Objective: To explore the intervention effects of different exercise modalities on executive function in school aged children, providing references for formulating exercise prescriptions to promote school aged children executive function. Methods: A systematic literature search was conducted using PubMed, Embase, Cochrane Library, Web of Science, CNKI, Wanfang, VIP and CBM to identify studies on the effects of exercises on executive function in school aged children. The search period spanned from the database inception to August 2025. Two researchers independently screened the literature, extracted data, and evaluated the risk of bias of the included studies. Network Meta analysis was performed using Stata 16.0. Results: A total of 51 studies involving 5 710 school aged children and seven modalities of exercises(control group,small ball sports,large ball sports,aerobic exercise,combined exercise,sport game,gymnastic and dance sports) were finally included. Network Meta analysis showed that, in terms of inhibitory control development of school aged children, small ball sports ( SMD =-0.98,95% CI =-1.32 to -0.64 ), large ball sports ( SMD =-0.64,95% CI =-0.91 to -0.36), and mixed sports ( SMD =-0.26,95% CI =-0.50 to -0.02]) were more effective than the control group; in terms of working memory, largeball sports ( SMD =-1.26,95% CI =-1.88 to -0.65) and small ball sports ( SMD =-0.91,95% CI =-1.64 to -0.19) were superior to the control group; in terms of improving cognitive flexibility, large ball sports ( SMD =-1.02,95% CI =-1.28 to -0.76), gymnastics and dance sports ( SMD =-0.80,95% CI =-1.21 to -0.40), and small ball sports ( SMD =-0.75,95% CI =-1.15 to -0.36) were more effective than the control group (all P <0.05). Surface under cumulative ranking curve(SUCRA) showed that small ball sports had the highest value (SUCRA=98.9%) in improving inhibitory control, while large ball sports achieved the highest score(SUCRA=92.6%) in enhancing working memory, and large ball sports also had the highest value(SUCRA=94.7%) in promoting cognitive flexibility. Conclusions For developing inhibitory control in school aged children, small ball sports are recommended as a priority. For enhancing working memory and cognitive flexibility, large ball sports are recommended.

Background Regulatory interactions between microRNAs (miRNAs) and messenger RNAs (mRNAs) are involved in the progression of pulmonary fibrosis, which can either promote or inhibit the development of this disease. Objective To explore the miRNA-mRNA regulatory network during the progression of silica (SiO₂)-induced pulmonary fibrosis in mice using integrated mRNA-seq and miRNA-seq analysis. Methods A mouse model of pulmonary fibrosis was established by dynamic SiO₂ dust exposure. The experimental design included a blank control group and four SiO₂-exposed groups (7, 14, 28, and 56 d, n=10 per group). Successful model induction was confirmed by histopathological analysis (HE and Masson staining), hydroxyproline (HYP) quantification, and expression of key fibrosis-related cytokines [fibroblast growth factor (FGF), interleukin-6 (IL-6), transforming growth factor-β (TGF-β), and tumor necrosis factor-α (TNF-α)]. Lung tissues from mice in each group were subjected to sequencing, and Mfuzz was used for time-series gene clustering to identify dynamic progression patterns. DESeq2 was utilized to identify differentially expressed genes (DEGs) and differentially expressed miRNAs. Enrichment analysis of DEGs was performed to identify critical signaling pathways and biological processes underlying pulmonary fibrosis progression. Expression of four selected miRNAs was subsequently validated by real-time quantitative polymerase chain reaction (RT-qPCR). The target mRNAs of key miRNAs were comprehensively predicted by integrating miRBase, starBase, and miRTarBase to construct the regulatory networks and investigate potential functions. Results SiO₂ exposure led to time-dependent aggravation of pulmonary fibrosis in mice, evidenced by increased fibrous deposition, elevated HYP levels (P < 0.01), and up-regulation of four kinds of pro-fibrotic cytokines (P < 0.01) compared with the NT group. Mfuzz clustering revealed the stage-specific characteristics. Compared to controls, 231, 662, 448, and 1020 DEGs were identified after SiO₂ exposure at 7, 14, 28, and 56 d, respectively, primarily enriched in immune responses and chemokine signaling. During critical fibrotic phases—7 d (acute inflammation and initiation) and 28 d (chronic inflammation and establishment)—18 differentially expressed miRNAs were identified; notably mmu-miR-135b-5p was significantly dysregulated at both time points. The expression trends of the four key miRNAs (mmu-miR-135b-5p, mmu-miR-708-5p, mmu-miR-21a-3p, and mmu-miR-205-5p) were consistent with the sequencing results. Furthermore, bioinformatics databases were used to predict the target mRNAs of key miRNAs. The constructed network highlighted critical miRNA-mRNA pairs—including mmu-miR-135b-5p and Meis1, mmu-miR-708-5p and Mmp25, mmu-miR-21a-3p and Cacna1d, mmu-miR-205-5p and Ereg which were closely associated with inflammatory response, extracellular matrix deposition, and fibroblast activation. Conclusion The progression of pulmonary fibrosis is accompanied by dynamic changes in miRNA-mRNA regulatory networks. The identified miRNA-target axes (e.g., miR-135b-5p and Meis1, mmu-miR-708-5p and Mmp25, mmu-miR-21a-3p and Cacna1d, and mmu-miR-205-5p and Ereg—) may play important roles in fibrogenesis and provide potential therapeutic targets for pulmonary fibrosis.

