BACKGROUND:Rheumatoid arthritis is widely prevalent worldwide,with its high incidence and universality that considerably affects patients' quality of life.Previous studies have focused on a few immune cells or cytokines,whereas this study comprehensively provides a more complete view of the immune mechanisms in rheumatoid arthritis.OBJECTIVE:To explore the causal relationship between 731 immune cell phenotypes and rheumatoid arthritis using the Mendelian randomization method,thereby providing evidence of causality.METHODS:The 731 immune cell phenotypes used in this study were sourced from the GWAScatalog database,jointly developed by the National Human Genome Research Institute(NHGRI)and the European Bioinformatics Institute(EBI).The rheumatoid arthritis data were from the Finngen database,developed by the Finnish Institute for Molecular Medicine(FIMM).The inverse variance weighting method was employed as the primary analytical approach.Additionally,multiple analytical methods,including MR-Egger,weighted mode,simple mode,and weighted median,were concurrently utilized to complement the final results.Sensitivity analyses(Cochran's Q test,MR-Egger regression,and MR-presso analysis)were also conducted to verify the stability and feasibility of the data.RESULTS AND CONCLUSION:(1)After excluding results through heterogeneity testing,the inverse variance weighting analysis indicated that 10 absolute cell counts,15 median fluorescence intensities of surface antigen levels,1 morphological characteristic,and 9 relative cell counts had a causal relationship with the occurrence of rheumatoid arthritis.(2)According to cell classification,this study found that seven types of B cells,seven types of classical dendritic cells,six types of mature T cells,four types of monocytes,three types of myeloid cells,three types of TBNK cells(lymphocyte subset T cells,B cells and natural killer cells),and five types of Tregs had a causal association with the occurrence of rheumatoid arthritis.(3)Through comprehensive bidirectional two-sample MR analysis,we demonstrated the complex causal relationships between multiple immune phenotypes and rheumatoid arthritis,highlighting the intricate interaction patterns between the immune system and rheumatoid arthritis.These results provide new biomarkers for the early screening and diagnosis of rheumatoid arthritis in China,and help to improve the diagnostic accuracy and sensitivity.

Objective: To explore the developmental trajectories of depression in children and adolescents and their association with family types, and to analyze the role of being an only child in the context, so as to provide a basis for early identification of mental health issues in children and adolescents. Methods: The study was a secondary analysis based on the existing database of the Jiangsu Provincial Student Common Diseases and Health Influencing Factors Monitoring and Intervention Project. A total of 11 502 students who had completed at least two measurements using the Chinese version of the Center for Epidemiologic Studies Depression Scale (CES-D) between 2022 and 2024, and had complete information on family type, gender, and age, were selected as the study subjects. Latent class trajectory modeling was used to identify depression developmental trajectories. Multinomial Logistic regression was applied to analyze the association between family type and depression developmental trajectories, and the interaction effect of family type and being an only child was tested. Results: Three types of depression developmental trajectories were identified among children and adolescents: low stable type (91.3%, 10 504 students), moderate rising type (4.3%, 500 students), and high declining type (4.3%, 498 students). Significant differences were observed among the different trajectory groups in terms of gender, age, parental education level, family type, baseline CES-D score, and baseline school type ( χ 2/H=17.48, 139.97, 19.72 , 30.77, 1 081.35, 220.81, all P <0.05). Multinomial Logistic regression analysis showed that, using the low stable type as the reference trajectory group and the nuclear family as the reference family type, after adjusting for confounding factors such as gender, age, and parental education level, single parent families ( OR=1.87, 95%CI= 1.16-3.03) and grandparent headed families ( OR=1.83, 95%CI =1.04-3.21) were significantly associated with the high declining type trajectory (both P <0.05). No significant association was found between family type and the moderate rising type trajectory (all P >0.05). The interaction effect between family type and being an only child was not statistically significant ( LRT=7.71, df=8, P =0.46). Conclusions Depressive symptoms in children and adolescents show heterogeneous developmental patterns during school age. Children and adolescents from single parent and intergenerational families are more likely to follow the high decreasing trajectory.

