AIM: To investigate the correlation between different severity grades of obstructive sleep apnea-hypopnea syndrome(OSAHS)and visual field defects as well asvisual evoked potential(VEP)parameters in patients with anterior ischemic optic neuropathy(AION). METHODS: A retrospective case-control study. Patients diagnosed with AION complicated by OSAHS at the Department of Ophthalmology, the Affiliated Xuzhou Municipal Hospital of Xuzhou Medical University, between June 2022 and October 2025 were selected as the study subjects. According to the AHI and mSaO2, the patients were divided into three groups: a mild group(AHI 5-15 events/h, mSaO2 85%-90%), moderate group(AHI 16-30 events/h, mSaO2 80%-85%), and severe group(AHI >30 events/h, mSaO2 <80%). General demographic data, retinal nerve fiber layer(RNFL)thickness, visual field defect indicators including mean defect(MD)and pattern standard deviation(PSD), as well as VEP parameters(P100 latency and amplitude)were compared among the three groups. RESULTS: This study included a total of 110 patients with AION complicated by OSAHS. Based on the severity of OSAHS, the patients were divided into a mild group of 37 patients(21 men and 16 women, mean age 62.15±9.37 y), a moderate group of 35 patients(20 men, 15 women; mean age 61.82±8.94 y), and a severe group of 38 patients(22 men, 16 women; mean age 63.02±9.61 y). There were no significant differences among the three groups in terms of age, sex, TG, TC, LDL-C, HDL-C levels, or AION severity(all P>0.05); however, there were significant differences in history of hypertension, history of diabetes, systolic blood pressure, diastolic blood pressure, and FPG levels(all P<0.05). The mean RNFL thickness in the severe group(63.27±5.58 μm)was significantly lower than that in the moderate group(74.14±6.28 μm)and the mild group(83.22±7.02 μm), and the moderate group was lower than the mild group(all P<0.05); The MD value(-11.57±1.82 dB)and PSD value(7.35±0.87 dB)in the severe group were both higher than those in the moderate group [(-7.62±1.31 dB),(4.89±0.62 dB)] and the mild group [(-4.38±1.05 dB),(2.57±0.45 dB)](all P<0.05); the P100 latency in the severe group(132.41±8.57 ms)was longer than that in the moderate group(118.75±7.32 ms)and the mild group(105.62±6.14 ms), and the amplitude(7.65±1.53 μV)was lower than that of the moderate group(11.24±1.89 μV)and the mild group(15.38±2.11 μV)(all P<0.05). Spearman's correlation analysis revealed that the severity of OSAHS was negatively correlated with the MD value(rs=-0.901, P<0.05)and positively correlated with the PSD value and P100 latency(rs=0.947, 0.807, P<0.05), and was negatively correlated with P100 amplitude(rs=-0.878, P<0.05). CONCLUSION:The severity of OSAHS is closely associated with RNFL thickness, visual field defects, and VEP parameters in patients with AION; the more severe the OSAHS, the more pronounced the structural and functional damage to the optic nerve. Monitoring AHI and mSaO2 can aid in assessing the condition of patients with AION and developing personalized intervention plans.

ObjectiveThis study aims to investigate the dynamic changes in general body parameters, blood glucose, and blood lipid profiles in obese cynomolgus monkeys, exploring the correlations among these parameters and providing a reference for research on the obese cynomolgus monkey model. Methods30 normal male cynomolgus monkeys aged 5 - 17 years old (with body mass index < 35 kg/m² and glycated hemoglobin content < 4.50%) and 99 spontaneously obese male cynomolgus monkeys (with body mass index ≥35 kg/m² and glycated hemoglobin content < 4.50%) were selected. Over a period of three years, their abdominal circumference, skinfold thickness, body weight, body mass index, fasting blood glucose, glycated hemoglobin, and four blood lipid indicators were monitored. The correlations between each indicator were analyzed using repeated measurement ANOVA, simple linear regression, and multiple linear regression correlation analysis method. Results Compared to the control group, the obese group exhibited significantly higher levels of abdominal circumference, skinfold thickness, body weight, body mass index, and triglyceride (P＜0.05). In the control group, skinfold thickness increased annually, while other indicators remained stable. Compared with the first year, the obese group showed significantly increased abdominal circumference, skinfold thickness, body weight, body mass index, triglyceride, and fasting blood glucose in the second year(P＜0.05), with this increasing trend persisting in the third year (P＜0.05). In the control group, the obesity incidence rates in the second and third years were 16.67% and 23.33%, respectively, while the prevalence of diabetes remained at 16.67%. In the obese group, the diabetes incidence rates were 29.29% and 44.44% in years 2 and 3, respectively. Among the 11-13 year age group, the incidence rates were 36.36% and 44.68%, while for the group older than 13 years, the rates were 28.13% and 51.35%. Correlation analysis revealed significant associations (P＜0.05) between fasting blood glucose and age, abdominal circumference, skinfold thickness, body weight, and triglyceride in the diabetic monkeys. Conclusion Long-term obesity can lead to the increases in general physical indicators and fasting blood glucose levels in cynomolgus monkeys, and an increase in the incidence of diabetes. In diabetic cynomolgus monkeys caused by obesity, there is a high correlation between their fasting blood glucose and age, weight, abdominal circumference, skinfold thickness, and triglyceride levels, which is of some significance for predicting the occurrence of spontaneous diabetes.