Background Regulatory interactions between microRNAs (miRNAs) and messenger RNAs (mRNAs) are involved in the progression of pulmonary fibrosis, which can either promote or inhibit the development of this disease. Objective To explore the miRNA-mRNA regulatory network during the progression of silica (SiO₂)-induced pulmonary fibrosis in mice using integrated mRNA-seq and miRNA-seq analysis. Methods A mouse model of pulmonary fibrosis was established by dynamic SiO₂ dust exposure. The experimental design included a blank control group and four SiO₂-exposed groups (7, 14, 28, and 56 d, n=10 per group). Successful model induction was confirmed by histopathological analysis (HE and Masson staining), hydroxyproline (HYP) quantification, and expression of key fibrosis-related cytokines [fibroblast growth factor (FGF), interleukin-6 (IL-6), transforming growth factor-β (TGF-β), and tumor necrosis factor-α (TNF-α)]. Lung tissues from mice in each group were subjected to sequencing, and Mfuzz was used for time-series gene clustering to identify dynamic progression patterns. DESeq2 was utilized to identify differentially expressed genes (DEGs) and differentially expressed miRNAs. Enrichment analysis of DEGs was performed to identify critical signaling pathways and biological processes underlying pulmonary fibrosis progression. Expression of four selected miRNAs was subsequently validated by real-time quantitative polymerase chain reaction (RT-qPCR). The target mRNAs of key miRNAs were comprehensively predicted by integrating miRBase, starBase, and miRTarBase to construct the regulatory networks and investigate potential functions. Results SiO₂ exposure led to time-dependent aggravation of pulmonary fibrosis in mice, evidenced by increased fibrous deposition, elevated HYP levels (P < 0.01), and up-regulation of four kinds of pro-fibrotic cytokines (P < 0.01) compared with the NT group. Mfuzz clustering revealed the stage-specific characteristics. Compared to controls, 231, 662, 448, and 1020 DEGs were identified after SiO₂ exposure at 7, 14, 28, and 56 d, respectively, primarily enriched in immune responses and chemokine signaling. During critical fibrotic phases—7 d (acute inflammation and initiation) and 28 d (chronic inflammation and establishment)—18 differentially expressed miRNAs were identified; notably mmu-miR-135b-5p was significantly dysregulated at both time points. The expression trends of the four key miRNAs (mmu-miR-135b-5p, mmu-miR-708-5p, mmu-miR-21a-3p, and mmu-miR-205-5p) were consistent with the sequencing results. Furthermore, bioinformatics databases were used to predict the target mRNAs of key miRNAs. The constructed network highlighted critical miRNA-mRNA pairs—including mmu-miR-135b-5p and Meis1, mmu-miR-708-5p and Mmp25, mmu-miR-21a-3p and Cacna1d, mmu-miR-205-5p and Ereg which were closely associated with inflammatory response, extracellular matrix deposition, and fibroblast activation. Conclusion The progression of pulmonary fibrosis is accompanied by dynamic changes in miRNA-mRNA regulatory networks. The identified miRNA-target axes (e.g., miR-135b-5p and Meis1, mmu-miR-708-5p and Mmp25, mmu-miR-21a-3p and Cacna1d, and mmu-miR-205-5p and Ereg—) may play important roles in fibrogenesis and provide potential therapeutic targets for pulmonary fibrosis.