Objective: To explore the interaction between school bullying and insomnia in relation to depression-anxiety-stress emotions among primary and secondary school students,so as to provide a basis for preventing negative emotional states in adolescents. Methods: In October 2024, a stratified cluster sampling method was used to select 3 058 students in grade 5-6 of primary, junior and senior high school in Sheyang County of Jiangsu Province. The Delaware Bullying Victimization Scale, Insomnia Severity Index, Depression-Anxiety-Stress Scale-21, and Study Condition Questionnaire were employed to investigate school bullying, insomnia, depression-anxiety-stress emotions, and academic performance. The χ 2 test and Logistic regression were used to analyze the association between school bullying and insomnia interactions and depression-anxiety-stress emotions among primary and secondary school students, multiplicative interaction analysis was conducted, and additive interaction analysis was performed using R software. Results: The detection rates of depression-anxiety-stress emotions among primary and secondary school students were 21.6%, 28.4% and 10.8%, respectively. The detection rates of physical bullying, relationship bullying, verbal bullying and cyberbullying in school bullying were 10.6%, 14.0%, 22.3%, and 6.2%, respectively. The detection rate for insomnia was 23.1%. Results from Logistic regression analysis showed that, after adjusting for relevant factors, physical, relational, verbal, and cyberbullying and insomnia were positively correlated with the detection rates of depression ( OR = 5.72- 10.93), anxiety ( OR =6.35-12.17), and stress emotions ( OR =5.97-14.52) among primary and secondary school students (all P <0.01). The multiplicative interaction between physical, relational, verbal, and cyberbullying and insomnia was positively correlated with the detection rates of depression ( OR =8.00-18.01), anxiety ( OR =11.35-17.76), and stress emotions ( OR =7.64-9.12) in primary and secondary school students (all P <0.01). Additive interactions were observed between physical, relational, verbal, and cyberbullying and insomnia in relation to the detection rates of depression, anxiety, and stress emotions among primary and secondary school students (both RERI and AP >0 and the credible interval excluded 0, SI >1 and the credible interval excluded 1). Conclusion School bullying and insomnia are associated with depression, anxiety, and stress emotions among primary and secondary school students, and they exhibit both multiplicative and additive interactions.

ObjectiveTo investigate the effect of Tougu Xiaotong capsules （TGXTC） on the regulation of chondrocyte PANoptosis， delay of chondrocyte degeneration， and improvement of the symptoms in knee osteoarthritis （KOA）. MethodsIn vivo experiments： 50 male C57BL/6 mice were randomly assigned into five groups （n=10 per group）： sham operation group， model group， low-dose TGXTC group （7.2 g·kg^-1）， high-dose TGXTC group （14.4 g·kg^-1）， and diclofenac sodium group （0.05 g·kg^-1）. Except for the sham group， KOA models were established in all other groups using the modified Hulth method. Following successful model induction， the TGXTC groups received daily oral gavage of 7.2 or 14.4 g·kg^-1 for 6 weeks， while the diclofenac sodium group received 0.05 g·kg^-1 solution daily over the same duration. Model evaluation was performed using Lequesne MG score； micro-computed tomography （micro-CT） was used to scan the knee， hematoxylin-eosin （HE） staining and safranin O-fast green staining were used to observe the morphology of