Objective: To explore the relationship of screen time and sleep duration with screening myopia among junior and senior high school students, so as to provide evidence for the prevention and control of myopia among students. Methods: From March to October 2024, 429 junior and senior high school students from a district of Guangzhou were selected using stratified cluster random sampling method. Standardized logarithmic visual acuity chart was used for vision assessment, while Questionnaire for the Physical Health Monitoring System of Students in Guangzhou was employed to collect students screen time and sleep duration. The Chi square test was used to compare differences across different groups, and binary Logistic regression analysis was employed to analyze the association of screen time and sleep duration with screening myopia. Results: The overall prevalence of screening myopia was 79.5%, with significant differences across educational stage, sex, screen time and sleep duration groups( χ 2=41.64, 9.75, 23.89 , 8.17, all P <0.05).Binary Logistic regression analysis revealed that, compared to the high screen time & insufficient sleep group, the low screen & sufficient sleep group ( OR=0.25, 95%CI =0.09-0.68), the low screen & insufficient sleep group ( OR= 0.27 , 95%CI =0.13-0.56), and the high screen & sufficient sleep group ( OR=0.26, 95%CI =0.10-0.70) exhibited significantly lower screening myopia risks (all P <0.05). After adjusting for sex and educational stage, low screen time & insufficient sleep was significantly associated with screening myopia ( OR=0.48, 95%CI =0.23-0.98); the multiplicative interaction term was statistically significant ( OR=0.99,95%CI =0.98-1.00)(both P <0.05). Conclusion The interaction effect between screen time and sleep duration in relation to screening myopia suggests a need to focus on daily routines and screen use habits among junior and senior high school students for ensuring sufficient sleep and limiting screen exposure.

Background Prolonged vibration exposure can lead to vascular endothelial cell dysfunction and cellular injury. However, research on the association between vibration and ferroptosis in vascular endothelial cells remains insufficient. Objective To explore whether occupational vibration exposure is associated with alterations in serum markers related to ferroptosis in patients with hand-arm vibration disease (HAVD), and to further investigate, through in vitro cell experiments, whether vibration exposure may induce ferroptosis in vascular endothelial cells. Methods ①A judgmental sampling method was employed to select 50 workers with HAVD (the HAVD group), 50 vibration-exposed workers without HAVD (the vibration exposure group), and 50 non–hand-transmitted vibration-exposed workers (the control group). Serum iron levels, malondialdehyde (MDA) content, and superoxide dismutase (SOD) levels were measured using serum iron assay kits, MDA detection kits, and SOD detection kits, respectively. One-way analysis of variance and binary logistic regression analysis were performed to examine the relationships between these indicators and HAVD. ②Human umbilical vein endothelial cells (HUVEC) were divided into a vibration group and a control group. The vibration group was subjected to vibration at 120 Hz with an acceleration of 6.5 m·s⁻² and further subdivided into four subgroups: 1 d 2 h, 1 d 4 h, 2 d 2 h, and 2 d 4 h. The control group was treated identically except for vibration exposure. Cellular iron (Fe²⁺) content and reduced glutathione (GSH) levels in HUVEC were measured using ferrous iron colorimetric assay kits and GSH colorimetric assay kits, respectively, to assess the effects of different vibration exposure schedules. Real-time quantitative polymerase chain reaction (RT-qPCR) was performed to detect the mRNA expression levels of ferroptosis-related genes, including acyl-CoA synthetase long-chain family member 4 (ACSL4), tumor suppressor protein P53 (P53), ferritin heavy chain 1 (FTH1), and glutathione peroxidase 4 (GPX4). Western blot analysis was conducted to determine the protein expression levels of ferroptosis-related markers in HUVEC. Results ①Compared with the control group, the patients in the HAVD group showed increased serum iron and MDA levels, along with decreased SOD levels (P<0.05). The logistic regression analysis indicated that elevated serum iron levels were significantly associated with an increased risk of HAVD (OR=4.034; 95%CI: 2.063, 7.887), and elevated MDA levels were also associated with an increased risk of HAVD (OR=1.523; 95%CI: 1.026, 1.936). ②Compared with the control group, increased intracellular Fe²⁺ content and decreased GSH content were observed in HUVECs in the 1 d 4 h and 2 d 4 h vibration subgroups (P<0.05). The RT-qPCR results showed that, compared with the control group, vibration exposures of 1 d 4 h and 2 d 4 h significantly upregulated the expression of ACSL4 and P53 (P<0.05), whereas the mRNA expression levels of GPX4 and FTH1 were downregulated in all vibration-exposed endothelial cells (P<0.05). The Western blot results revealed that, compared with the control group, the vibration exposure schedules of 1 d 2 h and 1 d 4 h significantly upregulated the protein expression levels of ACSL4 and P53 (P<0.05), while the vibration exposure schedules of 1 d 4 h, 2 d 2 h, and 2 d 4 h significantly downregulated the protein expression levels of FTH1 and GPX4 (P<0.05). Conclusion Occupational vibration exposure is associated with alterations in iron metabolism and oxidative stress status in workers with HAVD. The in vitro experiments further demonstrates that vibration stimulation induces intracellular iron accumulation and reduces antioxidant capacity in vascular endothelial cells, accompanied by dysregulated expression of ferroptosis-related molecules. These findings suggest that ferroptosis may play a role in vibration-induced vascular injury and the pathogenesis of HAVD.

