Objective: To investigate the prevalence and associated factors of depressive symptoms among junior and senior high school students in Beijing from 2019 to 2023, in order to provide a scientific basis for interventions targeting high risk groups. Methods: From 2019 to 2023, a stratified cluster random sampling method was used to select 88 927 junior and senior high school students from 16 districts in Beijing. The Center for Epidemiologic Studies Depression Scale(CES-D) was conducted to assess depressive symptoms. The Chi square test was used to compare the detection rates of depressive symptoms among different student groups, and the trend Chi square test was employed for trend analysis of detection rates across the years. Multivariate Logistic regression analysis was applied to examine the association between the detection of depressive symptoms and related factors among junior and senior high school students. Results: From 2019 to 2023, the prevalence rates of depressive symptoms among junior and senior high school students in Beijing were 20.45%, 18.19%, 16.64%, 17.89% and 18.17%, respectively, with an overall downward trend ( χ 2 trend =27.51, P <0.01). Multivariate Logistic regression analysis revealed that after adjusting for gender, monitoring year, educational stage,family structure,boarding status and has taken a medical leave of absence in the past year unhealthy dietary behaviors ( OR=1.80, 95%CI =1.73-1.87), physical inactivity ( OR=1.24, 95%CI =1.19-1.29), try smoking ( OR=1.46, 95%CI =1.35-1.58), try alcohol( OR=1.96, 95%CI =1.88-2.05), Internet addiction ( OR=3.88, 95%CI =3.57-4.22), and adverse ear related behavior ( OR=1.82, 95%CI =1.71-1.93) were all associated with an increased risk of depressive symptoms among junior and senior high school students (all P <0.05). Conclusions The prevalence depression symptoms among middle school students in Beijing showed a fluctuating downward trend from 2019 to 2023. Targeted interventions should be adopted to reduce the occurrence of depression symptoms among junior and senior high school students.

Objective: To understand the trends of classroom lighting and illumination of primary and secondary schools in Beijing from 2016 to 2023, so as to provide a scientific basis for targeted improvement measures. Methods: A sampling survey was conducted on the lighting and illumination indicators of 8 390 classrooms in primary and secondary schools in Beijing from 2016 to 2023. The survey included classroom daylight factor, window to floor area ratio, average illuminance and illuminance uniformity on the desks, average illuminance and illuminance uniformity on blackboards, as well as classroom lighting and blackboard illumination sources. Intergroup comparisons were performed using the Kruskal-Wallis H test and the Chi square test, and Spearman correlation analysis was used to examine the trend of classroom lighting and illumination changes. Results: Except the window to floor area ratio, the measured values and compliance rates of all lighting and illumination indicators showed an overall upward trend from 2016 to 2023 (daylight factor r = 0.27, χ 2 trend =206.80, average illuminance on the desk surface r =0.30, χ 2 trend =87.97, illuminance uniformity on the desk surface r =0.14, χ 2 trend =73.59, average illuminance on the blackboard r =0.33, χ 2 trend =477.43, illuminance uniformity on the blackboard r = 0.09, χ 2 trend =50.76) (all P ＜0.01). The lighting and illumination indicators of classrooms (included classroom daylight factor, average illuminance and illuminance uniformity on the desks, average illuminance and illuminance uniformity on blackboards) in urban schools, primary schools, and secondary schools from 2016 to 2023 showed an upward trend (urban r =0.23-0.40, χ 2 trend =88.66-392.18; primary school r =0.12-0.36, χ 2 trend =39.50-281.44; secondary schools r =0.06-0.31, χ 2 trend =11.79-213.73) (all P ＜ 0.01 ). The illuminance uniformity on the blackboard in suburban schools showed a downward trend ( r = -0.09, χ 2 trend =31.53, both P ＜0.01). The illuminance uniformity on the desk surface in suburban schools showed no significant change ( r =0.03, χ 2 trend =1.23, both P ＞0.05). The other indicators showed an upward trend (daylight factor r =0.28, χ 2 trend =40.69, average illuminance on the desk surface r =0.24, χ 2 trend =16.35, average illuminance on the blackboard r =0.25, χ 2 trend =118.05, all P ＜0.01). The trends of classroom and blackboard illumination sources were that fluorescent lamps decreased year by year and LED lamps increased by year (classroom illumination sources χ 2 trend =1 059.82, blackboard illumination sources χ 2 trend =1 070.25, both P ＜0.01). Conclusions The classroom lighting and illumination in primary and secondary schools in Beijing has shown an overall improving trend from 2016 to 2023. However, problems remain, such as limited improvement of illuminance uniformity indicators, late start and poor effect of reconstruction in suburban schools. Further improvements are still needed.