cartilage， transmission electron microscopy （TEM） was used to determine ultrastructural changes of PANoptosis. Multiple immunofluorescence （IF） co-localization assays was performed to detect the co-localization of cleaved Caspase-3， receptor-interacting protein 3 （RlPK3）， and the N-terminal domain of gasdermin D （GSDMD-N） in cartilage tissue， while western blot was employed to detect the expression levels of cleaved Caspase-3， RIPK3， and GSDMD-N. In vitro experiments： The knee cartilages of 4-week-old SD rats were isolated， and a chondrocyte in vitro culture system was established through mechanical digestion with 0.2% type Ⅱ collagenase. Second-generation chondrocytes were divided into three groups： the control group， the model group （pretreated with 10 mg·L^-1 lipopolysaccharide （LPS） for 24 h followed by treatment with 1 μmol·L^-1 nigericin for 4 h）， and the TGXTC treatment group （pretreated with 10 mg·L^-1 LPS for 24 h， followed by exposure to 1 μmol·L^-1 nigericin for 4 h and subsequently treated with 100 mg·L^-1 TGXTC for an additional 24 h）. The levels of reactive oxygen species （ROS）， apoptosis， necroptosis， and pyroptosis of chondrocytes were evaluated via fluorescence microscopy following staining with ROS detection， AO/EB and YO-PRO-1/PI staining kits. Transmission electron microscopy was utilized to investigate the ultrastructural changes associated with PANoptosis in cartilage tissue of KOA mice. Inflammatory cytokine levels （IL-1β and IL-18） were measured using ELISA. Western blot was conducted to assess protein expressions related to PANoptosis， including cleaved Caspase-3， cleaved Caspase-8， RIPK3， ZBP1， GSDMD-N， and NLRP3. ResultsCompared with the sham group， the Lequesne MG scores were significantly up-regulated（P<0.01） in the model group， and the pathological changes of cartilage were significantly， with joint spaces narrower， osteophyte formation increased， secere abrasion of cartilage surface. Ultrastructural analysis revealed pronounced chondrocyte apoptosis， necroptosis， and pyroptosis， along with markedly elevated expression of cleaved Caspase-3， RlPK3， and GSDMD-N in cartilage tissue （P<0.01）. In addition， The mean fluorescence intensities of ROS， orange-red fluorescence in AO/EB staining， green fluorescence and red fluorescence in YO-PRO-1/PI staining were increased of chondrocyte in the model group （P<0.01） . The levels of inflammatory factors IL-1β and IL-18 in the supernatant were increased （P<0.01）. The expression of PANoptosis related proteins （cleaved Caspase-3， cleaved Caspase-8， RIPK3， ZBP1， GSDMD-N， and NLRP3） were also significantly upregulated（P<0.05）. Compared to the model group， the TGXTC group demonstrated a significant improvement in various parameters of mice. These included a reduction in the Lequesne MG score， an increase in joint space， a decrease in osteophyte formation， diminished cartilage damage， reduced release of ROS， and alleviation of apoptotic， necroptotic， and pyroptotic processes in chondrocytes. Additionally， mitochondrial swelling and endoplasmic reticulum dilation were also mitigated. The levels of ROS as well as IL-1β and IL-18 were significantly decreased （P<0.05）. Furthermore， the expression levels of proteins associated with PANoptosis in cartilage tissue showed marked reductions （P<0.05）. Similar results were observed in chondrocytes： cleaved Caspase-3， cleaved Caspase-8， RIPK3， ZBP1， GSDMD-N， and NLRP3 exhibited significant decreases as well （P<0.05）. ConclusionTGXTC may mitigate chondrocytes degeneration and alleviate KOA symptoms by reducing oxidative stress and suppressing the activation of PANoptosis pathways.