The mitochondrial unfolded protein response(UPRmt)represents a crucial intracellular stress response mechanism that plays a fundamental role in maintaining mitochondrial and cellular homeostasis. Growing evidence suggests that dysregulation of UPRmt contributes significantly to the pathogenesis of various systemic disorders, including neurodegenerative diseases such as Parkinson's and Alzheimer's diseases, as well as age-related pathologies. Emerging research has particularly highlighted the involvement of UPRmt in ocular diseases, including cataracts, glaucoma, and diabetic retinopathy. This comprehensive review examines the physiological functions of UPRmt and its regulatory mechanisms in age-related eye diseases. The roles of key UPRmt downstream effector molecules in ocular cell populations such as lens epithelial cells, retinal pigment epithelial cells, and retinal ganglion cells are systematically analyzed. Importantly, the dual regulatory nature of UPRmt in ocular pathophysiology is discussed, that is, its moderate activation promotes mitochondrial homeostasis, mitigates oxidative stress, and suppresses inflammatory responses, its chronic or excessive activation triggers apoptotic pathways, induces metabolic dysfunction, and ultimately accelerates disease progression. By elucidating these mechanisms, our review provides novel insights into ocular disease pathogenesis and proposes potential therapeutic strategies targeting UPRmt modulation for the prevention and treatment of age-related eye disorders.

Diabetic cataract, a prevalent ocular complication of diabetes mellitus, arises from a complex interplay of pathological mechanisms, with oxidative stress and glycation stress playing central roles. Autophagy, a critical cellular self-protection mechanism, sustains intracellular homeostasis by selectively degrading damaged organelles and misfolded proteins, thereby counteracting the detrimental effects of oxidative and glycation stress under hyperglycemic conditions. Emerging evidence indicates a synergistic interaction between glycation stress and oxidative stress, which may exacerbate autophagic dysfunction and accelerate the onset and progression of diabetic cataract. However, the precise molecular mechanisms underlying this relationship remain incompletely understood. This review systematically examines the regulatory role of autophagy inthe pathogenesis of diabetic cataract, with a particular focus on how autophagic impairment influences disease progression under the combined effects of glycation and oxidative stress. By elucidating these mechanisms, the paper aims to provide novel insights into molecular diagnostic approaches and targeted therapeutic strategies for diabetic cataract.

Objective:To investigate whether deltoid ligament (DL) injury produces axial-plane rotational instability of the ankle in patients with chronic ankle instability (CAI).Methods:A retrospective study was conducted to analyze the 33 patients with CAI who had been treated at Department of Orthopaedics, The First Affiliated Hospital of Nanjing Medical University between January 2023 and December 2024. The cohort consisted of 17 males and 16 females with an age of (31.5±9.9) years. The patients were assigned into 2 groups based on the presence of DL injury: a lateral chronic ankle instability (LCAI) group ( n=17) and a rotational ankle instability (RAI) group ( n=16). Barefoot natural walking trials were performed in all patients. Three-dimensional kinematic data were synchronously collected using an optical motion capture system (12 cameras) and force plates. A lower extremity model was constructed to obtain shank axial rotation (internal/external rotation) and rear-foot inversion/eversion angles. Continuous relative phase (CRP) analysis was employed to assess shank-rearfoot movement coupling. The mean absolute relative phase (MARP) and deviation phase (DP) were calculated. Results:There was no statistically significant difference in the clinical baseline data between the 2 groups, indicating comparability ( P>0.05). Throughout the gait cycle, no significant differences were found in shank rotation angles or rear-foot eversion angles between the RAI group and the LCAI group. However, CRP analysis revealed that during the early stance phase (initial contact and loading response), shank-rearfoot coupling was significantly lower in the RAI group than in the LCAI group. In the early stance phase, the CRP values in the RAI group were significantly higher than those in the LCAI group. The CRP curve changes in the RAI group were consistently higher in the standce phase of the entire gait cycle than those in the LCAI group, and the peak value of the CRP curve was larger in the RAI group. Concurrently, the RAI group exhibited significantly higher MARP and DP values than the LCAI group (27.48°±14.54° versus 15.21°±9.56°; 26.02°±11.73° versus 17.83°±9.82°) (both P<0.05). Conclusion:DL injury significantly damages the axial rotational stability of the ankle joint and significantly exacerbates the mechanical instability of the ankle joint in CAI patients.