Radiotherapy is a cornerstone in the treatment of malignant tumors. It induces DNA damage through high-energy radiation, preferentially eliminating rapidly proliferating tumor cells. However, its clinical efficacy is often limited by tumor radioresistance and collateral damage to normal tissues. Consequently, elucidating the cellular response mechanisms to radiation stress and identifying key targets that can both sensitize tumor cells and protect normal tissues have become critical strategies for improving radiotherapy outcomes. Radiation stress triggers structural remodeling of the nucleolus, leading to the dissociation of certain ribosomal proteins from the ribosome and enabling them to acquire extra-ribosomal functions. Among these, RPL11 can be released and specifically binds to MDM2, thus inhibiting its E3 ubiquitin ligase activity, stabilizing p53, and mediating cell cycle arrest and apoptosis. The RPL11-MDM2-p53 pathway, acting as a signaling hub that links nucleolar dysfunction to cell fate determination, plays a pivotal role in maintaining genomic stability and regulating cellular responses to radiation. This review first introduces the basic characteristics of RPL11 and elucidates the molecular basis of radiation-induced ribosomal stress. It then outlines the core regulatory mechanisms of the cell cycle. On this basis, it focuses on the mechanisms by which radiation-induced RPL11 regulates the cell cycle and analyzes the specific effects of RPL11 on cell cycle. Furthermore, it discusses the role of the RPL11-MDM2-p53 pathway in cell cycle regulation. Finally, it explores the role of this pathway in maintaining genomic stability and determining cell fate, and highlights its potential value as a target for radiosensitization, aiming to provide new perspectives for enhancing tumor radiosensitivity and reducing damage to normal tissues.

Radiotherapy is a cornerstone in the treatment of malignant tumors. It induces DNA damage through high-energy radiation, preferentially eliminating rapidly proliferating tumor cells. However, its clinical efficacy is often limited by tumor radioresistance and collateral damage to normal tissues. Consequently, elucidating the cellular response mechanisms to radiation stress and identifying key targets that can both sensitize tumor cells and protect normal tissues have become critical strategies for improving radiotherapy outcomes. Radiation stress triggers structural remodeling of the nucleolus, leading to the dissociation of certain ribosomal proteins from the ribosome and enabling them to acquire extra-ribosomal functions. Among these, RPL11 can be released and specifically binds to MDM2, thus inhibiting its E3 ubiquitin ligase activity, stabilizing p53, and mediating cell cycle arrest and apoptosis. The RPL11-MDM2-p53 pathway, acting as a signaling hub that links nucleolar dysfunction to cell fate determination, plays a pivotal role in maintaining genomic stability and regulating cellular responses to radiation. This review first introduces the basic characteristics of RPL11 and elucidates the molecular basis of radiation-induced ribosomal stress. It then outlines the core regulatory mechanisms of the cell cycle. On this basis, it focuses on the mechanisms by which radiation-induced RPL11 regulates the cell cycle and analyzes the specific effects of RPL11 on cell cycle. Furthermore, it discusses the role of the RPL11-MDM2-p53 pathway in cell cycle regulation. Finally, it explores the role of this pathway in maintaining genomic stability and determining cell fate, and highlights its potential value as a target for radiosensitization, aiming to provide new perspectives for enhancing tumor radiosensitivity and reducing damage to normal tissues.