ObjectiveTo investigate the effect of Tougu Xiaotong capsules （TGXTC） on the regulation of chondrocyte PANoptosis， delay of chondrocyte degeneration， and improvement of the symptoms in knee osteoarthritis （KOA）. MethodsIn vivo experiments： 50 male C57BL/6 mice were randomly assigned into five groups （n=10 per group）： sham operation group， model group， low-dose TGXTC group （7.2 g·kg^-1）， high-dose TGXTC group （14.4 g·kg^-1）， and diclofenac sodium group （0.05 g·kg^-1）. Except for the sham group， KOA models were established in all other groups using the modified Hulth method. Following successful model induction， the TGXTC groups received daily oral gavage of 7.2 or 14.4 g·kg^-1 for 6 weeks， while the diclofenac sodium group received 0.05 g·kg^-1 solution daily over the same duration. Model evaluation was performed using Lequesne MG score； micro-computed tomography （micro-CT） was used to scan the knee， hematoxylin-eosin （HE） staining and safranin O-fast green staining were used to observe the morphology of cartilage， transmission electron microscopy （TEM） was used to determine ultrastructural changes of PANoptosis. Multiple immunofluorescence （IF） co-localization assays was performed to detect the co-localization of cleaved Caspase-3， receptor-interacting protein 3 （RlPK3）， and the N-terminal domain of gasdermin D （GSDMD-N） in cartilage tissue， while western blot was employed to detect the expression levels of cleaved Caspase-3， RIPK3， and GSDMD-N. In vitro experiments： The knee cartilages of 4-week-old SD rats were isolated， and a chondrocyte in vitro culture system was established through mechanical digestion with 0.2% type Ⅱ collagenase. Second-generation chondrocytes were divided into three groups： the control group， the model group （pretreated with 10 mg·L^-1 lipopolysaccharide （LPS） for 24 h followed by treatment with 1 μmol·L^-1 nigericin for 4 h）， and the TGXTC treatment group （pretreated with 10 mg·L^-1 LPS for 24 h， followed by exposure to 1 μmol·L^-1 nigericin for 4 h and subsequently treated with 100 mg·L^-1 TGXTC for an additional 24 h）. The levels of reactive oxygen species （ROS）， apoptosis， necroptosis， and pyroptosis of chondrocytes were evaluated via fluorescence microscopy following staining with ROS detection， AO/EB and YO-PRO-1/PI staining kits. Transmission electron microscopy was utilized to investigate the ultrastructural changes associated with PANoptosis in cartilage tissue of KOA mice. Inflammatory cytokine levels （IL-1β and IL-18） were measured using ELISA. Western blot was conducted to assess protein expressions related to PANoptosis， including cleaved Caspase-3， cleaved Caspase-8， RIPK3， ZBP1， GSDMD-N， and NLRP3. ResultsCompared with the sham group， the Lequesne MG scores were significantly up-regulated（P<0.01） in the model group， and the pathological changes of cartilage were significantly， with joint spaces narrower， osteophyte formation increased， secere abrasion of cartilage surface. Ultrastructural analysis revealed pronounced chondrocyte apoptosis， necroptosis， and pyroptosis， along with markedly elevated expression of cleaved Caspase-3， RlPK3， and GSDMD-N in cartilage tissue （P<0.01）. In addition， The mean fluorescence intensities of ROS， orange-red fluorescence in AO/EB staining， green fluorescence and red fluorescence in YO-PRO-1/PI staining were increased of chondrocyte in the model group （P<0.01） . The levels of inflammatory factors IL-1β and IL-18 in the supernatant were increased （P<0.01）. The expression of PANoptosis related proteins （cleaved Caspase-3， cleaved Caspase-8， RIPK3， ZBP1， GSDMD-N， and NLRP3） were also significantly upregulated（P<0.05）. Compared to the model group， the TGXTC group demonstrated a significant improvement in various parameters of mice. These included a reduction in the Lequesne MG score， an increase in joint space， a decrease in osteophyte formation， diminished cartilage damage， reduced release of ROS， and alleviation of apoptotic， necroptotic， and pyroptotic processes in chondrocytes. Additionally， mitochondrial swelling and endoplasmic reticulum dilation were also mitigated. The levels of ROS as well as IL-1β and IL-18 were significantly decreased （P<0.05）. Furthermore， the expression levels of proteins associated with PANoptosis in cartilage tissue showed marked reductions （P<0.05）. Similar results were observed in chondrocytes： cleaved Caspase-3， cleaved Caspase-8， RIPK3， ZBP1， GSDMD-N， and NLRP3 exhibited significant decreases as well （P<0.05）. ConclusionTGXTC may mitigate chondrocytes degeneration and alleviate KOA symptoms by reducing oxidative stress and suppressing the activation of PANoptosis pathways.

