AIM:To investigate the effects of high-altitude hypoxic exposure on retinal injury and the associated changes in oxidative stress-related indicators in rats. METHODS: Twenty-four healthy male Sprague-Dawley(SD)rats were randomly divided into a plain group and a high-altitude group, with 12 rats(24 eyes)in each group. Rats in the plain group were housed under normoxic conditions in an SPF-grade animal facility, whereas rats in the high-altitude group were placed in a special environmental chamber simulating an altitude of 6 000 m for 7 d. Optical coherence tomography(OCT)was used to assess retinal layer architecture and quantify retinal thickness. Hematoxylin-eosin(HE)staining was performed to observe retinal histopathological changes. Immunofluorescence(IF)was used to detect the expression of hypoxia-inducible factor-1α(HIF-1α)in retinal tissue. Transmission electron microscopy(TEM)was applied to examine the ultrastructure of retinal ganglion cells(RGCs). Enzyme-linked immunosorbent assay(ELISA)was used to measure the levels of malondialdehyde(MDA), total superoxide dismutase(T-SOD), and reduced glutathione(GSH)in retinal tissue. In addition, intracellular reactive oxygen species(ROS)levels in retinal tissue were assessed using the 2',7'-dichlorodihydrofluorescein diacetate(DCFH-DA)fluorescent probe. RESULTS: OCT examination revealed disorganized retinal architecture in the high-altitude group, with increased inner and middle ring thickness and decreased outer ring thickness compared with the plain group(all P<0.05). HE staining showed varying degrees of retinal layer damage, blurred layer boundaries, loosely arranged RGCs, and partial cellular necrosis in the high-altitude group. IF analysis demonstrated significantly increased HIF-1α expression in the inner nuclear layer of the high-altitude group(P<0.01). TEM revealed mitochondrial swelling, disrupted cristae, and reduced matrix electron density in RGCs of the high-altitude group. ELISA and fluorescence probe assays showed significantly elevated MDA levels and ROS fluorescence intensity, accompanied by decreased T-SOD and GSH levels in the retinal tissue of the high-altitude group(all P<0.05). CONCLUSION: Exposure to a high-altitude hypoxic environment induces marked morphological and ultrastructural damage in the rat retina and significantly enhances oxidative stress, suggesting that oxidative stress may play a critical role in retinal injury induced by high-altitude hypoxia.

Objective: To investigate the status of condom use and its influencing factors among men who have sex with men (MSM), so as to provide a basis for improving condom utilization rates and AIDS prevention and control in this population. Methods: From May to October 2024, a snowball sampling method was employed to recruit MSM in Songjiang District, Shanghai Municipality. Self-administered questionnaires were used to collect data on demographic characteristics, AIDS-related knowledge, sexual behaviors, pre-exposure prophylaxis (PrEP) and post-exposure prophylaxis (PEP), and condom use in the past six months. Multivariable logistic regression model was used to analyze the influencing factors for consistent condom use. Results: A total of 921 MSM were surveyed, with a median age of 29.00 (interquartile range, 9.00) years. Among them, 697 (75.68%) were aware of AIDS-related knowledge, 826 (89.69%) expressed willingness to use PrEP, and 835 (90.66%) were willing to use PEP. Additionally, 787 (85.45%) MSM reported their age at first homosexual intercourse as ≥18 years, while 519 (56.35%) reported consistent condom use in the past six months. Multivariable logistic regression analysis revealed that MSM who were aware of AIDS-related knowledge (OR=0.582, 95% CI: 0.423-0.801), willing to use PrEP (OR =0.611, 95% CI: 0.385-0.969), and whose age at first homosexual intercourse was <18 years (OR=0.480, 95% CI: 0.330-0.700) were less likely to consistent use condoms. Conclusion The proportion of consistent condom use among the MSM remains relatively low, which is primarily associated with AIDS-related knowledge, willingness to use PrEP, and the age at first homosexual intercourse.