Radiotherapy is a cornerstone in the treatment of malignant tumors. It induces DNA damage through high-energy radiation, preferentially eliminating rapidly proliferating tumor cells. However, its clinical efficacy is often limited by tumor radioresistance and collateral damage to normal tissues. Consequently, elucidating the cellular response mechanisms to radiation stress and identifying key targets that can both sensitize tumor cells and protect normal tissues have become critical strategies for improving radiotherapy outcomes. Radiation stress triggers structural remodeling of the nucleolus, leading to the dissociation of certain ribosomal proteins from the ribosome and enabling them to acquire extra-ribosomal functions. Among these, RPL11 can be released and specifically binds to MDM2, thus inhibiting its E3 ubiquitin ligase activity, stabilizing p53, and mediating cell cycle arrest and apoptosis. The RPL11-MDM2-p53 pathway, acting as a signaling hub that links nucleolar dysfunction to cell fate determination, plays a pivotal role in maintaining genomic stability and regulating cellular responses to radiation. This review first introduces the basic characteristics of RPL11 and elucidates the molecular basis of radiation-induced ribosomal stress. It then outlines the core regulatory mechanisms of the cell cycle. On this basis, it focuses on the mechanisms by which radiation-induced RPL11 regulates the cell cycle and analyzes the specific effects of RPL11 on cell cycle. Furthermore, it discusses the role of the RPL11-MDM2-p53 pathway in cell cycle regulation. Finally, it explores the role of this pathway in maintaining genomic stability and determining cell fate, and highlights its potential value as a target for radiosensitization, aiming to provide new perspectives for enhancing tumor radiosensitivity and reducing damage to normal tissues.

Objective To determine the related substances in esmolol hydrochloride injection by HPLC method. Methods A Waters XBridge TM C₁₈ （4.6 mm×150 mm,5 µm） column packed with octadecylsilane-bonded silica gel was used, with phosphate buffer （3.0 g of potassium dihydrogen phosphate was taken, dissolved in water and diluted to 650 ml）-acetonitrile-methanol （65∶15∶20） as the mobile phase A, and mobile phase A mixed with methanol （65∶35） as the mobile phase B. The related substances in the test sample and those generated after forced degradation were qualitatively and quantitatively analyzed by the impurity reference standard method, with an injection volume of 20 μl, a column temperature of 30℃, a flow rate of 1.0 ml/min and a detection wavelength of 222 nm. Results The separation between esmolol hydrochloride and neighboring impurities as well as between each impurity was greater than 1.5; the impurities showed good linearity in their respective linear ranges （r>0.999）. The average recovery of impurity a （Imp-a） was 99.1% with an RSD of 0.56%; the average recovery of impurity b（Imp-b）was 96.0% with an RSD of 0.98%; the average recovery of impurity c （Imp-c） was 100.7% with an RSD of 1.24%; the average recovery of impurity d （Imp-d） was 99.0% with an RSD of 0.12%; the average recovery of impurity e （Imp-e） was 100.7% with an RSD of 0.64%; and the impurity f （Imp-f） average recovery was 101.7% with an RSD of 3.26%; impurity g （Imp-g） average recovery was 99.1% with an RSD of 1.45%. Conclusion This method could evaluate the quality of esmolol hydrochloride injection more accurately than the current standard and could provide data reference for the quality evaluation system.

Zhishi Shaoyaosan is the 34^th prescription in the Catalogue of Ancient Classic Formulas （Second Batch） published by the National Administration of Traditional Chinese Medicine in 2023. It is widely used in clinical practice and has a definite curative effect. However， there is currently a lack of its ancient literature analysis and textual research， and there is no corresponding Chinese patent medicine preparation. By consulting and combing the relevant ancient books of traditional Chinese medicine， this paper analyzes and conducts textual research of the origin， composition， measurement， administration， and efficacy of Zhishi Shaoyaosan. The results show that Zhishi Shaoyaosan is derived from Essentials from the Golden Cabinet written by Zhang Zhongjing in the Eastern Han Dynasty. It is mainly recorded in the name of Zhishi Shaoyaosan in the literature of the past dynasties. The prescription is composed of Aurantii Fructus Immaturus and Paeoniae Radix Alba. The processing method is stir-frying Aurantii Fructus Immaturus to scorch and using raw Paeoniae Radix Alba. The dose of the prescription recorded in the ancient books is mainly an equal amount of Aurantii Fructus Immaturus and Paeoniae Radix Alba in one square-cun spoon， taken three times a day， which is converted into a modern dose of 1.5 g each time （0.75 g Aurantii Fructus Immaturus and 0.75 g Paeoniae Radix Alba each time）. The components of the prescription are ground into powder and taken with barley porridge， three times a day. The efficacy is to break stagnated Qi， harmonize blood， and relieve restlessness and pain. It is mainly used to treat postpartum abdominal pain， acute pelvic inflammatory disease， acute cholecystitis and intestinal diseases， stroke sequelae， and other diseases. This study combs and analyzes the ancient literature recording Zhishi Shaoyaosan and clarifies the key information of the prescription， which provides a basis for promoting the research and development of its patent medicine.

