Objective To investigate the status quo of limited social participation in young patients with ankylosing spondylitis (AS), and analyze its influencing factors. Methods Using the random number table method, a simple random sampling method was employed to select 320 young patients with ankylosing spondylitis who were admitted to the First Affiliated Hospital of Naval Medical University from June 2023 to June 2025. Chinese version of social participation scale was applied to evaluate the level of social participation of patients. The above patients were classified into unlimited group (n=148) and limited group (n=172). Logistic regression analysis was performed to analyze the independent influencing factors for limited social participation. Results Compared with the unlimited group, the limited group exhibited longer course of AS, higher BASDAI score, BASFI score, HAMA score, HAMD score and ASQoL score as well as lower PSSS score (P<0.05). Logistic regression analysis suggested that course of disease, high disease activity score, high anxiety score, high depression scores and low social support scores are the relevant factors for the restricted social participation of young patients with ankylosing spondylitis. Conclusion The phenomenon of limited social participation is common in young patients with AS, and its occurrence is the result of a combination of factors such as disease course, disease activity, anxiety, depression and social support level.

Objective To explore the evaluation value of serum follistatin like protein 1(FSTL1)and glu-cose regulatory protein 78(GRP78)on disease severity and readmission in elderly patients with chronic ob-structive pulmonary disease(COPD).Methods A total of 100 elderly COPD patients(COPD group)treated in this hospital from March 2020 to May 2023 were selected as COPD group,and were divided into grade Ⅰ(35 cases),grade Ⅱ(46 cases)and grade Ⅲ(19 cases)according to the severity of the disease.Another 100 elderly volunteers who underwent physical examination during the same period were selected as the control group.Serum FSTL1 and GRP78 levels were detected by enzyme-linked immunosorbent assay(ELISA).Spearman and Pearson correlation were used to analyze the correlation between serum FSTL1 and GRP78 lev-els and general data.The evaluation value of serum FSTL1 and GRP78 levels in COPD patients on disease se-verity and readmission was analyzed by receiver operating characteristics(ROC)curve.Results Compared with the control group,serum levels of FSTL1 and GRP78 in COPD group were significantly increased(P＜0.05).Serum levels of FSTL1 and GRP78 in COPD patients increased with the severity of the disease(P＜0.05).Compared with non-readmission group,the serum levels of FSTL1 and GRP78 in readmission group were significantly increased(P＜0.05).Spearman correlation analysis showed that serum FSTL1 and GRP78 levels were positively correlated with smoking history,hypertension history and disease severity(P＜0.05).Pearson correlation analysis showed that serum FSTL1 and GRP78 levels were negatively correlated with arte-rial oxygen pressure(PaO2),the ratio of forced expiratory volume in the first second to forced vital capacity(FEV1/FVC),and the percentage of forced expiratory volume in the first second to expected value(FEV1％pred),with significance(P＜0.05),while it was positively correlated with the partial pressure of carbon diox-ide(PaCO2),with significance(P＜0.05).ROC curve analysis showed that serum FSTL1,GRP78 and their combined assessment of disease severity and readmitted area under the curve(AUC)were higher in COPD pa-tients,and the combination was significantly better than the single assessment(P＜0.05).Conclusion Serum levels of FSTL1 and GRP78 are significantly increased in COPD patients,which are correlated with the severi-ty of the disease and have a high value in evaluating the severity of the disease and readmission.