BACKGROUND:Previous studies have demonstrated that the cannabinoid type Ⅰ receptor can enhance the proliferation and neural differentiation of neural stem cells and mesenchymal stem cells.Moreover,cannabinoid type Ⅰ also governs the proliferation and mineralization capacity of human apical papilla stem cells.However,there are relatively few investigations concerning the impact of cannabinoid type Ⅰ overexpression on the neural differentiation of human apical papilla stem cells.OBJECTIVE:To investigate the effect of cannabinoid type Ⅰ on neural differentiation of human apical papilla stem cells in vitro.METHODS:Healthy third molars with immature root tips that need to be removed for orthodontic treatment were collected,and human apical papilla stem cells were isolated and cultured by tissue block method combined with enzyme digestion method.Cannabinoid type Ⅰ gene was introduced into human apical papilla stem cells by lentivirus-mediated transfection technique.A blank control group,a negative control group,and cannabinoid type Ⅰ overexpression group were set up.The transfection effect of overexpression of cannabinoid type Ⅰ lentivirus on human apical papilla stem cells was verified by Western Blot.The control group,negative control group,cannabinoid type Ⅰ overexpression group and cannabinoid type Ⅰ overexpression+AM251(cannabinoid type Ⅰ receptor antagonist)group were set up.Cell proliferation was detected by CCK-8 assay at 1,5,and 10 days after neural induction.On day 10 of neural induction,the expression levels of TH,NeuroD-1,and NCAM1 genes were detected by qRT-PCR,and the protein expression levels of Nestin and TUBB3 were detected by immunofluorescence.RESULTS AND CONCLUSION:(1)Compared with the blank control group and the negative control group,the expression of cannabinoid receptor Ⅰ protein in the cannabinoid receptor Ⅰ overexpression group was significantly increased,and the difference was significant(P＜0.05).(2)Compared with the blank control group and the negative control group,the proliferation ability of human apical papilla stem cells in the cannabinoid type Ⅰ overexpression group was the strongest at 5 and 10 days after neural induction(P＜0.05).(3)Compared with the blank control group and the negative control group,the mRNA expression of NeuroD-1,NCAM1,and TH in the stem cells of the human apical papilla in the cannabinoid type Ⅰ overexpression group was significantly increased,and the fluorescence intensity of Nestin and TUBB3 was significantly enhanced(P＜0.05).(4)Compared with the cannabinoid type Ⅰ overexpression group,the proliferation ability,mRNA expression level of NeuroD-1,NCAM1,and TH,as well as the fluorescence intensity of Nestin and TUBB3,were significantly decreased in the cannabinoid type Ⅰ overexpression+AM251 group(P＜0.05).These findings conclude that overexpression of cannabinoid type Ⅰ promoted the proliferation and neural differentiation of human apical dentin papilla stem cells.

BACKGROUND:Previous studies have demonstrated that the cannabinoid type Ⅰ receptor can enhance the proliferation and neural differentiation of neural stem cells and mesenchymal stem cells.Moreover,cannabinoid type Ⅰ also governs the proliferation and mineralization capacity of human apical papilla stem cells.However,there are relatively few investigations concerning the impact of cannabinoid type Ⅰ overexpression on the neural differentiation of human apical papilla stem cells.OBJECTIVE:To investigate the effect of cannabinoid type Ⅰ on neural differentiation of human apical papilla stem cells in vitro.METHODS:Healthy third molars with immature root tips that need to be removed for orthodontic treatment were collected,and human apical papilla stem cells were isolated and cultured by tissue block method combined with enzyme digestion method.Cannabinoid type Ⅰ gene was introduced into human apical papilla stem cells by lentivirus-mediated transfection technique.A blank control group,a negative control group,and cannabinoid type Ⅰ overexpression group were set up.The transfection effect of overexpression of cannabinoid type Ⅰ lentivirus on human apical papilla stem cells was verified by Western Blot.The control group,negative control group,cannabinoid type Ⅰ overexpression group and cannabinoid type Ⅰ overexpression+AM251(cannabinoid type Ⅰ receptor antagonist)group were set up.Cell proliferation was detected by CCK-8 assay at 1,5,and 10 days after neural induction.On day 10 of neural induction,the expression levels of TH,NeuroD-1,and NCAM1 genes were detected by qRT-PCR,and the protein expression levels of Nestin and TUBB3 were detected by immunofluorescence.RESULTS AND CONCLUSION:(1)Compared with the blank control group and the negative control group,the expression of cannabinoid receptor Ⅰ protein in the cannabinoid receptor Ⅰ overexpression group was significantly increased,and the difference was significant(P＜0.05).