor-assisted soft robotic glove training did not demonstrate superiority over supervised GRASP for upper limb function post-stroke. Exploratory subgroup analyses identified a signal suggesting improved distal hand motor recovery in participants with greater baseline impairment with sufficient therapy exposure.

Dyslipidaemia remains a leading cause of death in Germany despite an improving therapeutic landscape, with many patients not achieving guideline-recommended low-density lipoprotein cholesterol (LDL-C) goals. Bempedoic acid, an adenosine triphosphate citrate lyase inhibitor, is a recent addition to the therapeutic landscape with proven efficacy in randomised controlled trials; however, its use varies between centres. We aimed to assess the short-term, real-world effectiveness of bempedoic acid in lowering LDL-C levels in patients in Germany.

This retrospective, observational study was conducted using data from patients with primary hypercholesterolaemia or mixed dyslipidaemia, collected before and approximately 3 months after initiating bempedoic acid in 7 specialised lipid outpatient clinics in Germany.

Data were analysed from a total of 641 patients, with a mean age (standard deviation [SD]) of 63.2 (11.3) years. The addition of bempedoic acid significantly reduced LDL-C levels from a mean of 133.6 mg/dL at baseline to 101.8 mg/dL after 3 months (p < 0.001). The mean within-patient LDL-C reduction was 31.8 mg/dL and the mean patient-level percentage change was -17.5%. Mean patient-level changes were -4.9% for HDL-C and -12.0% for total cholesterol; triglycerides did not change significantly. At 3 months, patients not receiving any lipid-lowering therapy (LLT) other than bempedoic acid had a mean patient-level LDL-C reduction of 27.1%; corresponding mean reductions were 23.7% with ezetimibe, 20.3% with PCSK9 inhibitor therapy, 9.0% with statin therapy and 6.1% with statin plus ezetimibe. Suspected adverse events were documented in 218/641 patients (34.0%), and 171/641 (26.7%) had discontinued bempedoic acid by follow-up. Myalgia was the most commonly reported adverse event in patients discontinuing treatment (75 cases).

Findings from this real-world, multicentre study conducted in Germany show that bempedoic acid may present an effective treatment option for patients with hypercholesterolaemia who are already receiving LLT, in addition to being an effective option for patients not receiving/tolerating other LLTs. The magnitude of LDL-C reduction differed across background treatment strategies, while suspected adverse events and treatment discontinuation were common in this specialist-care cohort.

Stroke is one of the leading causes of death and disability in China and imposes a substantial disease burden. Population aging has further increased the challenges of stroke prevention and control among middle-aged and older adults. Although environmental relative humidity (RH) is considered an important environmental determinant of health, existing evidence regarding its association with stroke remains inconsistent, with prospective evidence from Chinese populations being particularly limited. This study aims to investigate the association between environmental RH and the risk of incident stroke among middle-aged and older adults in China and to assess the mediating role of frailty and potential gender differences in this association.

A dynamic-entry cohort was constructed using data from the 2011, 2013, 2015, and 2018 waves of the China Health and Retirement Longitudinal Study (CHARLS), with a total of 19 582 participants ultimately included. Participants were followed from the date of the first interview at which they met the eligibility criteria until the first report of incident stroke, loss to follow-up, or the end of follow-up in 2020. Hourly RH at each participant's place of residence was obtained from ERA5 reanalysis dataset, and the mean RH during the year preceding enrollment was calculated. Participants were categorized into low-, moderate-, and high-humidity groups according to tertiles, with the low-humidity group serving as the reference. Incident stroke was defined as the first self-reported physician diagnosis of stroke during follow-up. Cox proportional hazards models were used to estimate HR and 95% CI, with sequential adjustment for sociodemographic characteristics, health behaviors, mean temperature during the year preceding enrollment, and other potential confounders. Gender-stratified analyses were also performed. Counterfactual-based mediation analysis was conducted to assess the mediating effect of the frailty index (FI), and nonparametric bootstrap resampling with 5 000 repetitions was used to estimate the proportion mediated by FI and its uncertainty.