Objective: To explore the association between mental health and muscle strength among Chinese adolescents aged 13- 18, providing a theoretical foundation and intervention strategies for mental health promotion. Methods: Data were obtained from the 2019 Chinese National Survey on Students Constitution and Health, including 98 631 Chinese adolescents aged 13- 18. Psychological distress was assessed by using the Kessler Psychological Distress Scale (K10), and mental well being was measured with the Warwick-Edinburgh Mental Well being Scale (WEMWBS). Based on the gender and age specific Z scores of various test items [grip strength, standing long jump, pull ups (for males), and sit ups (for females)], muscle strength index (MSI) was constructed to evaluate the comprehensive level of muscle strength in adolescents. According to the Dual factor Model (DFM) of mental health, participants were categorized into four groups:troubled, symptomatic but content, vulnerable, and complete mental health. Gender differences were analyzed by using Chi-square tests, trends were tested with Cochran-Armitage tests, and multinomial Logistic regression models were applied to assess associations between muscle strength and mental health among adolescents. Results: In 2019, 37.4% of Chinese adolescents aged 13-18 were reported of high mental distress, and 59.9% were reported of low mental well being. Boys had significantly lower rates of high mental distress (35.3%) and low mental well being (55.6%) compared to girls (39.4%, 64.3%), and the differences were of statistical significance ( χ 2=176.13, 780.42, both P <0.05). In 2019, the rate of complete mental health among adolescents showed a downward trend with increasing age ( χ 2 trend = 258.47) and a gradual upward trend with increasing muscle strength levels ( χ 2 trend =123.14)，and both boys and girls exhibited similar trends ( χ 2 trend =103.83, 168.46; 57.00 , 67.34) (all P <0.05). The results of the unordered multiclass Logistic regression model showed that after controlling for confounding factors such as age and gender, when the completely pathological group as a reference, for every 1 unit increase in MSI in adolescents, the likelihood of being in a completely mental health state increased by 29% ( OR = 1.29); for every unit increase in the Z-score for pull ups, the likelihood of being in a completely mental health state increased by 6% ( OR =1.06) among boys; for every 1 unit increase in sit up Z score, the likelihood of being in a completely mental health state increased by 19% ( OR =1.19) among girls (all P <0.05). Conclusions The mental health status of Chinese adolescents is not good enough. Muscle strength is positively associated with mental health.

Objective To quantitatively assess the association of short-term exposure to polycyclic aromatic hydrocarbons (PAHs) in ambient fine particulate matter (PM2.5) with residents mortality. Methods A time-stratified case-crossover study was conducted from 2020 to 2022 among 10606 non-accidental residents by using the Guangzhou Cause of Death Surveillance System in Conghua District, Guangzhou. Exposure levels of PAHs in PM_2.5 and meteorological data during the study period were obtained from the Center for Disease Control and Prevention in Conghua District and the China Meteorological Administration Land Data Assimilation System (CLDAS-V2.0), respectively. Conditional Poisson regression model was used to estimate the exposure-response association between PAHs and the mortality risk. Results Fluoranthene, chrysene, benzo[k]fluoranthene, benzo[a]pyrene, and indeno[1,2,3-cd]pyrene were significantly associated with an increased risk of mortality. For every one interquartile range increase in exposure levels, the non-accidental mortality risks increased by 8.33% (95% CI: 1.80%, 15.27%), 4.67% (95% CI: 1.86%, 7.57%), 6.07% (95% CI: 2.08%, 10.21%), 4.62% (95% CI: 1.85%, 7.47%), and 4.70% (95% CI: 0.53%, 9.03%), respectively. The estimated non accidental deaths attributable to exposure to fluoranthene, chrysene, benzo[k]fluorine, benzo[a]pyrene and indine[1,2,3-cd]pyrene were 5.91%, 6.08%, 6.51%, 6.46%, and 4.21%, respectively. Conclusions Short-term exposure to PAHs in PM_2.5, including fluoranthene, chrysene, benzo[k]fluoranthene, benzo[a]pyrene and indine[1,2,3-cd]pyrene, was significantly associated with an increased risk of mortality among residents.