(2)Compared with the blank control group and the negative control group,the proliferation ability of human apical papilla stem cells in the cannabinoid type Ⅰ overexpression group was the strongest at 5 and 10 days after neural induction(P＜0.05).(3)Compared with the blank control group and the negative control group,the mRNA expression of NeuroD-1,NCAM1,and TH in the stem cells of the human apical papilla in the cannabinoid type Ⅰ overexpression group was significantly increased,and the fluorescence intensity of Nestin and TUBB3 was significantly enhanced(P＜0.05).(4)Compared with the cannabinoid type Ⅰ overexpression group,the proliferation ability,mRNA expression level of NeuroD-1,NCAM1,and TH,as well as the fluorescence intensity of Nestin and TUBB3,were significantly decreased in the cannabinoid type Ⅰ overexpression+AM251 group(P＜0.05).These findings conclude that overexpression of cannabinoid type Ⅰ promoted the proliferation and neural differentiation of human apical dentin papilla stem cells.

ObjectiveSpinal cord injury (SCI) directly impairs the regulatory function of the autonomic nervous system, induces intestinal dysfunction, and significantly reduces patients’ quality of life. Preclinical studies have shown that electroacupuncture (EA) therapy can regulate the brain-gut axis and is used to treat central nervous system diseases such as major depressive disorder, Alzheimer’s disease and Parkinson’s disease. Recent research has established that fecal microbiota transplantation (FMT) from EA-treated SCI rats restored intestinal motility and colonic morphology. However, it remains unclear whether the regulation of gut microbiota by EA therapy directly contributes to neural repair after SCI. This study aims to explore whether gut microbiota mediates the neuroprotective effect of EA in the treatment of SCI and its possible mechanism. MethodsThe study employed RNA transcriptome analysis of spinal cord tissue to characterize gene expression profiles and to identify key signaling pathways following EA treatment for SCI. Hematoxylin-Eosin (HE) staining and Nissl staining were used to observe the morphological changes in spinal cord tissue. Western blot (WB) and enzyme-linked immunosorbent assay (ELISA) were applied to detect the effects of EA on the expression of proteins related to nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3 (NLRP3) -dependent pyroptosis. Using 16S rDNA sequencing, the study observed alterations in gut microbiota diversity and community composition in SCI rats. Prior to establishing SCI models, rats were pretreated with an antibiotic cocktail to induce gut dysbiosis, and the effects on intestinal function and spinal cord neural repair were evaluated. FMT was performed to investigate the regulatory effects of post-EA FMT on motor function, general status, liver and spleen indices, and NLRP3-mediated pyroptosis in SCI rats. ResultsEA improved motor function and reduced regulated neuronal cell death in SCI rats. Transcriptomic analysis demonstrated the activation of immune- and inflammation-related pathways post-SCI, including NOD-like receptors, nuclear factor-kappa B(NF-κB), and Toll-like receptor (TLR) pathways. EA primarily influenced intestinal inflammation and autoimmune functions. 16S rDNA sequencing illustrated that EA did not alter the diversity of gut microbiota. However, EA altered the gut microbiota composition in SCI rats, increasing Lactobacillus and Akkermansia genera while rebalancing the Firmicutes/Bacteroidetes ratio. Furthermore, depletion of gut microbiota by antibiotics disrupted the intestinal barrier, reduced the expression of intestinal barrier proteins Zonula Occludens-1 (ZO-1) and Occludin, elevated serum lipopolysaccharide-binding protein (LBP) levels, exacerbated spinal cord tissue damage, and hindered motor function recovery in SCI rats. FMT from donors treated with EA reduced LBP levels in the intestine, blood, and spinal cord of rats, inhibited the TLR4 myeloid differentiation primary response protein 88 (MyD88)-NF‑κB pathway and NLRP3-dependent pyroptosis, and improved motor function. On the other hand, FMT treatment resulted in decreased body weight and food intake, whereas FMT using EA-treated donors effectively alleviated these alterations. ConclusionEA effectively alleviated neuroinflammatory responses in rats with SCI, primarily through regulating the gut microbiota and suppressing the NLRP3-dependent pyroptosis signaling pathway.