ObjectiveTo investigate the mechanisms by which the combination of berberine （BBR） and baicalin （BAI） ameliorates type 2 diabetes mellitus （T2DM） due to internal accumulation of dampness-heat from the perspectives of gut microbiota and metabolomics. MethodsAntibiotics were used to induce pseudo-sterile mice. Thirty pseudo-sterile mice were randomized into a normal fecal microbiota transplantation group （n=10） and a T2DM （syndrome of internal accumulation of dampness-heat） fecal microbiota transplantation group （n=20）. The mice were then administrated with suspensions of fecal microbiota from healthy volunteers and a patient with T2DM due to internal accumulation of dampness-heat by gavage， respectively. Each mouse received 200 µL suspension every other day for a total of 15 times to reshape the gut microbiota. The T2DM model mice were then assigned into a model group （n=8） and a BBR-BAI group （n=11）. BBR was administrated at a dose of 200 mg·kg^-1， and BAI was administrated in a ratio of BBR-BAI 10∶1 based on preliminary research findings. The administration lasted for 8 consecutive weeks. Fasting blood glucose （FBG）， glycated hemoglobin （HbA1c）， insulin （INS）， triglycerides （TG）， total cholesterol （CHOL）， low-density lipoprotein cholesterol （LDL-C）， high-density lipoprotein cholesterol （HDL-C）， aspartate aminotransferase （AST）， and alanine aminotransferase （ALT） levels were measured to evaluate the effects of the BBR-BAI combination on glucose and lipid metabolism and liver function in T2DM mice. Hematoxylin-eosin staining was employed to observe pathological changes in the colon tissue. The expression of claudin-1， zonula occludens-1 （ZO-1）， and occludin in the colon tissue was determined by Western blot. Real-time quantitative polymerase chain reaction（Real-time PCR） was employed to assess the levels of tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β）， and interleukin-6 （IL-6） in the colon tissue. The fecal microbiota composition and differential metabolites were analyzed by 16S rRNA sequencing and ultra-high performance liquid chromatography-quadrupole-time of flight tandem mass spectrometry （UPLC-Q-TOF-MS）， respectively. ResultsThe BBR-BAI combination lowered the FBG， HbA1c， and INS levels （P<0.05， P<0.01） and alleviated insulin resistance （P<0.01） in T2DM mice. Additionally， BBR-BAI elevated the levels of ZO-1， occludin， and claudin-1 （P<0.05， P<0.01） and down-regulated the expression levels of TNF-α， IL-1β， and IL-6 in the colon （P<0.05， P<0.01）. The results of 16S rRNA sequencing showed that BBR-BAI increased the relative abundance of Ligilactobacillus， Phascolarctobacterium， and Akkermansia （P<0.05）， while significantly decreasing the relative abundance of Alistipes， Odoribacter， and Colidextribacter （P<0.05）. UPLC-Q-TOF-MS identified 28 differential metabolites， which were primarily involved in arachidonic acid metabolism and α-linolenic acid metabolism. ConclusionBBR-BAI can ameliorate T2DM due to internal accumulation of dampness-heat by modulating the relative abundance of various bacterial genera in the gut microbiota and the expression of fecal metabolites.

