Mitochondria are the center of intracellular energy metabolism.Mitochondrial dynamics refers to the dynamic process of mitochondrial fusion and fission,which plays an important role in maintaining mitochondrial homeostasis and central nervous system function.Optic atrophy 1(OPA1)is a key factor involved in mitochondrial dynamics.OPA1 acts by regulating mitochondrial fusion and fission,reducing oxidative stress,inhibiting apoptosis,and promoting mitochondrial autophagy,to maintain the dynamic changes in mitochondrial quantity,structure,and biological function.Numerous studies have shown that OPA1-mediated mitochondrial dynamics plays an important role in ischemic stroke,Alzheimer's disease,Parkinson's disease,spinal cord injury,multiple sclerosis,and other central nervous system diseases.Here we review the regulatory mechanism of OPA1 in terms of mitochondrial dynamics and the important role of mitochondrial function mediated by OPA1 in central nervous system diseases,to provide new ideas for clinical treatment.

The objective of this study was to evaluate the protective effect and possible related mechanisms of Sophora subprostrate polysaccharide(SSP)on intestinal epithelial cell injury in-duced by Tert-Butyl hydroperoxide(TBHP).The optimal dose of TBHP and the safe concentra-tion range of SSP were determined using the MTT method.In this study,IPEC-J2 cells were divid-ed into five groups:the control group,the model group,the SSPL group,the SSPM group and the SSPH group,and the cell morphology,cell survival rate and LDH release rate were observed and measured.The content of intracellular reactive ROS was observed and determined by DCFH-DA staining.The content of MDA in the supernatant and the antioxidant index of cells were determined by the reagent kit.Transcriptome technology was employed to analyze the potential mechanisms by which SSP mitigates oxidative damage in IPEC-J2 cells.The results showed that treatment with 625 μmol/L TBHP for 2 h significantly reduced the activity of IPEC-J2 cells,markedly increased LDH release(P＜0.05),inhibited CAT superoxide SOD and glutathione GPX activities(P＜0.05),and significantly elevated MDA and ROS levels(P＜0.05).Compared to the model group,after SSP treatment,intracellular ROS levels were significantly reduced(P＜0.05),while CAT,SOD,and GPX activities were significantly increased(P＜0.05),and MDA content and LDH re-lease were significantly decreased(P＜0.05)in a dose-dependent manner.Transcriptome analysis revealed that TBHP treatment significantly altered the transcriptional profiles of IPEC-J2 cells,while SSP treatment could restore the transcriptional profiles of the damaged cells to a certain ex-tent.Gene ontology(GO)and Kyoto encyclopedia of genes and genomes(KEGG)indicated that the differentially expressed genes between the CC and TBHP groups were significantly enriched in oxidative phosphorylation,ribosome,and other pathways.Meanwhile,the differentially expressed genes between the SSP and TBHP groups were mainly enriched in oxidative phosphorylation,ap-optosis,glyoxylate and dicarboxylate metabolism,and other pathways.These results suggest that TBHP may disrupt normal oxidative respiration in IPEC-J2 cells by affecting oxidative phospho-rylation and interfering with metabolism pathways involving glycine,serine,and threonine,leading to oxidative damage in intestinal epithelial cells.Conversely,SSP treatment may potentially restore oxidative phosphorylation processes,alleviate lysosomal damage,reduce cell apoptosis,and miti-gate oxidative damage in intestinal epithelial cells through modulation of oxidative phosphoryla-tion,apoptosis,and lysosomal pathways.This discovery provides a theoretical basis for the clinical application of SSP in alleviating oxidative damage in the porcine intestinal tract.

Vascular cognitive impairment (VCI), caused by cerebrovascular dysfunction, severely impacts the quality of life in the elderly population, yet effective therapeutic approaches remain limited. Mitophagy, a selective mitochondrial quality-control mechanism, has emerged as a critical focus in neurological disease research. Accumulating evidence indicates that mitophagy modulates oxidative stress, neuroinflammation, and neuronal apoptosis. Key signaling pathways associated with mitophagy—including PINK1/Parkin, BNIP3/Nix, FUNDC1, PI3K/Akt/mTOR, and AMPK—have been identified as potential therapeutic targets for VCI. This review summarizes the mechanistic roles of mitophagy in VCI pathogenesis and explores emerging therapeutic strategies targeting these pathways, aiming to provide novel insights for clinical intervention and advance the development of effective treatments for VCI.