ObjectiveSpinal cord injury (SCI) directly impairs the regulatory function of the autonomic nervous system, induces intestinal dysfunction, and significantly reduces patients’ quality of life. Preclinical studies have shown that electroacupuncture (EA) therapy can regulate the brain-gut axis and is used to treat central nervous system diseases such as major depressive disorder, Alzheimer’s disease and Parkinson’s disease. Recent research has established that fecal microbiota transplantation (FMT) from EA-treated SCI rats restored intestinal motility and colonic morphology. However, it remains unclear whether the regulation of gut microbiota by EA therapy directly contributes to neural repair after SCI. This study aims to explore whether gut microbiota mediates the neuroprotective effect of EA in the treatment of SCI and its possible mechanism. MethodsThe study employed RNA transcriptome analysis of spinal cord tissue to characterize gene expression profiles and to identify key signaling pathways following EA treatment for SCI. Hematoxylin-Eosin (HE) staining and Nissl staining were used to observe the morphological changes in spinal cord tissue. Western blot (WB) and enzyme-linked immunosorbent assay (ELISA) were applied to detect the effects of EA on the expression of proteins related to nucleotide-binding domain leucine-rich repeat and pyrin domain-containing receptor 3 (NLRP3) -dependent pyroptosis. Using 16S rDNA sequencing, the study observed alterations in gut microbiota diversity and community composition in SCI rats. Prior to establishing SCI models, rats were pretreated with an antibiotic cocktail to induce gut dysbiosis, and the effects on intestinal function and spinal cord neural repair were evaluated. FMT was performed to investigate the regulatory effects of post-EA FMT on motor function, general status, liver and spleen indices, and NLRP3-mediated pyroptosis in SCI rats. ResultsEA improved motor function and reduced regulated neuronal cell death in SCI rats. Transcriptomic analysis demonstrated the activation of immune- and inflammation-related pathways post-SCI, including NOD-like receptors, nuclear factor-kappa B(NF-κB), and Toll-like receptor (TLR) pathways. EA primarily influenced intestinal inflammation and autoimmune functions. 16S rDNA sequencing illustrated that EA did not alter the diversity of gut microbiota. However, EA altered the gut microbiota composition in SCI rats, increasing Lactobacillus and Akkermansia genera while rebalancing the Firmicutes/Bacteroidetes ratio. Furthermore, depletion of gut microbiota by antibiotics disrupted the intestinal barrier, reduced the expression of intestinal barrier proteins Zonula Occludens-1 (ZO-1) and Occludin, elevated serum lipopolysaccharide-binding protein (LBP) levels, exacerbated spinal cord tissue damage, and hindered motor function recovery in SCI rats. FMT from donors treated with EA reduced LBP levels in the intestine, blood, and spinal cord of rats, inhibited the TLR4 myeloid differentiation primary response protein 88 (MyD88)-NF‑κB pathway and NLRP3-dependent pyroptosis, and improved motor function. On the other hand, FMT treatment resulted in decreased body weight and food intake, whereas FMT using EA-treated donors effectively alleviated these alterations. ConclusionEA effectively alleviated neuroinflammatory responses in rats with SCI, primarily through regulating the gut microbiota and suppressing the NLRP3-dependent pyroptosis signaling pathway.