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by synovial inflammation, joint destruction, and functional impairment. Angiogenesis plays a key role in the pathological progression of RA with dysfunction of endothelial cells to promote synovial inflammation, sustain pannus formation, subsequently leading to joint damage. Colquhounia Root Tablets (CRT), a Chinese patent drug, has shown a satisfying clinical efficacy in treating RA, while the underlying mechanism by which CRT inhibits RA-associated angiogenesis remains unclear. In this study, we applied a research approach combining transcriptomic data analysis, bio-network mapping, and in vivo and in vitro experiments to explore the molecular mechanisms of CRT in suppressing angiogenesis in RA. Animal welfare and experimental procedures follow the regulations of the Animal Ethics Committee of Institute of Basic Theory for Chinese Medicine, China Academy of Chinese Medical Sciences (ratification number: IBTCMCACMS21-2307-06). Network analysis identified that key genes such as nucleotide-binding oligomerization domain-containing protein 2 (NOD2), SMAD family member 3 (SMAD3), and vascular endothelial growth factor A (VEGFA) significantly enriched in pathways related to NOD-like receptor signaling and VEGF signaling, indicating that CRT may inhibit angiogenesis by regulating vascular endothelial cell function with modulating angiogenesis-related pathways. In vivo data showed that CRT significantly reduced the positive expression of CD31 and VEGF in the ankle joint of adjuvant-induced arthritis (AIA) rats. In vitro data further confirmed that CRT effectively inhibited VEGF-induced migration, invasion, and tube formation in HUVECs, while significantly reduced the expression of angiogenesis-related factors VEGF/CD31/Ang-1, as well as the positive expression of VEGF and CD31 in HUVECs. Furthermore, CRT markedly decreased the protein expression of NOD2, VEGFA, and SMAD3. In conclusion, these findings indicate that CRT may inhibit the RA-related angiogenesis by targeting the NOD2/SMAD3/VEGF signaling axis to improve endothelial cell function, enriching the scientific connotation of CRT in inhibiting pathological angiogenesis in RA and also offer new insights for clinical prevention and treatment of RA.

ObjectiveTo explore the mechanism of action of Wendantang on ApoE^-/- hyperlipidemic mice using non-targeted metabolomics technology. MethodsMale C57BL/6J mice served as the normal control group （n=6）， and they were fed with regular chow， while male ApoE^-/- mice constituted the high-fat group （n=30）， and they were fed with a 60% high-fat diet. After 11 weeks of model establishment， the mice in the high-fat group were randomly divided into the model group， simvastatin group （3.3 mg·kg^-1）， and high-dose， medium-dose， and low-dose groups of Wendantang （26， 13， 6.5 g·kg^-1， respectively， in terms of crude drug amount）， with six mice in each group. The normal control group and the model group were gavaged with an equivalent volume of normal saline， and all groups continued to be fed their respective diets， receiving daily medication for 10 weeks with weekly body weight measurements. Serum levels of total cholesterol （TC）， triglycerides （TG）， high-density lipoprotein cholesterol （HDL-C）， low-density lipoprotein cholesterol （LDL-C）， free fatty acids （NEFA）， blood glucose （GLU）， alanine aminotransferase （ALT）， and aspartate aminotransferase （AST） were detected in the mice. Pathological changes in liver tissue were observed using hematoxylin-eosin （HE） staining， and ultra-performance liquid chromatography-quadrupole time-of-flight mass spectrometry （UPLC-Q-TOF-MS/MS） was employed for metabolomic analysis of mouse liver tissue. ResultsCompared to the normal control group， the model group exhibited significantly increased body weight， blood lipid levels， and liver function （P<0.05， P<0.01）， with disordered liver tissue structure， swollen hepatocytes， and accompanying vacuolar fatty degeneration and inflammatory cell infiltration. Compared to the model group， the simvastatin group and Wendantang groups showed significantly reduced body weight， TG， NEFA， GLU， ALT， and AST levels （P<0.05， P<0.01）， with a significant increase in HDL-C levels （P<0.05， P<0.01）， demonstrating a dose-dependent effect. The lesion of the liver tissue section was obviously improved after administration， tending towards a normal liver tissue morphology. Analysis of liver metabolites revealed 86 differential metabolites between the normal control group and the model group， with the high-dose group of Wendantang able to regulate 56 of these metabolites. Twenty-two differential metabolites associated with hyperlipidemia were identified， mainly including chenodeoxycholic acid， hyocholic acid， taurine， glycocholic acid， dihydroceramide， hydroxy sphingomyelin C14∶1， arachidonic acid， and linoleic acid， enriching 22 metabolic pathways， with 4 being the most significant （P<0.05）， namely primary bile acid biosynthesis， sphingolipid metabolism， unsaturated fatty acid biosynthesis， and linoleic acid metabolism pathways. ConclusionWendantang can improve blood lipid levels and liver function in ApoE^-/- hyperlipidemic mice， which may be related to the regulation of primary bile acid biosynthesis， sphingolipid metabolism， unsaturated fatty acid biosynthesis， and linoleic acid metabolism pathways.