BACKGROUND:Rheumatoid arthritis is widely prevalent worldwide,with its high incidence and universality that considerably affects patients' quality of life.Previous studies have focused on a few immune cells or cytokines,whereas this study comprehensively provides a more complete view of the immune mechanisms in rheumatoid arthritis.OBJECTIVE:To explore the causal relationship between 731 immune cell phenotypes and rheumatoid arthritis using the Mendelian randomization method,thereby providing evidence of causality.METHODS:The 731 immune cell phenotypes used in this study were sourced from the GWAScatalog database,jointly developed by the National Human Genome Research Institute(NHGRI)and the European Bioinformatics Institute(EBI).The rheumatoid arthritis data were from the Finngen database,developed by the Finnish Institute for Molecular Medicine(FIMM).The inverse variance weighting method was employed as the primary analytical approach.Additionally,multiple analytical methods,including MR-Egger,weighted mode,simple mode,and weighted median,were concurrently utilized to complement the final results.Sensitivity analyses(Cochran's Q test,MR-Egger regression,and MR-presso analysis)were also conducted to verify the stability and feasibility of the data.RESULTS AND CONCLUSION:(1)After excluding results through heterogeneity testing,the inverse variance weighting analysis indicated that 10 absolute cell counts,15 median fluorescence intensities of surface antigen levels,1 morphological characteristic,and 9 relative cell counts had a causal relationship with the occurrence of rheumatoid arthritis.(2)According to cell classification,this study found that seven types of B cells,seven types of classical dendritic cells,six types of mature T cells,four types of monocytes,three types of myeloid cells,three types of TBNK cells(lymphocyte subset T cells,B cells and natural killer cells),and five types of Tregs had a causal association with the occurrence of rheumatoid arthritis.(3)Through comprehensive bidirectional two-sample MR analysis,we demonstrated the complex causal relationships between multiple immune phenotypes and rheumatoid arthritis,highlighting the intricate interaction patterns between the immune system and rheumatoid arthritis.These results provide new biomarkers for the early screening and diagnosis of rheumatoid arthritis in China,and help to improve the diagnostic accuracy and sensitivity.

OBJECTIVE To summarize the procedural management practice of hospital infection review for new medical technologies and projects so as to provide references for other medical institutions.METHODS The data with the respect to review of new technologies and projects were collected from Zhejiang Provincial Hospital of Chinese Medicine between 2018 and 2023,and the process of review and management practice were summarized.The potential risk for infection was evaluated by establishing the evaluation indexes for nosocomial infection man-agement of new technologies and projects and conducting procedural management of the review so as to make clear of the corresponding prevention and control measures.The tracking closed-loop management was carried out for the new technologies and projects that have been already implemented.RESULTS Totally 629 items of new medical technologies and projects were involved in the review and tracking closed-loop management,including 499(79.33％)medical technologies and pharmacy-related projects and 130(20.67％)nursing.The result of review showed that there were 606(96.34％)items with'approval',14(2.23％)items with'approval after revision',3(0.48％)items with'approval after reexamination,and 6(0.95％)items with'disapproval'.The result of risk as-sessment indicated that there were 5(0.79％)items of high-risk projects and 624(99.21％)items of low-risk pro-jects.There was no severe nosocomial infection or infection cluster incident during the tracking of clinical applica-tion of the approved items.CONCLUSION The risk of nosocomial infection has been controlled from the origin through the practice,which further standardizes the clinical application of the new technologies and projects and provides evidence for normalized application of the new technologies and projects in the medical institutions.