Methods: Fifty patients who underwent UBE-TLIF and 50 patients who underwent W-TLIF, each with >2 years of follow-up, were retrospectively analyzed. Outcomes included operative parameters, time to postoperative mobilization, paravertebral muscle atrophy and fat infiltration rates, clinical scores (Visual Analog Scale [VAS], Oswestry Disability Index [ODI], Japanese Orthopaedic Association [JOA]), modified Macnab criteria, fusion rates, and complications. Results: Compared with W-TLIF, the UBE-TLIF group had significantly less intraoperative blood loss, shorter operative times, and lower postoperative drainage volumes (p <0.05). The UBE-TLIF group showed faster postoperative recovery and shorter hospital stays. At 6 months, 1 year, and 2 years, W-TLIF patients had higher multifidus and erector spinae atrophy, and greater paravertebral muscle fat infiltration (p <0.05). The UBE-TLIF group also had lower VAS and ODI scores at 1 year and 2 years (p <0.05) and fewer surgical complications (6% vs. 10%). Fusion rates (94% vs. 92%) and modified Macnab outcomes (88% vs. 86%) were comparable (p >0.05). Conclusions UBE-TLIF is associated with reduced intraoperative trauma, quicker recovery, and fewer complications. In the long-term, it better preserves paravertebral muscle integrity and provides superior pain and functional outcomes.

Background Occupational disease diagnosis appraisal is an appeal procedure initiated when a party disagrees with the occupational disease diagnosis conclusion. It is a legal procedure to safeguard the health rights of employees and the legitimate rights and interests of employers. Objective To analyze the data of occupational disease diagnosis appraisal in Shanghai, identify existing problems, and provide suggestions for improving. Methods Statistical analysis was conducted on basic situation, characteristics of workers and employers, disease classification, and consistency between diagnosis and appraisal conclusions of all occupational disease diagnosis appraisal cases from 2012 to 2024. All diagnosis conclusions were named in accordance with the Classified Catalogue of Occupational Diseases included employers were classified according to the Measures for the Statistical Classification of Large, Medium, Small and Micro Enterprises" and the Notice on Adjusting the Provisions for Classifying Enterprise Registration Types; industry classification followed the Industrial Classification for National Economic Activities (GB/T 4754-2017). Results From 2012 to 2024, a total of 260 cases of occupational diseases diagnosis appraisal were closed. The main diagnosis were 138 cases of ear, nose, throat, and oral diseases (53.1%), chemical poisoning (18.8%), and pneumoconiosis and other respiratory diseases (16.2%). The proportion of ear, nose, throat, and oral diseases gradually increased (2022 excluded). The incidence of annual municipal and provincial cases decreased by 76.3% and 85.0% respectively (2024 vs 2012). The consistency rate of conclusions between appraisal and diagnosis gradually increased. The total consistency rates between final appraisals and diagnostic conclusions were 81.5%, and 79.7%, 87.8%, 100.0%, 85.0% for ear, nose, throat, and oral diseases, chemical poisoning, and pneumoconiosis and other respiratory system diseases, respectively. Specifically, the consistency rates were 80.1% and 80.0% for noise-induced deafness and chronic benzene poisoning. In terms of inconsistency reasons, "inconsistent interpretation of standards and excessive discretion in standard application" accounted for 43.8%, followed by "failure to correctly apply standards" (31.3%) and and "discrepancies in occupational exposure history recognition" (15.6%). Conclusion The revisions and improvements of the legal system for occupational disease diagnosis appraisal have played a positive role in improving the consistency of conclusions between appraisal and diagnosis of occupational diseases in Shanghai. It is suggested to further strengthening the publicity and training of occupational disease diagnosis standards to improve the quality of occupational disease diagnosis.