Mitochondria are the center of intracellular energy metabolism.Mitochondrial dynamics refers to the dynamic process of mitochondrial fusion and fission,which plays an important role in maintaining mitochondrial homeostasis and central nervous system function.Optic atrophy 1(OPA1)is a key factor involved in mitochondrial dynamics.OPA1 acts by regulating mitochondrial fusion and fission,reducing oxidative stress,inhibiting apoptosis,and promoting mitochondrial autophagy,to maintain the dynamic changes in mitochondrial quantity,structure,and biological function.Numerous studies have shown that OPA1-mediated mitochondrial dynamics plays an important role in ischemic stroke,Alzheimer's disease,Parkinson's disease,spinal cord injury,multiple sclerosis,and other central nervous system diseases.Here we review the regulatory mechanism of OPA1 in terms of mitochondrial dynamics and the important role of mitochondrial function mediated by OPA1 in central nervous system diseases,to provide new ideas for clinical treatment.

The objective of this study was to evaluate the protective effect and possible related mechanisms of Sophora subprostrate polysaccharide(SSP)on intestinal epithelial cell injury in-duced by Tert-Butyl hydroperoxide(TBHP).The optimal dose of TBHP and the safe concentra-tion range of SSP were determined using the MTT method.In this study,IPEC-J2 cells were divid-ed into five groups:the control group,the model group,the SSPL group,the SSPM group and the SSPH group,and the cell morphology,cell survival rate and LDH release rate were observed and measured.The content of intracellular reactive ROS was observed and determined by DCFH-DA staining.The content of MDA in the supernatant and the antioxidant index of cells were determined by the reagent kit.Transcriptome technology was employed to analyze the potential mechanisms by which SSP mitigates oxidative damage in IPEC-J2 cells.The results showed that treatment with 625 μmol/L TBHP for 2 h significantly reduced the activity of IPEC-J2 cells,markedly increased LDH release(P＜0.05),inhibited CAT superoxide SOD and glutathione GPX activities(P＜0.05),and significantly elevated MDA and ROS levels(P＜0.05).Compared to the model group,after SSP treatment,intracellular ROS levels were significantly reduced(P＜0.05),while CAT,SOD,and GPX activities were significantly increased(P＜0.05),and MDA content and LDH re-lease were significantly decreased(P＜0.05)in a dose-dependent manner.Transcriptome analysis revealed that TBHP treatment significantly altered the transcriptional profiles of IPEC-J2 cells,while SSP treatment could restore the transcriptional profiles of the damaged cells to a certain ex-tent.Gene ontology(GO)and Kyoto encyclopedia of genes and genomes(KEGG)indicated that the differentially expressed genes between the CC and TBHP groups were significantly enriched in oxidative phosphorylation,ribosome,and other pathways.Meanwhile,the differentially expressed genes between the SSP and TBHP groups were mainly enriched in oxidative phosphorylation,ap-optosis,glyoxylate and dicarboxylate metabolism,and other pathways.These results suggest that TBHP may disrupt normal oxidative respiration in IPEC-J2 cells by affecting oxidative phospho-rylation and interfering with metabolism pathways involving glycine,serine,and threonine,leading to oxidative damage in intestinal epithelial cells.Conversely,SSP treatment may potentially restore oxidative phosphorylation processes,alleviate lysosomal damage,reduce cell apoptosis,and miti-gate oxidative damage in intestinal epithelial cells through modulation of oxidative phosphoryla-tion,apoptosis,and lysosomal pathways.This discovery provides a theoretical basis for the clinical application of SSP in alleviating oxidative damage in the porcine intestinal tract.

Objective:To construct a nursing quality evaluation index system for knee ligament injury to provide a basis for standardizing the nursing practice and improving the nursing quality of knee ligament injury.Methods:Based on the three-dimensional quality structure model of "structure-process-outcome" proposed by Donabedian, the quality evaluation index system for knee ligament injury specialties was constructed through literature review, brainstorming, and Delphi expert consultation from April to June 2023.Results:Sixteen experts were included in the inquiry. The effective recovery rate of the two rounds of expert correspondence questionnaires was 16/16, the expert authority coefficient was 0.95, and the Kendell harmony coefficients of the expert correspondence were 0.116 and 0.122, respectively (both P<0.05). The final constructed knee ligament injury specialty care quality evaluation index system contained 3 primary indicators (structural quality, process quality and outcome quality), 16 secondary indicators, and 69 tertiary indicators.Conclusions:The specialized nursing quality evaluation index system for knee ligament injury constructed in this study is scientific and reliable, which can provide a basis for the evaluation and assessment of the nursing quality of knee ligament injury specialties and promote the continuous improvement of their nursing quality.