Objective:To evaluate the relationship between superoxide dismutase 2 (SOD2) lactylation and nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy-ferroptosis during cerebral ischemia-reperfusion (IR) in mice.Methods:Thirty-six clean-grade male C57BL/6 mice, aged 8-10 weeks, weighing 22-25 g, were divided into 4 groups ( n=9 each) using a table of random numbers: sham operation group (Sham group), cerebral IR group (IR group), IR+ glycolysis inhibitor 2-DG group (IR+ 2-DG group), and IR+ 2-DG+ NCOA4 overexpression group (IR+ 2-DG+ LvNCOA4 group). The model of cerebral IR injury was established by occlusion of the middle cerebral artery for 1 h followed by 24 h of reperfusion using the intraluminal suture method in anesthetized animals. 2-DG 250 mg/kg was intraperitoneally injected at 90 min before ischemia in IR+ 2-DG and IR+ 2-DG+ LvNCOA4 groups. The lentivirus overexpressing NCOA4 2 μl was injected into the ventricles at 7 days before ischemia in IR+ 2-DG+ LvNCOA4 group. The percentage of cerebral infarct volume was determined, the viable neurons were counted, and the levels of reactive oxygen species (ROS), malondialdehyde (MDA), and glutathione (GSH) were measured by enzyme-linked immunosorbent assay. The expression of SOD2, lysine 114 lactylation of superoxide dismutase 2 (SOD2-K114la), NCOA4, microtubule-associated protein 1 light chain 3β (LC3B), and acyl-CoA synthetase long-chain family member 4 (ACSL4) was determined by Western blot. Mitochondrial morphology was examined by electron microscopy. Results:Compared with Sham group, the percentage of cerebral infarct volume was significantly increased, the number of viable neurons was decreased, the levels of ROS and MDA were elevated, the content of GSH was reduced, the expression of SOD2-K114la, NCOA4, LC3B and ACSL4 was up-regulated, the expression of SOD2 was down-regulated ( P<0.05), and the mitochondrial injury was aggravated in IR group. Compared with IR group, the percentage of cerebral infarct volume was significantly decreased, the number of viable neurons was increased, the mitochondrial injury was alleviated, the levels of ROS and MDA were decreased, the content of GSH was increased, the expression of SOD2-K114la, NCOA4 and ACSL4 was down-regulated, and the expression of SOD2 and LC3B was up-regulated in IR+ 2-DG group ( P<0.05). Compared with IR+ 2-DG group, the percentage of cerebral infarct volume was significantly increased, the number of viable neurons was decreased, the levels of ROS and MDA were elevated, the content of GSH was reduced, and the expression of NCOA4, LC3B and ACSL4 was up-regulated ( P<0.05), no significant change was found in the expression of SOD2 and SOD2-K114la ( P>0.05), and the mitochondrial injury was aggravated in IR+ 2-DG+ LvNCOA4 group. Conclusions:SOD2 lactylation promotes NCOA4-mediated ferritinophagy-ferroptosis by enhancing oxidative stress, thereby contributing to the cerebral IR injury in mice.

By integrating existing research,this paper systematically analyzes the impact of exercise training in low-temperature environments on immune regulation and infection defense,in order to explore its potential benefits and risks.Strictly following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses:2020(PRISMA 2020)guidelines,multiple databases were systematically reviewed,to include original studies on the impact of exercise training in low-temperature environments on immune regulation and infection defense,and to evaluate the quality of the studies.The 25 included literature indicated that moderate-intensity exercise training in low-temperature environments could cause an increase in white blood cell count,neutrophils and natural killer cells,changes in both pro-inflammatory and anti-inflammatory factors,and predominant upregulation of most mucosal immunity level,as well as accelerated infection recovery in several studies.High-intensity exercise training in low-temperature environments has shown an immunosuppressive trend in individual studies,and physiological indicators such as body temperature,heart rate and metabolism have also been affected to varying degrees.This suggests that moderate-intensity exercise training in a low-temperature environment is conducive to enhancing immunity and preventing infection,which is of great significance for health management and occupational protection in cold climates.Reasonable control of exercise intensity and duration in a low-temperature environment is crucial for preventing immunosuppression.

Objective:To analyze the effects of fluorine exposure on calcium ion metabolism and the expression of related calcium-regulating proteins in the kidneys of rats.Methods:Forty-five 5-week-old specific pathogen-free male Wistar rats (weighed 90 - 120 g) were selected and divided into three groups according to the randomized numeric table: 0 (control), 50, and 100 mg/L fluorine exposure groups, with 15 rats in each group. The control group was given deionized water, while the 50 and 100 mg/L fluorine exposure groups were given sodium fluoride solutions containing 50 and 100 mg/L fluorine ions, respectively. After 12 weeks, urine samples were collected, and kidneys and blood were harvested. Urinary fluorine levels were measured using a fluoride ion-selective electrode method. Calcium ion levels in the urine, kidneys, and serum were determinated using the methylthymol blue microplate method. The protein expression levels of transient receptor potential vanilloid receptor 5 (TRPV5), calbindin-D28K (CB-D28K), sodium-calcium exchanger-1 (NCX1), Klotho and plasma membrane calcium ATPase 1b (PMCA1b) in the kidneys were detected by Western blotting and immunohistochemistry.Results:The urinary fluorine levels in the control group and the 50 and 100 mg/L fluorine exposure groups were (0.48 ± 0.09), (20.01 ± 1.68), (37.45 ± 2.45) mg/L, respectively, with statistically significant differences between the groups ( F = 929.58, P < 0.001). Significant differences in calcium ion levels in urine, kidneys, and serum were observed among the three groups ( F = 14.66, 11.09, 10.31, P < 0.05). Compared with the control group, the 100 mg/L fluorine exposure group exhibited higher levels of calcium ion in the urine and kidneys, and lower serum calcium ion levels ( P < 0.05). The results of Western blotting analysis revealed that the protein expression levels of TRPV5 and CB-D28K in the kidneys increased with the increase of fluorine exposure level ( Z = 2.11, 2.11, P = 0.035). The protein expression level of NCX1 in the kidneys showed a decreasing trend with increasing fluorine exposure level ( Z = - 2.11, P = 0.035). Significant differences were also observed in the protein expression levels of Klotho and PMCA1b among the three groups ( F = 8.93, 7.08, P < 0.05). Compared with the control group, the 100 mg/L fluorine exposure group showed higher level of Klotho protein expression and lower level of PMCA1b protein expression in the kidneys ( P < 0.05). Immunohistochemical results indicated significant differences in the protein expression levels of TRPV5, CB-D28K, NCX1, and Klotho in the kidneys of the three groups ( F = 27.56, 24.94, 16.05, 32.72, P < 0.05). Compared with the control group, the protein expression levels of TRPV5, CB-D28K, and Klotho in kidneys of 50 and 100 mg/L fluorine exposure groups were higher, while the protein expression levels of NCX1 were lower ( P < 0.05). Conclusion:Fluorine exposure may cause calcium ion metabolism disorders by regulating the expression levels of Klotho and other calcium-regulating proteins in the kidneys.