Objective: To investigate the iodine nutrition status of children in water borne iodine excess areas in Hebei Province, so as to provide references for scientific prevention and control of water borne iodine excess hazards. Methods: From March to September each year during 2018 to 2023, a cross sectional survey was conducted in 39 water borne iodine excess counties (measured in 2017) from 5 cities (Cangzhou, Hengshui, Xingtai, Handan and Langfang) in Hebei Province. The survey included the detection of iodine content in residents drinking water, the measurement of thyroid volume in children aged 6-12, the detection of salt iodine and urinary iodine. The iodine nutrition status and water iodine distribution of 6-12 year-old children were evaluated from different perspectives such as years, gender, and age. Kruskal-Wallis H- test, Mann-Whitney U test and Chi square test were used for group comparison. Results: A total of 38 755 children were surveyed from 2018 to 2023, and 1 270 drinking water samples were tested across the province. The mass volume concentration of iodine in water showed a decreasing trend over the years ( Z= -30.87, P <0.01). Among 38 470 salt samples monitored from children s home, 24 790 were not non iodized salt, with a non iodized salt rate of 64.44%. A total of 31 989 urine samples were collected from children aged 8-10 years, with the median urine iodine was 245.94 μg/L. Comparing the results of urinary iodine in children from different years, the median urinary iodine from 2018 to 2023 were 328.0, 339.3, 267.8, 279.1, 291.3, 186.5 μg/L, respectively, with statistically significant differences ( H= 4 138.40 , P <0.01). Further pairwise comparisons showed that the median urinary iodine of children in 2023 was lower than in all other years ( Z =-51.59 to -11.41, all P <0.01). Among children aged 6-12 years, 1 150 cases of goiter were detected and the rate of goiter was 3.0%; and the goiter rates in boys and girls were 2.8% and 3.1%, with no significant difference between the sexes ( χ 2= 2.76, P >0.05). There were significant differences in the rate of goiter among different years and ages ( χ 2=324.02, 191.61, both P <0.05). Conclusions With the progress of water reform in water borne iodine excess areas of Hebei Province, children s iodine nutrition has reduced from excessive state to suitable state. It is necessary to continue to expand the coverage of water based iodine reduction projects, and strengthen the monitoring of iodine nutrition status of key populations in water borne iodine excess areas.

ObjectiveTo develop a nomogram-based risk prediction model for chronic obstructive pulmonary disease (COPD) incidence among the community-dwelling population aged 40 years old and above, so as to provide targeted references for the screening and prevention of COPD. MethodsBased on a natural population cohort in suburban Shanghai, a total of 3 381 randomly selected participants aged ≥40 years underwent pulmonary function tests between July and October 2021. Cox stepwise regression analysis was used to develop overall and gender-specific risk prediction models, along with the construction of corresponding risk nomograms. Model predictive performance was evaluated using the C-indice, area under the curve (AUC) values, and Brier score. Stability was assessed through 10-fold cross-validation and sensitivity analysis. ResultsA total of 3 019 participants were included, with a median follow-up duration of 4.6 years. The COPD incidence density was 17.22 per 1 000 person-years, significantly higher in males (32.04/1 000 person-years) than that in females (7.38/1 000 person-years) (P<0.001). The overall risk prediction model included the variables such as gender, age, education level, BMI, smoking, passive smoking, and respiratory comorbidities. The male-specific model incorporated the variables such as age, BMI, respiratory comorbidities, and smoking, while the female-specific model included age, marital status, respiratory comorbidities, and pulmonary tuberculosis history. The C-indices for the overall, male-specific, and female-specific models were 0.829, 0.749, and 0.807, respectively. The 5-year AUC values were 0.785, 0.658, and 0.811, with Brier scores of 0.103, 0.176, and 0.059, respectively. Both 10-fold cross-validated C-indices and sensitivity analysis (excluding participants with a follow-up duration of <6 months) yielded C-indices were above 0.740. ConclusionThis study developed concise and practical overall and gender-specific COPD risk prediction models and corresponding nomograms. The models demonstrated robust performance in predicting COPD incidence, providing a valuable reference for identifying high-risk populations and formulating targeted screening and personalized management strategies.