Objective: Data on syncopal donation-related vasovagal reaction (DRVR) collected from 74 blood centers between 2020 and 2023 was statistically analyzed to provide a reference for developing preventive strategies against syncopal DRVR. Methods: Data on blood donation adverse reactions and basic information of donors from 2020 to 2023 were collected through the information management system at monitoring sentinel sites. Statistical analysis was performed on the following aspects of syncopal DRVR: characteristics of donors who experienced syncope, reported incidence, triggers, duration, presence and occurrence time of syncope-related trauma, clinical management including outpatient and inpatient treatment, and severity grading. Results: From 2020 to 2023, 45 966 donation-related adverse reactions were recorded. Of these, 1 665 (3.72%) cases were syncopal DRVR. The incidence of syncopal DRVR decreased with age, being the highest in the 18-22 age group. Incidence was significantly higher in female donors than male donors, in first-time donors than repeat donors, and in university and individual donors than group donors (all P<0.05). There was no statistically significant difference among different blood donation locations (P>0.05). The top three triggers were tension, fatigue, and needle phobia or fear of blood. Among syncopal DRVR cases, 60.36% occurred during blood collection, 87.63% lasted for less than 60 seconds, and 5.05% were accompanied by trauma. Notably, 57.14% of these traumas occurred after donor had left the blood collection site. Syncope severity was graded based on required treatment: grade 1 (fully recovered without treatment, 95.50%); grade 2 (recovered after outpatient treatment, 4.02%); and grade 3 (recovered after inpatient treatment, 0.48%). Conclusion: By analyzing the data of syncopal DRVR cases, it is possible to provide a reference for formulating blood donor safety policies.

Objective To analyze the death rate and life loss of injuries in Jinshan District of Shanghai from 1990 to 2023, and to provide a scientific basis for the formulation of injury prevention and control measures. Methods Excel 2010 was used to establish a database for injury death reports in Jinshan District from 1990 to 2023, and the crude mortality rate, standardized mortality rate, age-specific mortality rate, potential years of life lost (PYLL), rate of potential years of life lost (PYLLR) and standardized rate of potential years of life lost (SPYLLR) were calculated. Results From 1990 to 2023, the crude mortality rate due to injuries in Jinshan District was 52.25/100 000, while the standardized mortality rate was 36.95/100 000. Based on the standardized mortality rate, the top four causes of injury-related deaths were traffic accidents, falls, drowning, and suicide. Traffic accidents ranked first as the leading cause of death for both males (19.30/100 000) and females (8.41/100 000). The top cause of death for the 0-14 years old group was drowning, the 15-64 years old group was traffic accidents, and the 65 years old and above was falls. Over the 34-year period, according to SPYLLR, the top four causes of death for both genders were consistently traffic accidents, drowning, suicide, and falls. Conclusion From 1990 to 2023, traffic accidents, falls, drowning, and suicide have been the primary causes of injury-related deaths in Jinshan District, Shanghai. It is essential to develop targeted prevention and control strategies based on the specific characteristics of these injury-related fatalities.