Kinesiophobia commonly exists among patients after anterior cruciate ligament reconstruction(ACLR),and severe kinesiophobia can affect the patients'rehabilitation outcomes and prognosis,which is not conducive to their physical and mental health.This paper reviews the overview,assessment tools,influencing factors,and interventions methods of kinesiophobia in patients after ACLR,analyzes the existing problems,and puts forward the outlook for future research.It aims to strengthen the attention of orthopedic nursing staff to the kinesiophobia in patients after ACLR,and provides references for further proposing a scientific and reasonable management plan.

Kinesiophobia commonly exists among patients after anterior cruciate ligament reconstruction(ACLR),and severe kinesiophobia can affect the patients'rehabilitation outcomes and prognosis,which is not conducive to their physical and mental health.This paper reviews the overview,assessment tools,influencing factors,and interventions methods of kinesiophobia in patients after ACLR,analyzes the existing problems,and puts forward the outlook for future research.It aims to strengthen the attention of orthopedic nursing staff to the kinesiophobia in patients after ACLR,and provides references for further proposing a scientific and reasonable management plan.

Objective:To explore the association between weight change from age 20 to middle age and diabetes risk.Methods:A total of 10 104 residents over 40 years old were recruited in Guangzhou. The final analysis data set is a cohort of 6 272 patients from the REACTION study. Quartile of weight changes from age 20 to middle-age was used as an independent variable to explore its association with newly diagnosed diabetes. Simple and multivariable logistic regression analysis were used to calculate OR and 95% CI. Results:The prevalence of newly diagnosed diabetes in study cohort was 15.7%. Weight changes from age 20 to middle-age was significantly higher in diabetes group( P<0.001). Logistic regression analysis found in general population and overweight people [24.0≤body mass index(BMI)<28.0 kg/m 2], after adjusting for gender, age, educational level, family history of diabetes, drinking, SBP, waist circumference, cholesterol, high-density lipoprotein-cholesterol(HDL-C), TG, ALT, AST, the risk of diabetes increased in line with the magnitude of weight change( P=0.081). While in group of lean, normal and obese adult, no significant association has been found. Conclusion:The risk of diabetes increased with weight change in general population and overweight people, indicating that weight change in adults after age of 20 was positively associated with diabetes. It is suggested the importance of weight management in the prevention of dialetes.

Background Arsenic is recognized as a kind of developmental toxicant, which can pass through the placenta barrier and induce health defects in offspring. However, the effects of environmental levels of arsenic exposure during gestation on the reproductive system of adult male offspring remain unclear. Objective To investigate the impact of environmental levels of arsenic exposure during gestation on testosterone synthesis and sperm quality in F1 adult male rats. Methods Forty sexually mature Wistar female rats were randomly divided into four groups according to body weight, namely control group, low-dose sodium arsenite (NaAsO₂) group, middle-dose NaAsO₂ group, and high-dose NaAsO₂ group. They were mated with sexually mature Wistar male rats in a ratio of 2:1, and the day with presence of a vaginal plug or spermatozoa in the vaginal smear was designated as gestational day 0 (GD0). Pregnant rats were provided drinking water containing 0, 1, 5,^, or 25 mg·L⁻¹ NaAsO₂ until delivery. At postnatal day 70, the F1 male rats were euthanized. Anogenital distance was measured, testis and epididymis were weighed, and associated organ coefficients were calculated. Epididymal sperm quality was evaluated. The histological changes of testis were observed. The levels of testosterone and estradiol in serum were determined with ELISA kit. The testicular mRNA relative expression levels of key steroidogenic enzymes were determined by quantitative real-time PCR. The protein relative expression levels of key steroidogenic enzymes were determined by Western blotting. Results Compared with the control group, the testicular coefficients and epididymis coefficients were increased in the low- and middle-dose groups (P<0.05), and the epididymis coefficient was also increased in the high-dose group (P<0.05). As for the percentage of sperm motility, compared to the control group, grade Ⅰ sperm cells were increased in the low-dose group, but significantly decreased in the middle- and high-dose groups; grade Ⅱ and Ⅲ sperm cells were decreased in the low- and high-dose groups; grade Ⅳ sperm cells were significantly increased in the middle- and high-dose groups; all the differences above were statistically significant (P<0.05). Compared with the control group, there was a significant increase in serum testosterone levels in all treated groups (P<0.05), and the serum estradiol levels were significantly decreased in the high-dose group (P<0.05). Meanwhile, compared with the control group, the relative mRNA expression levels of Hsd3β1 and Cyp19a1 were decreased (P<0.05), while those of StAR and Cyp11a1 were increased in the high-dose group (P<0.05). In addition, the relative protein expression levels of CYP11A1 were significantly increased in all treated groups compared with the control group (P<0.05). Conclusion Environmental levels of arsenic exposure during gestation can up-regulate testosterone level and reduce sperm quality, and is a potential risk for reproductive dysfunction in adult male offspring.