BACKGROUND: Asthma is a common chronic inflammatory airway disease and intermittent hypoxia is increasingly recognized as a factor that may impact disease progression. The present study investigated whether intermittent hypoxia (IH) could aggravate asthma by promoting hypoxia-inducible factor-1α (HIF-1α)/nucleotide-binding oligomerization domain (NOD)-like receptor pyrin domain-containing protein 3 (NLRP3)/interleukin (IL)-1β-dependent pyroptosis and the inflammatory response and further elucidated the underlying molecular mechanisms involved. METHODS: A total of 49 patients diagnosed with severe bronchial asthma and diagnosed by polysomnography were enrolled at Tongji Hospital, Tongji Medical College of Huazhong University of Science and Technology, between January 2022 and December 2022, and their general data and induced sputum were collected. BEAS-2B cells were treated with IL-13 and subjected to IH. An ovalbumin (OVA)-treated mouse model was also used to assess the effects of chronic intermittent hypoxia (CIH) on asthma. Pyroptosis, the inflammatory response, and related signalling pathways were assessed in vivo and in vitro . RESULTS: In this study, as the apnoea and hypopnea index (AHI) increased, the proportion of patients with uncontrolled asthma increased. The proportions of neutrophils and the levels of IL-6, IL-8, HIF-1α and NLRP3 in induced sputum were related to the AHI. NLRP3-mediated pyroptosis, which could be mediated by the HIF-1α signalling pathway, was activated in IL-13 plus IH-treated BEAS-2B cells and in the lungs of OVA/CIH mice. HIF-1α downregulation significantly reduced lung pyroptosis and ameliorated neutrophil inflammation by modulating the NLRP3/IL-1β pathway both in vitro and in vivo . Similarly, pretreatment with LW6, an inhibitor of HIF-1α, effectively blocked the generation of inflammatory cytokines in neutrophils. In addition, administration of the NLRP3 activator nigericin obviously increased lung neutrophil inflammation. CONCLUSIONS Obstructive sleep apnoea-hypopnea syndrome (OSAHS) is a risk factor for asthma exacerbation. IH aggravates neutrophil inflammation in asthma via NLRP3/IL-1β-dependent pyroptosis mediated by the HIF-1α signalling pathway, which should be considered a potential therapeutic target for the treatment of asthma with OSAHS.
NLR Family, Pyrin Domain-Containing 3 Protein/metabolism* ; Humans ; Asthma/metabolism* ; Animals ; Pyroptosis/physiology* ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism* ; Mice ; Signal Transduction/physiology* ; Male ; Hypoxia/metabolism* ; Female ; Interleukin-1beta/metabolism* ; Adult ; Inflammation/metabolism* ; Middle Aged ; Mice, Inbred C57BL

This study investigates the pharmacokinetics and metabolic characteristics of three marine-derived piericidins as potential drug leads for kidney disease: piericidin A (PA) and its two glycosides (GPAs), glucopiericidin A (GPA) and 13-hydroxyglucopiericidin A (13-OH-GPA). The research aims to facilitate lead selection and optimization for developing a viable preclinical candidate. Rapid absorption of PA and GPAs in mice was observed, characterized by short half-lives and low bioavailability. Glycosides and hydroxyl groups significantly enhanced the absorption rate (13-OH-GPA > GPA > PA). PA and GPAs exhibited metabolic instability in liver microsomes due to Cytochrome P450 enzymes (CYPs) and uridine diphosphoglucuronosyl transferases (UGTs). Glucuronidation emerged as the primary metabolic pathway, with UGT1A7, UGT1A8, UGT1A9, and UGT1A10 demonstrating high elimination rates (30%-70%) for PA and GPAs. This rapid glucuronidation may contribute to the low bioavailability of GPAs. Despite its low bioavailability (2.69%), 13-OH-GPA showed higher kidney distribution (19.8%) compared to PA (10.0%) and GPA (7.3%), suggesting enhanced biological efficacy in kidney diseases. Modifying the C-13 hydroxyl group appears to be a promising approach to improve bioavailability. In conclusion, this study provides valuable metabolic insights for the development and optimization of marine-derived piericidins as potential drug leads for kidney disease.
Animals ; Male ; Mice ; Aquatic Organisms/chemistry* ; Biological Availability ; Cytochrome P-450 Enzyme System/metabolism* ; Glucuronosyltransferase/metabolism* ; Microsomes, Liver/metabolism* ; Molecular Structure ; Biological Products/pharmacokinetics* ; Pyridines/pharmacokinetics*