ObjectiveTo investigate pulmonary function levels and associated influencing factors among rural elderly in Guangzhou， to identify high-risk populations for poor pulmonary function， and to reveal the relationship between the influencing factors of pulmonary function. MethodsWe recruited 1 500 residents aged 60 to 94 years from rural area of Conghua District， Guangzhou City using convenience sampling in 2023. Data on demographics， body measurements， medical history and lifestyle were collected via face-to-face questionnaires and physical examination. Meanwhile， expiratory function parameters including forced expiratory volume in one second （FEV1）， forced vital capacity （FVC）， FEV1/FVC， and the prevalence of airflow obstruction （AFO） were assessed using a portable spirometer. Age and sex distribution of pulmonary function in older adults at 5-year intervals was reported， and risk factors of AFO using multifactorial logistic regression models were analyzed. Furthermore， path analysis was further employed to explore the role of lifestyle in the association between other influencing factors and lung function. ResultsAmong the 1 500 participants， the median age was 71 years （67-75）， and 44.2% were male. Subjects identified as AFOs were generally older， more likely male， less educated， and had lower rates of moderate to vigorous physical activity （＜1 time/week） and lower lean body mass. Mean FEV1/FVC ratio was （82.0±16.4） %. FEV1/FVC was （79.80±17.58） % in men and （83.66±15.22） % in women. Older age， lower education， male sex and leanness were negatively associated with all pulmonary function outcomes （all P values＜0.05）. Path analysis identified that age， gender， marital status， occupation and income may influence pulmonary function indirectly through lifestyle. ConclusionRural elderly in Guangzhou exhibited lower pulmonary function levels， and male sex， non-married status， advanced age， lower education， smoking habits， insufficient engagement in moderate to vigorous physical activity， and lean body type were all associated with worse pulmonary function.

ObjectiveTo analyse the efficacy and mechanism of Guizhi Fulingwan in regulating sex hormone disorders in rats with benign prostatic hyperplasia （BPH）. MethodsThirty male SD rats were randomly divided into a sham group， a model group， a finasteride group （0.45 mg·kg^-1·d^-1）， and low-dose and high-dose groups of Guizhi Fulingwan （0.135， 0.337 5 g∙kg^-1∙d^-1）， with six in each group. The BPH model was prepared by subcutaneous injection of 3.5 mg∙kg^-1∙d^-1 testosterone propionate after debridement surgery in all groups except the sham group. The rats in the sham group and the model group were administered with an equal volume of saline by gavage， and the rest of the groups were administered with the corresponding medicinal solution by gavage for 35 days. Histopathology in rats was evaluated by prostate wet weight， volume， index， and hematoxylin-eosin （HE） staining. The serum sex hormone levels of testosterone （T）， dihydrotestosterone （DHT）， and estradiol （E₂） were determined by enzyme-linked immunosorbent assay. The protein expression of the androgen receptor （AR） was detected by immunohistochemistry. The serum metabolism profiles of rats in the sham group， the model group， and the high-dose group of Guizhi Fulingwan were compared by ultra-high performance liquid chromatography tandem Fourier transform mass spectrometry （UHPLCQ Exactive） to screen for metabolic markers and to obtain relevant metabolic pathways. ResultsCompared with those in the sham group， the wet weight， volume， index， serum sex hormone level， and AR protein expression of the prostate in the model group were all elevated （P<0.05， P<0.01）， and the histomorphology showed pathological changes. Compared with those in the model group， the wet weight， volume， index， serum sex hormone level， and AR protein expression of the prostate in the intervention groups showed a decreasing trend （P<0.05， P<0.01）， and histopathology was improved. Serum metabolomics analysis obtained a total of 40 metabolic markers related to the intervention effect of Guizhi Fulingwan， such as dehydrosafynol， hyoscyamine， and lumichrome， which were involved in the pathways of autophagy， riboflavin metabolism， and retrograde endocannabinoid signaling. ConclusionGuizhi Fulingwan can effectively regulate sex hormone disorders in BPH rats， and its mechanism may be related to autophagy， riboflavin metabolism， and retrograde endocannabinoid signaling.