Glaucoma,characterized by optic nerve damage and progressive damage to retinal ganglion cells(RGCs),is the leading cause of irreversible blindness.However,the specific mechanism of RGC damage has not been fully elucida-ted.In recent years,there is increasing evidence that microglia,especially disease-associated microglia(DAM),may play an important role in glaucomatous ganglion cell injury.In this paper,we reviewed the role and mechanism of DAM in RGC damage in glaucoma,aiming to provide new insights for further research on the mechanism of RGC damage and subsequent protection of RGCs.

Objective To investigate the impact of high mobility group box 1(HMGB1)on hydrogen peroxide(H2O2)-induced DNA damage and senescence in lens epithelial cells(LECs)under oxidative stress conditions.Methods Fluorescent quantitative real-time polymerase chain reaction(RT-PCR)technology was used to detect the mRNA expres-sion of HMGB1 in the anterior capsule tissue of patients with age-related cataract(ARC group)and epiretinal membrane(control group).Western blot analysis was employed to examine the changes in the protein expression of HMGB1 in the LEC line SRA01/04 after treatment with varying concentrations of H2O2(0,100,200,and 400 μmol·L-1).The optimal concentration was selected for subsequent establishment of a cellular oxidative damage model.The cultured SRA01/04 cells were divided into three groups:Control(untreated),HA(transfected with the control plasmid HA),and OE-HMGB1 groups(transfected with the HMGB1 plasmid).The mRNA and protein expression levels of HMGB1 were detected by RT-PCR and Western blot.The cultured SRA01/04 cells were divided into three groups:H2O2(treated with 400 μmol·L-1 H2O2),H2O2+HA(transfected with the control plasmid HA and simultaneously treated with 400 μmol·L-1 H2O2),and H2O2+OE-HMGB1 groups(transfected with the HMGB1 plasmid and simultaneously treated with 400 μmol·L-1 H2O2).Immunofluorescence was used to detect DNA oxidative damage in cells from each group.Western blot analysis was per-formed to assess the protein expression levels of phosphorylated histone H2A(γH2A),tumor protein p53(P53),cyclin-dependent kinase inhibitor 1A(P21),and cyclin-dependent kinase inhibitor 2A(P16)in cells from each group.Additional-ly,senescence-associated-β-galactosidase(SA-β-gal)staining was conducted to detect senescent changes in cells from each group.Results RT-PCR results indicated that the relative mRNA expression level of HMGB1 in the anterior capsule tissue of the ARC group was significantly decreased,compared with that in the control group(P＜0.001).Furthermore,in the H2O2-induced oxidative damage model,the relative protein expression level of HMGB1 decreased with the increase of the concentration of H2O2.Both RT-PCR and Western blot analyses revealed that the mRNA and protein expression levels of HMGB1 were both significantly elevated in the OE-HMGB1 group,compared with those in the HA group(both P＜0.001).The immunofluorescence staining results demonstrated that the protein expression of γH2A and the fluorescence intensity in the H2O2+OE-HMGB1 group were significantly decreases,compared with those in H2O2 and H2O2+HA groups(all P＜0.001).SA-β-gal staining results showed that the H2O2+OE-HMGB1 group had significantly less cells stained by SA-β-gal than H2O2 and H2O2+HA(both P＜0.001).Additionally,Western blot analysis revealed that,compared with those in H2O2 and H2O2+HA groups,the relative expression levels of senescence-associated proteins P53,P21,and P16 were significantly decreased in the H2O2+OE-HMGB1 group(all P＜0.01).Conclusion HMGB1 inhibits the accumula-tion of damaging DNA and senescence in LECs by enhancing DNA damage repair capabilities.