Objective: To explore the relationship of physical activity (PA) and sedentary behavior (SB) with cardiorespiratory fitness (CRF) among middle schoold students in Tibet, so as to provide empirical references for improving the cardiorespiratory fitness and health levels of adolescents in Tibet. Methods: From August to December 2020, 1 225 junior and senior high school students were selected from 2 middle schools in Lhasa, Tibet Autonomous Region, using the stratified cluster random sampling method. Triaxial accelerometers were used to evaluate PA and SB behaviors, and the 20 meter shuttle run was employed to assess CRF among the middle school students. Isochronous substitution modeling was used to analyze the associations of SB, low intensity physical activity (LPA), and moderate vigorous physical activity (MVPA) with CRF, and the saturation threshold effect in the dose response relationship between MVPA and CRF was analyzed through restricted cubic spline and two stage linear regression. Results: After adjusting for covariates such as gender, body mass index and sleep quality score, isotemporal substitution analysis showed that among junior high school students aged 13-15, replacing 30 minutes of SB ( B =1.73) or LPA ( B =2.38) with MVPA were positively associated with CRF (both P <0.05). Among senior high school students aged 16-18, replacing SB ( B =0.99) or LPA ( B =1.38) with MVPA were also positively associated with CRF (both P <0.05). Restricted cubic spline and two piecewise linear regression analyses indicated that only middle school girls aged 13-18 exhibited a saturation threshold effect between MVPA and CRF (logarithmic likelihood ratio test=0.03), with the optimal CRF improvement observed at 60 minutes of MVPA per day ( B=0.13, P ＜ 0.01). Conclusions Reducing SB and LPA while increasing MVPA can improve CRF in Tibetan middle school students. To maximize CRF improvement, middle school girls should engage in at least 60 minutes of MVPA daily.

Objective To investigate the mechanisms of 6-hydroxygenistein(6-OHG)in the treatment of high-altitude hypoxia-induced lung injury.Methods The intersection targets of 6-OHG and high-altitude hypoxia-induced lung injury were identified using databases,including Swiss Target Prediction,SuperPred,GeneCards,and OMIM.The STRING database and Cytoscape software were used to construct a protein interaction network for the intersection targets of drugs and diseases,and targets with degree values greater than the median were identified as key targets.GO and KEGG enrichment analyses of key targets were performed using the DAVID database to identify relevant signaling pathways.The Maestro 13.7 software was used for molecular docking validation.A large hypobaric hypoxic chamber was used to establish a high-altitude lung injury model in mice.A total of 42 male BALB/c mice were randomly assigned to 3 groups(n=14 in each group),including a normal control group,which was exposed to the environmental conditions at the altitude of 1400 m and received a single intraperitoneal injection of normal saline,a model group,which received a single intraperitoneal injection of normal saline,and a 6-OHG group,which received a single intraperitoneal injection of 6-OHG at 100 mg/kg.Then,1 h after drug administration,mice in the model and 6-OHG groups were placed in a large hypobaric hypoxic simulation chamber for animal experiments.Then,they ascended to an altitude of 8 000 m at a speed of 10 m/s,remained in that environment for 24 h,and then descended to an altitude of 3500 m.Mice in the three groups were sacrificed,and their lung tissues were extracted to measure the water content in the lungs.Pathological changes were observed using HE staining,and the levels of malondialdehyde(MDA),H2O2,total superoxide dismutase(T-SOD),and glutathione(GSH)were measured.Western blot was performed to determine the expression levles of p-PI3K/PI3K,p-AKT/AKT,hypoxia-inducible factor 1α(HIF-1α),and vascular endothelial growth factor(VEGF)proteins.Results Key targets such as serine/threonine protein kinase 1(AKT1),HIF-1α,epidermal growth factor receptor(EGFR),matrix metalloproteinase 9(MMP9),and peroxisome proliferator-activated receptor A(PPARA)were identified.GO and KEGG enrichment analyses showed that the targets of 6-OHG in the treatment of high altitude hypoxia-induced lung injury were mainly involved in PI3K/AKT,HIF-1α/VEGF,tumor necrosis factor(TNF),and other signaling pathways.The results of animal experiments demonstrated that compared with the model group,the 6-OHG group showed significant improvement in the pathological damage of lung tissues induced by high altitude hypoxia,presenting statistically significant differences in the levels of MDA,H2O2,GSH,and T-SOD(P＜0.01).The results of Western blot assay revealed statistically significant differences in the p-PI3K/PI3K,p-AKT/AKT,HIF-1α,and VEGF levels in the lung tissues of the 6-OHG group compared with those of the model group(P＜0.01).The molecular docking results showed that 6-OHG could form stable binding with PI3K,AKT,HIF-1α,and VEGF.Conclusion 6-OHG may alleviate lung injury induced by high altitude hypoxia in mice by activating the PI3K/AKT signaling pathway and inhibiting the HIF/VEGF signaling pathway.