Objective To elucidate how the overexpression of cystathionine-β-synthase(CBS)plays an antihypertensive role by affecting peroxisome proliferator-activated receptor γ coactivator-1α(PGC-1α)expression.Methods The adeno-associated viruses(AAVs),ones that overexpressed CBS,and another knocked down PGC-1α,were injected into the hypothalamic paraventricular nucleus(PVN)of spontaneously hypertensive rats(SHRs).The rats'blood pressure was monitored,and the level of norepinephrine(NE)was examined by ELISA;PVN inflammatory response,oxidative stress and tyrosine hydroxylase(TH)expression were detected with RT-qPCR and immunofluorescence.Results PVN overexpression of CBS could increase the transcription level of CBS(by 3.8 times,P＜0.05)and PGC-1α(by 1.6 times,P＜0.05)in PVN of SHR.PVN overexpression of CBS could reduce blood pressure in SHR(from 177.81 mmHg to 128.77 mmHg,P＜0.001),but PVN knockdown of PGC-1αweakened such effect(from 128.77 mmHg to 152.79 mmHg,P＜0.05).PVN overexpression of CBS could alleviate PVN inflammatory response and oxidative stress,but this effect was weakened or even eliminated when knocking down PGC-1α was performed at the same time.Conclusion PVN overexpression of CBS can reduce blood pressure in SHR,and this effect may be achieved by increasing the transcriptional level of PGC-1α,alleviating PVN inflammatory response,oxidative stress,and improving sympathetic nerve excitation.

The prefrontal cortex (PFC) plays a pivotal role in orchestrating higher-order emotional and cognitive processes, a function that depends on the precise modulation of synaptic activity. Although pharmacological studies have demonstrated that dopamine signaling through dopamine D1 receptor (DRD1) in the PFC is essential for these functions, the cell-type-specific and molecular mechanisms underlying the neuromodulatory effects remain elusive. Using cell-type-specific knockout mice and patch-clamp recordings, we investigated the regulatory role of DRD1 on neurons and astrocytes in synaptic transmission and plasticity. Furthermore, we explored the mechanisms by which DRD1 on astrocytes regulate synaptic transmission and plasticity at the cellular level, as well as emotional and cognitive functions at the behavioral level, through two-photon imaging, microdialysis, high-performance liquid chromatography, transcriptome sequencing, and behavioral testing. We found that conditional knockout of the Drd1 in astrocytes (CKO^AST) increased glutamatergic synaptic transmission and long-term potentiation (LTP) in the medial prefrontal cortex (mPFC), whereas Drd1 deletion in pyramidal neurons did not affect synaptic transmission. The elevated level of d-serine in the mPFC of CKO^AST mice increased glutamatergic transmission and LTP through NMDA receptors. In addition, CKO^AST mice exhibited abnormal emotional and cognitive function. Notably, these behavioral changes in CKO^AST mice could be reversed through the administration of d-serine degrease to the mPFC. These results highlight the critical role of the astrocytic DRD1 in modulating mPFC synaptic transmission and plasticity, as well as higher brain functions through d-serine, and may shed light on the treatment of mental disorders.