Background Exposure to air pollutants increases the risk of diseases in multiple systems, including respiratory and cardiovascular systems, yet its association with neurological diseases remains unclear. Objective To quantitatively evaluate the association between short-term exposure to air pollutants and outpatient and emergency visits for neurological diseases, identify potential susceptible populations, and quantify associated disease burden. Methods Daily 24-hour average concentrations of fine particulate matter (PM_2.5), inhalable particulate matter (PM₁₀), sulfur dioxide (SO₂), nitrogen dioxide (NO₂), and carbon monoxide (CO), daily maximum 8-hour average concentration of ozone (O₃), daily meteorological data (24-hour average temperature, 24-hour average relative humidity), and data on daily outpatient and emergency department visits for neurological diseases from two hospitals in Conghua District, Guangzhou, China, were collected from 2015 to 2022. A time-stratified case-crossover design was adopted, and a conditional Poisson regression model was constructed to analyze the association between air pollution exposure and neurological disease visits. Two-pollutant models and sensitivity analysis were used to validate model stability. Stratified analyses by season (cold season: from November to March; warm season: from April to October), sex (male, female), and age (≤45 years, 46–60 years, ≥61 years) were performed to identify vulnerable group. Additionally, the number and proportion of neurological disease visits attributable to short-term air pollutant exposure were calculated. Results A total of 72 673 outpatient and emergency department visits for neurological diseases were included during the study period. Most of the patients were middle-aged and elderly individuals (69.89% were over 45 years old) and females (60.25%). The results of single-pollutant models showed that for each interquartile range (IQR) increase in exposure to PM_2.5, PM₁₀, SO₂, NO₂, CO, and O₃, the risk of outpatient and emergency department visits for neurological diseases increased by 7.54% (95%CI: 4.69%, 10.46%), 6.66% (95%CI: 3.92%, 9.46%), 16.72% (95%CI: 10.58%, 23.19%), 8.12% (95%CI: 4.82%, 11.53%), 5.60% (95%CI: 2.34%, 8.97%), and 6.11% (95%CI: 2.91%, 9.40%), respectively. The results of the two-pollutant model showed that the association between PM_2.5 and SO₂ exposure and outpatient and emergency department visits for neurological diseases were relatively stable. The stratified analyses showed that the effect of SO₂ was stronger in the cold season. It was estimated that 8.32% (95%CI: 5.55%, 10.96%) and 6.65% (95%CI: 4.27%, 8.96%) of the outpatient and emergency department visits were attributable to short-term exposure to SO₂ and PM_2.5, respectively. Conclusion Exposure to PM_2.5 and SO₂ is associated with increased risks of outpatient and emergency visits for neurological diseases. SO₂ shows stronger effects during the cold season, and exposure to air pollution contributes to up to 8.32% of neurological disease visits.

Objective:To investigate the safety, feasibility and efficacy of trans-oral robotic surgery in the treatment of lingual thyroglossal duct cyst. Methods:The clinical data of 21 patients with lingual thyroglossal duct cyst underwent trans-oral robotic surgery from May 2017 to March 2025 were analyzed retrospectively. Results:The cysts in all 21 patients were successfully excised by trans-oral robotic surgery. The mean robotic set-up and exposure time, operation time, estimated intraoperative blood loss and recovery time for oral intake were （14.3±7.2） min （[range 5.0-32.0]min）, （17.0±8.4） min （range[6.0-36.0]min）, （8.4±5.9） mL （range[2.0-25.0]mL） and （2.1±2.2） days （range[0-7]days）, respectively. No patients required tracheostomy, and no severe postoperative complications occurred. The patients were followed up for 2 to 96 months, with median follow-up time of 47 months, and 1 recurrence was observed. Conclusion:Excision of lingual thyroglossal duct cyst by trans-oral robotic surgery is safe and feasible, with rapid recovery and low recurrence rate, which is worth popularizing in clinical practice.
Humans ; Thyroglossal Cyst/surgery* ; Robotic Surgical Procedures/methods* ; Retrospective Studies ; Female ; Male ; Adult ; Treatment Outcome ; Middle Aged ; Adolescent

Acute kidney injury (AKI) has high morbidity and mortality, but effective clinical drugs and management are lacking. Previous studies have suggested that macrophages play a crucial role in the inflammatory response to AKI and may serve as potential therapeutic targets. Emerging evidence has highlighted the importance of forkhead box protein O1 (FoxO1) in mediating macrophage activation and polarization in various diseases, but the specific mechanisms by which FoxO1 regulates macrophages during AKI remain unclear. The present study aimed to investigate the role of FoxO1 in macrophages in the pathogenesis of AKI. We observed a significant upregulation of FoxO1 in kidney macrophages following ischemia-reperfusion (I/R) injury. Additionally, our findings demonstrated that the administration of FoxO1 inhibitor AS1842856-encapsulated liposome (AS-Lipo), mainly acting on macrophages, effectively mitigated renal injury induced by I/R injury in mice. By generating myeloid-specific FoxO1-knockout mice, we further observed that the deficiency of FoxO1 in myeloid cells protected against I/R injury-induced AKI. Furthermore, our study provided evidence of FoxO1's pivotal role in macrophage chemotaxis, inflammation, and migration. Moreover, the impact of FoxO1 on the regulation of macrophage migration was mediated through RhoA guanine nucleotide exchange factor 1 (ARHGEF1), indicating that ARHGEF1 may serve as a potential intermediary between FoxO1 and the activity of the RhoA pathway. Consequently, our findings propose that FoxO1 plays a crucial role as a mediator and biomarker in the context of AKI. Targeting macrophage FoxO1 pharmacologically could potentially offer a promising therapeutic approach for AKI.