BACKGROUND:Mitochond rial biogenesis in skeletal muscle and its regulatory mechanisms during exercise have become focal points of research.Pathways such as AMP-activated protein kinase,peroxisome proliferator-activated receptory coactivator 1α,mitogen-activated protein kinase,calcium-regulated signaling play profound roles in exercise-induced mitochondrial biogenesis,impacting muscle metabolic optimization,enhanced athletic performance,and the prevention of metabolic diseases.However,the interactions among these pathways,their regulatory mechanisms,and their comprehensive effects on exercise-induced mitochondrial biogenesis in skeletal muscle remain unclear.OBJECTIVE:To explore the signaling pathways related to mitochondrial biogenesis in skeletal muscle,precisely analyze the induction and regulatory details of exercise within these pathways,and clearly elucidate the principles by which exercise-activated signaling pathways promote mitochondrial generation and functional enhancement.This will establish a theoretical foundation for improving muscle metabolism,enhancing exercise efficiency,and preventing metabolic diseases.METHODS:An extensive literature search was conducted using China National Knowledge Infrastructure(CNKI),WanFang,VIP,PubMed,and Web of Science.The latest publications related to mitochondrial biogenesis in skeletal muscle and its regulatory mechanisms were collected from inception to August 2024.By integrating findings from multiple signaling pathways,the regulatory mechanisms of exercise on mitochondrial biogenesis were systematically reviewed,with a focus on the interactions and synergistic mechanisms of AMP-activated protein kinase,peroxisome proliferator-activated receptor y coactivator 1α,protein kinase A,mitogen-activated protein kinase,calcium-regulated signaling pathways.RESULTS AND CONCLUSION:(1)Mitochondrial biogenesis in skeletal muscle is a complex biological process involving the coordinated regulation of multiple signaling pathways.This process aims to optimize the metabolic capacity,fatigue resistance,and overall athletic performance of skeletal muscle in response to changes in energy demand and external stress.The core mechanisms include the interactions and regulation of key factors such as AMP-activated protein kinase,peroxisome proliferator-activated receptor gamma coactivator 1α,and mitogen-activated protein kinase.(2)AMP-activated protein kinase senses the cellular energy status and activates peroxisome proliferator-activated receptor gamma coactivator 1α,thereby promoting mitochondrial biogenesis.Peroxisome proliferator-activated receptor gamma coactivator 1α,as the main regulator of mitochondrial biogenesis in skeletal muscle,can modulate the synthesis of mitochondrial proteins and DNA,enhance the antioxidant stress response,and improve mitochondrial function.(3)The mitogen-activated protein kinase signaling pathway,particularly p38 mitogen-activated protein kinase,further promotes mitochondrial generation by activating peroxisome proliferator-activated receptor gamma coactivator 1α during stress responses.(4)Additionally,calcium signaling and protein kinase A pathways play significant roles in the metabolic regulation of skeletal muscle.(5)Exercise can significantly enhance mitochondrial biogenesis capacity in skeletal muscle by activating these multiple signaling pathways,optimizing cellular metabolic efficiency,increasing muscle endurance,and improving athletic performance.(6)Future research should focus on in-depth exploration of the interaction mechanisms among AMP-activated protein kinase,peroxisome proliferator-activated receptor gamma coactivator1α,mitogen-activated protein kinases,and calcium signaling under different exercise intensities and modalities;strengthen studies across diverse age groups,genders,and health conditions;validate the universality and population-specificity of research findings;investigate the intricate mechanisms of emerging regulatory factors such as FNIP1 and PERM1 and their potential in exercise interventions;and promote the translation of exercise health research outcomes into clinical applications.