Objective To investigate the molecular targets and signaling pathways involved in the therapeutic effects of Lishukang Capsule(LSK)in a rat model of high-altitude pulmonary edema(HAPE)using a proteomics-based approach.Methods A total of 60 male Wistar rats were randomly assigned to a control group,a HAPE model group,3 LSK treatment groups receiving low-,medium-,and high-dose LSK,respectively,and a Rhodiola rosea(also known as Hongjitian[HJT]in pinyin,a Chinese Romanization system)control group.After HAPE modeling,the pharmacodynamic effects were assessed and the optimal LSK dose was determined using HE stains,inflammatory cytokine quantification,lung tissue water content,and the protein concentration in bronchoalveolar lavage.Label free quantitative proteomic profiling was then applied to identify differentially expressed proteins(DEPs)in the optimal dose group,using a screening threshold of over 1.5-fold change and P<0.05.The selected DEPs were validated with Western blotting,followed by Gene Ontology(GO)enrichment and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway enrichment analysis.Results The medium-dose LSK group exhibited significant anti-HAPE effects.Findings from the proteomic analysis revealed,in the comparison with the control group,267 DEPs were identified in the HAPE group.In the comparison with the HAPE group,225 DEPs were identified in the medium-dose LSK group.A total of 112 DEPs in the control group were normalized following LSK treatment in the medium-dose LSK group.In addition,GO enrichment analysis of proteins differentially expressed between the HAPE and LSK group showed that these DEPs were mainly enriched in 12 biological processes,2 cellular components,and 5 molecular functions.KEGG pathway analysis showed that LSK activated pathways associated with cell adhesion molecules,glycosaminoglycan biosynthesis,DNA replication/nucleotide excision repair,transcriptional dysregulation in cancer,and Herpes simplex virus type 1(HSV-1)infection,while inhibiting pathways associated with glycerophospholipid metabolism.Some differentially expressed proteins with potential functions were verified by Western blotting,including AGPAT5,NCAM1,SRSF3,and PLA2.These differentially expressed proteins were significantly expressed in the normal group,HAPE group,and LSK group,and the validation results were consistent with proteomic findings,indicating the high reliability of the proteomic results.Conclusion LSK exerts a significant protective effect against HAPE.Proteomic analysis suggests that its therapeutic action may be mediated through activating pathways involved in cell adhesion molecules,glycosaminoglycan biosynthesis,DNA replication/nucleotide excision repair,transcriptional dysregulation in cancer,and HSV-1 infection,alongside inhibition of pathways associated with glycerophospholipid metabolism.The key DEPs identified in these pathways may play crucial roles in the preventive and therapeutic effects of LSK on HAPE.