Objective:To explore the correlation between skeletal muscle mass and strength with metabolic syndrome in children.Methods:This cross-sectional study was conducted involving 383 children aged 10 to 15 years who visited the Department of Child Health Care, Children′s Hospital of Nanjing Medical University from June 2021 to December 2022. Their height, weight, waist circumference, body composition, grip strength and blood pressure were measured. Relative skeletal muscle mass, muscle-to-fat ratio, and grip strength-to-body weight index were calculated. The levels of fasting blood glucose, lipids and insulin were tested. Homeostasis model assessment of insulin resistance (HOMA-IR) was calculated. Children were divided into the metabolic syndrome group and the non-metabolic syndrome group. Independent t test or Mann-Whitney U test etc. was used to compare the difference between groups. Spearman correlation analysis and binary Logistic regression were used to investigate the correlation between skeletal muscle mass and strength and metabolic syndrome. The area under the curve (AUC) of receiver operating characteristic (ROC) curve was used to compare the accuracy of the index of skeletal muscle in predicting metabolic syndrome in children. Results:Among the 383 children, 282 (73.6%) were male, at the age of 11.4 (10.6, 12.5) years. There were 216 children (56.4%) diagnosed with obesity and 90 children (23.5%) diagnosed with metabolic syndrome. Relative skeletal muscle mass, muscle-to-fat ratio, and grip strength-to-body weight index of the metabolic syndrome group were all lower than those in the non-metabolic syndrome group (all P<0.001). After adjusting for sex and age, relative skeletal muscle mass, muscle-to-fat ratio, and grip strength-to-body weight index were all negatively correlated with body mass index ( r=-0.84, -0.38, -0.63), waist circumference ( r=-0.76, -0.36, -0.70), systolic blood pressure ( r=-0.42, -0.21, -0.38), diastolic blood pressure ( r=-0.33, -0.18, -0.24), triglycerides ( r=-0.29, -0.13, -0.23), fasting insulin ( r=-0.28, -0.20, -0.29), and HOMA-IR ( r=-0.26, -0.18, -0.26) (all P<0.05), and positively correlated with high-density lipoprotein cholesterol ( r=0.38, 0.13, 0.31, all P<0.01). After adjusting for sex and age, high relative skeletal muscle mass, high muscle-to-fat ratio, and high grip strength-to-body weight index all decreased the risks of metabolic syndrome ( OR=0.80, 0.55, 0.90), obesity ( OR=0.53, 0.64, 0.82), hypertension ( OR=0.86, 0.58, 0.92), low high-density lipoprotein cholesterol ( OR=0.83, 0.62, 0.92), hypertriglyceridemia ( OR=0.88, 0.78, 0.96). After adjusting for sex and age, high relative skeletal muscle mass and high grip strength-to-body weight index all decreased the risks of hyperglycemia ( OR=0.93 and 0.95, all P<0.05). ROC curve analysis showed that the relative skeletal muscle mass, muscle-to-fat ratio, and grip strength-to-body weight index all had good predictive accuracy of metabolic syndrome in children (AUC=0.79, 0.71, 0.76), with optimal cutoff values of 40%, 1.2, and 35%, respectively. Conclusions:High relative skeletal muscle mass, high muscle-to-fat ratio, and high grip strength-to-body weight index are all protective factors for metabolic syndrome in children. Regular measurement of skeletal muscle mass and grip strength can aid in the early identification and prevention of obesity and metabolic syndrome during childhood .