Objective To investigate the effects of DNA Cross-Link Repair 1A(DCLRE1A)on mitochondrial func-tion in lens epithelial cells(LECs).Methods Thirty eyes from 30 patients with age-related cataracts(ARC)were select-ed and divided into three groups:cortical type(ARCC group),nuclear type(ARNC group),and posterior subcapsular type(ARPC group),with 10 cases in each group.Additionally,10 eyes from 10 age-matched patients diagnosed with epiretinal membrane and having clear lenses were selected as the control group.Western blot was used to detect the ex-pression levels of DCLRE1A protein in the anterior capsule tissues of patients in each group and in the lens epithelial cell line(SRA01/04)treated with hydrogen peroxide(H2O2)in vitro and overexpressed DCLRE1A model(OE-DCLRE1A group).The effects of overexpressed DCLRE1A on the expression levels of mitochondrial transcription factor(TFAM)and peroxisome proliferator-activated receptor-γ coactivator-1α(PGC1α)proteins were also detected.Normal cultured SRA01/04 cells were randomly divided into Control group(untreated),H2 O2 group,H2 O2+HA group(transfected with control plasmid HA),and H2O2+OE-DCLRE1A group(transfected with DCLRE1A plasmid).RT-PCR was used to measure mtD-NA expression in each group cells.Changes in mitochondrial membrane potential(MMP)and mitochondrial reactive oxy-gen species(ROS)in each group were detected by immunofluorescence staining.Results Western blot analysis showed that compared with the control group cells,the relative expression levels of DCLRE1A protein in the anterior capsule tis-sues of patients in the ARCC,ARNC,and ARPC groups were all decreased,with statistically significant differences(all P＜0.001).In the in vitro H2O2-induced oxidative damage model,compared with the Control group,the relative expression level of DCLRE1A protein in the H2O2 group was significantly decreased(P＜0.001).The overexpression efficiency results of DCLRE1A showed that,compared with the Control group,the relative expression level of DCLRE1A protein in the OE-DCLRE1A group cells was significantly increased,with statistical significance(P＜0.001).RT-PCR results showed that compared with the H2O2+HA group,the expression level of mtDNA in the H2O2+OE-DCLRE1A group was significantly in-creased(P＜0.001).Western blot analysis showed that compared with the H2O2+HA group,the relative expression levels of TFAM and PGC1α proteins in the H2O2+OE-DCLRE1A group were significantly increased(P＜0.001).Immunofluores-cence staining results showed that compared with the H2O2+HA group,the MMP level in the H2O2+OE-DCLRE1A group was significantly restored,and the accumulation of mitochondrial ROS was reduced(P＜0.001).Conclusion Under H2O2-induced oxidative stress conditions,DCLRE1A promotes the repair of damaged mtDNA in LECs by regulating mito-chondrial biogenesis,thereby reducing LEC apoptosis and participating in the occurrence and development of ARC.

Objective:To introduce the research and innovations around the application of aquatic rehabilitation techniques in the treatment of lumbago, and to summarize specific methods and applications in aeromedicine. Literature resource and selection Literature on the prevention and treatment of lumbago using aquatic rehabilitation techniques as well as on the rehabilitation of lumbago in pilots was retrieved and selected. Literature quotation Sixty-one references were cited. Literature synthesis Aquatic rehabilitation techniques can be classified into shower therapy, immersion therapy, and aquatic exercise therapy according to treatment regimens. Among them, immersion therapy and aquatic exercise therapy are commonly used in the treatment of lumbago. Aquatic rehabilitation techniques can effectively alleviate patients′ lumbago, improve their functional disorders, and enhance their quality of life. Prior to aquatic therapy, patients with lumbago need to have their motor function assessed to tailor the treatment protocol based on diagnostic findings and specific therapeutic objectives. Aquatic rehabilitation techniques, when used to prevent and treat lumbago in pilots under convalescence, are not only more effective than land-based training, but also more accessible to pilots due to their comfort and compliance. Many of our military rehabilitation and convalescent centers in China have integrated modern aquatic rehabilitation techniques into rehabilitation treatment by drawing on their rich water resources so as to improve the physical and mental health, social adaptability and military adaptability of pilots. Conclusions:When used for the prevention and treatment of lumbago, aquatic rehabilitation techniques are highly effective, safe and enjoyable, so they should be made more accessible to pilots during convalescence.

The glymphatic system is an important pathway for fluid drainage and metabolic waste clearance in the central nervous system. Its core mechanism involves the active cerebrospinal fluid-interstitial fluid circulation process mediated by perivascular spaces and aquaporin-4 channels located on astrocytic endfeet. This process is crucial for eliminating neurotoxic substances such as β-amyloid and tau proteins, as well as maintaining homeostasis in the central nervous system. Recent studies have shown that dynamic changes in the glymphatic system are associated with recovery after ischemic stroke. This article elaborates on the role of the glymphatic system in ischemic stroke and evaluates its potential value as a novel therapeutic target, providing new insights for post-stroke treatment strategies.