During a median follow-up of 7 years, 1 235 participants (6.31%) developed incident stroke. Cox regression analyses showed that, compared with the low-humidity group, both the moderate- and high-humidity groups had increased risks of incident stroke. In the fully adjusted model, the HR was 1.119 (95% CI 1.033 to 1.213) for the moderate-humidity group and 1.279 (95% CI 1.227 to 1.331) for the high-humidity group (both P<0.01), with effect estimates progressively attenuated as the degree of model adjustment increased. Gender-stratified analyses showed that the association was more pronounced in men. In the fully adjusted model, the HRs among men were 1.145 (95% CI 1.031 to 1.272) for the moderate-humidity group and 1.352 (95% CI 1.268 to 1.442) for the high-humidity group. Among women, the risk was also elevated in the high-humidity group (HR=1.186, 95% CI 1.092 to 1.288), whereas the association for the moderate-humidity group was attenuated and not statistically significant (HR=1.082, 95% CI 0.954 to 1.227). Mediation analysis indicated that the total effect of environmental RH on incident stroke risk was statistically significant (P<0.01). RH was associated with frailty level (β=0.22, P<0.01), and frailty mediated 22.0% of the association between RH and incident stroke risk.

Higher environmental RH is associated with an increased risk of incident stroke among middle-aged and older adults in China, and this association may be partially mediated through frailty. Gender differences were observed, with the association being more pronounced in men. These findings suggest that exposure to high-humidity environments should be considered in primary stroke prevention and healthy aging management, with enhanced risk identification and health guidance for potentially high-risk subgroups, particularly individuals with frailty and men.

It remains unclear whether the degree of fragmentation modifies the adverse health outcomes associated with prolonged sedentary behavior. This study aims to investigate the associations of objectively measured sedentary patterns with incident cardiovascular disease (CVD), mortality, and life expectancy.

This prospective cohort study included 89 010 UK Biobank participants (median age 63.5 years, 56.5% women) who provided 3 to 7 valid days of wrist accelerometer data. Daily sedentary time and number of sedentary breaks were the metrics of interest. Four overall sedentary behavior patterns were identified by joint classification of sedentary time and number of sedentary breaks. Outcomes were all-cause mortality, CVD incidence and mortality, CVD-free life expectancy, and total life expectancy. Multivariable Cox proportional hazards models were used to evaluate the associations of sedentary behavior metrics with all-cause mortality and CVD incidence, whereas Fine-Gray competing-risk models were used to evaluate their associations with cardiovascular mortality, with non-CVD death treated as a competing event. Restricted cubic splines were used to assess potential nonlinear associations. Multi-state survival analyses were performed to estimate CVD-free life expectancy. Isotemporal substitution models were used to estimate the effects of replacing sedentary time with moderate-to-vigorous physical activity (MVPA).

During a median follow-up of 8.0 years, 3 730 deaths occurred, including 1 223 CVD deaths and 8 883 incident CVD cases. Total sedentary time showed J-shaped dose-response associations with all-cause and cardiovascular mortality and a linear association with increased CVD incidence. The number of sedentary breaks showed L-shaped associations with risks of all-cause mortality and CVD mortality. Compared to the least sedentary group, participants with prolonged sedentary time (≥10 h/d) and a low degree of fragmentation (sedentary break <12 bouts/d) had a 51.5% higher risk of all-cause mortality [hazard ratio (HR)=1.515, 95% confidence interval (CI) 1.380 to 1.663], a 55.3% higher risk of cardiovascular mortality (subdistribution HR=1.553, 95% CI 1.325 to 1.820), and a 10.0% higher risk of incident CVD (HR=1.100, 95% CI 1.030 to 1.174). At age 50, the loss of life expectancy was primarily observed in CVD-free years (men: -2.770 years, 95% CI -3.392 to -2.148; women: -3.113 years, 95% CI -3.794 to -2.432). Notably, a higher frequency of sedentary breaks attenuated the increased mortality risk and the loss of CVD-free life expectancy associated with prolonged sedentary time. Nevertheless, replacing sedentary behavior with MVPA reduced the risk of mortality and CVD incidence among all sedentary participants, regardless of levels of fragmentation.

Prolonged sedentary time and its uninterrupted accumulation patterns are associated with greater risks of mortality and CVD, alongside reductions in CVD-free life expectancy. The increased mortality risk and the loss of CVD-free years may be mitigated by frequent interruptions to sedentary behavior.