Objective:To evaluate the relationship between superoxide dismutase 2 (SOD2) lactylation and nuclear receptor coactivator 4 (NCOA4)-mediated ferritinophagy-ferroptosis during cerebral ischemia-reperfusion (IR) in mice.Methods:Thirty-six clean-grade male C57BL/6 mice, aged 8-10 weeks, weighing 22-25 g, were divided into 4 groups ( n=9 each) using a table of random numbers: sham operation group (Sham group), cerebral IR group (IR group), IR+ glycolysis inhibitor 2-DG group (IR+ 2-DG group), and IR+ 2-DG+ NCOA4 overexpression group (IR+ 2-DG+ LvNCOA4 group). The model of cerebral IR injury was established by occlusion of the middle cerebral artery for 1 h followed by 24 h of reperfusion using the intraluminal suture method in anesthetized animals. 2-DG 250 mg/kg was intraperitoneally injected at 90 min before ischemia in IR+ 2-DG and IR+ 2-DG+ LvNCOA4 groups. The lentivirus overexpressing NCOA4 2 μl was injected into the ventricles at 7 days before ischemia in IR+ 2-DG+ LvNCOA4 group. The percentage of cerebral infarct volume was determined, the viable neurons were counted, and the levels of reactive oxygen species (ROS), malondialdehyde (MDA), and glutathione (GSH) were measured by enzyme-linked immunosorbent assay. The expression of SOD2, lysine 114 lactylation of superoxide dismutase 2 (SOD2-K114la), NCOA4, microtubule-associated protein 1 light chain 3β (LC3B), and acyl-CoA synthetase long-chain family member 4 (ACSL4) was determined by Western blot. Mitochondrial morphology was examined by electron microscopy. Results:Compared with Sham group, the percentage of cerebral infarct volume was significantly increased, the number of viable neurons was decreased, the levels of ROS and MDA were elevated, the content of GSH was reduced, the expression of SOD2-K114la, NCOA4, LC3B and ACSL4 was up-regulated, the expression of SOD2 was down-regulated ( P<0.05), and the mitochondrial injury was aggravated in IR group. Compared with IR group, the percentage of cerebral infarct volume was significantly decreased, the number of viable neurons was increased, the mitochondrial injury was alleviated, the levels of ROS and MDA were decreased, the content of GSH was increased, the expression of SOD2-K114la, NCOA4 and ACSL4 was down-regulated, and the expression of SOD2 and LC3B was up-regulated in IR+ 2-DG group ( P<0.05). Compared with IR+ 2-DG group, the percentage of cerebral infarct volume was significantly increased, the number of viable neurons was decreased, the levels of ROS and MDA were elevated, the content of GSH was reduced, and the expression of NCOA4, LC3B and ACSL4 was up-regulated ( P<0.05), no significant change was found in the expression of SOD2 and SOD2-K114la ( P>0.05), and the mitochondrial injury was aggravated in IR+ 2-DG+ LvNCOA4 group. Conclusions:SOD2 lactylation promotes NCOA4-mediated ferritinophagy-ferroptosis by enhancing oxidative stress, thereby contributing to the cerebral IR injury in mice.

Objective:Using bacterial culture as the gold standard, to evaluate the agreement of rapid antigen detection test (RADT) and rapid nucleic acid test (RNAT) in diagnosing group A Streptococcus (GAS) pharyngitis in pediatric outpatients, and assess their potential clinical utility. Methods:This cross-sectional study prospectively collected throat swab specimens and clinical data of 338 children diagnosed with acute pharyngitis at the Department of Outpatient Beijing Children′s Hospital, Capital Medical University, between July 2023 and February 2024. The specimens were tested for GAS bacterial culture, RADT and RNAT. Using bacterial culture results as the reference standard, Kappa consistency analysis was performed to assess the diagnostic concordance between RADT and RNAT. Chi-square test was used to compare clinical characteristics between cases diagnosed by different methods.Results:In the 338 children diagnosed with pharyngitis, 195 were male and 143 were female, with an age at the visit of 7.4 (5.9, 7.4) years. The positivive rates for GAS detection were 25.7% (87/338) by bacterial culture, 20.7% (70/338) by RADT, and 41.7% (141/338) by RNAT. In terms of diagnostic performance, RADT exhibited a higher specificity (96.8% (243/251)) and better agreement with bacterial culture results ( κ=0.73), whereas RNAT showed greater sensitivity (95.4% (83/87)) but lower specificity (76.9% (193/251)) and moderate agreement ( κ=0.61). Among the 87 children with positive bacterial culture for GAS, 56 were male and 31 were female, with an age at visit of 7.3 (6.2, 8.8) years. Clinically, body temperature predominantly ranged from 38.1 to 39.0 ℃ in 48 cases (55.2%), and common accompanying symptoms included sore throat 62 cases (71.3%), cough 33 cases (37.9%), and cervical lymphadenopathy or tenderness 16 cases (18.4%). On physical examination, tonsillar enlargement was present in 73 cases (83.9%) and exudate in 37 cases (42.5%). The McIsaac score was most frequently 4 points, observed in 37 cases (42.5%). Laboratory tests showed a peripheral white blood cell (WBC) count of 14.5 (12.3, 18.7)×10?/L and C-reactive protein (CRP) concentration of 22.0 (10.1, 41.4) mg/L. There were no statistically significant differences in the proportion of fever, sore throat, cough, tender cervical lymphadenopathy, tonsillar exudates, or tonsillar enlargement, nor in WBC count or CRP, among children who tested positive by RADT, RNAT, or bacterial culture (all P>0.05). Conclusions:Compared with bacterial culture,the RADT demonstrates higher specificity, while the RNAT exhibits greater sensitivity. Both methods show good concordance with culture results and may serve as effective adjunctive tools for the early screening of GAS pharyngitis.