OBJECTIVE: To investigate the potential mechanism by which electroacupuncture (EA) induces macrophage polarization to promote muscle satellite cell proliferation and differentiation, accelerating the repair of acute skeletal muscle injury. METHODS: Forty-two SPF-grade SD rats were randomly divided into three groups: a blank group (n=6), a model group (n=18), and an EA group (n=18). The model and EA groups established acute blunt contusion model of the right gastrocnemius muscle using a self-made striking device. From day 1 after modeling, rats in the EA group received EA at "Chengshan" (BL57) and "Yanglingquan" (GB34) on the right side, using disperse-dense wave with a frequency of 2 Hz/100 Hz and a current of approximately 2 mA. The EA treatment was administered once daily for 30 minutes for 3, 7, or 14 days based on the designated sampling time points. Gait analysis was performed using the Cat Walk XT^TM system. Hematoxylin-eosin (HE) staining was used to observe the morphological changes in the gastrocnemius muscle. Masson staining was applied to evaluate collagen fiber content. Immunofluorescence was used to detect the expression of proliferating cell nuclear antigen (PCNA) in muscle satellite cells. Immunohistochemistry was used to assess the expression levels of CD68 and CD206, markers of macrophages. Serum levels of pro-inflammatory cytokines (TNF-α, IL-1β) and anti-inflammatory cytokines (IL-10, IL-13) were detected using ELISA. RESULTS: Compared with the blank group, the model group showed a significant reduction in average movement speed on days 3 and 7 after modeling (P<0.05), and a decrease in the right hind limb stride length on day 3 (P<0.05). Compared with the model group, the EA group showed increased average movement speed and right hind limb stride length on day 7 (P<0.05). In the blank group, the gastrocnemius muscle on the right side showed uniform and consistent inter-fiber spacing, with neatly and regularly arranged muscle cells. In contrast, the model group exhibited enlarged inter-fiber spacing, edema, and significant infiltration of red blood cells and inflammatory cells, with progressively increasing fibrosis over time. By day 14 after modeling, the EA group showed a return to baseline levels of inflammatory cell infiltration, and the degree of fibrosis was significantly lower than that observed in the model group. Compared with the blank group, the ratio of collagen fibers in the gastrocnemius muscle of the model group increased significantly on days 3, 7, and 14 after modeling (P<0.05). Compared with the model group, the EA group exhibited a lower collagen fiber ratio on days 3, 7, and 14 (P<0.05). Compared with the blank group, PCNA positive expression in the gastrocnemius muscle of the model group was significantly increased on days 3, 7, and 14 after modeling (P<0.05). Compared with the model group, the EA group exhibited significantly higher PCNA positive expression on days 3 and 7 (P<0.05). Compared with the blank group, the model group showed a significant increase in CD68-positive macrophage expression in the gastrocnemius muscle on day 3 after modeling (P<0.05), while CD206-positive macrophage expression increased on days 3, 7, and 14 (P<0.05). Compared with the model group, CD68 expression was significantly lower in the EA group on day 3 (P<0.05), whereas CD206 expression was significantly higher on days 3 and 7 (P<0.05), peaking on day 7 with CD206 expression. Compared with the blank group, serum TNF-α levels were significantly elevated in the model group on days 3 and 7 after modeling (P<0.05), while serum IL-1β levels were increased on days 3, 7, and 14 (P<0.05). Serum IL-10 and IL-13 levels were significantly higher on day 7 after modeling (P<0.05). Compared with the model group, the EA group exhibited lower serum TNF-α level on day 3 (P<0.05) and reduced serum IL-1β levels on days 3 and 7 (P<0.05), while serum IL-10 and IL-13 levels were significantly increased on day 7 (P<0.05). CONCLUSION EA could promote the repair of acute blunt contusion-induced gastrocnemius muscle injury by regulating the proliferation and differentiation of muscle satellite cells. This process is closely related to macrophage polarization.
Animals ; Electroacupuncture ; Rats, Sprague-Dawley ; Rats ; Macrophages/immunology* ; Muscle, Skeletal/immunology* ; Male ; Humans ; Female ; Tumor Necrosis Factor-alpha/immunology* ; Cell Proliferation