BACKGROUND:Mitochond rial biogenesis in skeletal muscle and its regulatory mechanisms during exercise have become focal points of research.Pathways such as AMP-activated protein kinase,peroxisome proliferator-activated receptory coactivator 1α,mitogen-activated protein kinase,calcium-regulated signaling play profound roles in exercise-induced mitochondrial biogenesis,impacting muscle metabolic optimization,enhanced athletic performance,and the prevention of metabolic diseases.However,the interactions among these pathways,their regulatory mechanisms,and their comprehensive effects on exercise-induced mitochondrial biogenesis in skeletal muscle remain unclear.OBJECTIVE:To explore the signaling pathways related to mitochondrial biogenesis in skeletal muscle,precisely analyze the induction and regulatory details of exercise within these pathways,and clearly elucidate the principles by which exercise-activated signaling pathways promote mitochondrial generation and functional enhancement.This will establish a theoretical foundation for improving muscle metabolism,enhancing exercise efficiency,and preventing metabolic diseases.METHODS:An extensive literature search was conducted using China National Knowledge Infrastructure(CNKI),WanFang,VIP,PubMed,and Web of Science.The latest publications related to mitochondrial biogenesis in skeletal muscle and its regulatory mechanisms were collected from inception to August 2024.By integrating findings from multiple signaling pathways,the regulatory mechanisms of exercise on mitochondrial biogenesis were systematically reviewed,with a focus on the interactions and synergistic mechanisms of AMP-activated protein kinase,peroxisome proliferator-activated receptor y coactivator 1α,protein kinase A,mitogen-activated protein kinase,calcium-regulated signaling pathways.RESULTS AND CONCLUSION:(1)Mitochondrial biogenesis in skeletal muscle is a complex biological process involving the coordinated regulation of multiple signaling pathways.This process aims to optimize the metabolic capacity,fatigue resistance,and overall athletic performance of skeletal muscle in response to changes in energy demand and external stress.The core mechanisms include the interactions and regulation of key factors such as AMP-activated protein kinase,peroxisome proliferator-activated receptor gamma coactivator 1α,and mitogen-activated protein kinase.(2)AMP-activated protein kinase senses the cellular energy status and activates peroxisome proliferator-activated receptor gamma coactivator 1α,thereby promoting mitochondrial biogenesis.Peroxisome proliferator-activated receptor gamma coactivator 1α,as the main regulator of mitochondrial biogenesis in skeletal muscle,can modulate the synthesis of mitochondrial proteins and DNA,enhance the antioxidant stress response,and improve mitochondrial function.(3)The mitogen-activated protein kinase signaling pathway,particularly p38 mitogen-activated protein kinase,further promotes mitochondrial generation by activating peroxisome proliferator-activated receptor gamma coactivator 1α during stress responses.(4)Additionally,calcium signaling and protein kinase A pathways play significant roles in the metabolic regulation of skeletal muscle.(5)Exercise can significantly enhance mitochondrial biogenesis capacity in skeletal muscle by activating these multiple signaling pathways,optimizing cellular metabolic efficiency,increasing muscle endurance,and improving athletic performance.(6)Future research should focus on in-depth exploration of the interaction mechanisms among AMP-activated protein kinase,peroxisome proliferator-activated receptor gamma coactivator1α,mitogen-activated protein kinases,and calcium signaling under different exercise intensities and modalities;strengthen studies across diverse age groups,genders,and health conditions;validate the universality and population-specificity of research findings;investigate the intricate mechanisms of emerging regulatory factors such as FNIP1 and PERM1 and their potential in exercise interventions;and promote the translation of exercise health research outcomes into clinical applications.

Objective This study aims to investigate and analyze the effects of the incentive-coordination-supervision mechanism applied to training management of medical staff under the modern hospital management system.Methods A total of 84 medical staff members working at the hospital from February 2022 to February 2024 were selected for the study.They were di-vided into a reference group(n=42,February 2022 to February 2023)and a study group(n=42,March 2023 to February 2024)based on the time period.The reference group underwent routine management,while the study group underwent manage-ment based on the incentive-coordination-supervision mechanism.The quality of management,occurrence of adverse events,management satisfaction,and core competencies were compared between the two groups.Results The study group had higher scores in cultural construction,reward and punishment mechanism,reporting system,and communication and coordination mech-anism than the reference group(all P＜0.05).The occurrence rate of adverse events was lower in the study group than in the reference group(7.14％vs 23.81％)(P＜0.05).The study group had higher satisfaction rates in management methods,man-agement content,management forms,and communication skills(95.24％,92.86％,97.62％,and 95.24％,respectively)compared to the reference group(78.57％,73.81％,76.19％,and 73.81％,respectively)(all P＜0.05).The study group had higher scores in all core competencies compared to the reference group(all P＜0.05).Conclusion The application of the incentive-coordination-supervision mechanism in training management of medical staff shows favorable effects,improving the qual-ity of management,management satisfaction,and core competencies,and reducing the occurrence of adverse events.