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.

Diabetic kidney disease （DKD） is one of the main causes of chronic kidney disease. Both traditional Chinese medicine （TCM） and western medicine have their own advantages in the prevention and treatment of DKD， but there are also many difficulties. By analysis of the difficulties faced by TCM and western medicine in the differentiation and treatment of DKD， based on the theory of "miniature masses in the renal collaterals"， combined with long-term clinical practice， "internal heat leading to mass" is proposed as the core pathogenesis of DKD. Therefore， a trinity model of "disease-syndrome-symptom" for differentiation and treatment of DKD based on the core pathogenesis has been proposed. This model highlights the status of the core pathogenesis of "internal heat leading to mass" in DKD， and conducts a three-dimensional identification from the perspectives of disease， syndrome and symptom， so as to inspire clinical practice.

ObjectiveTo explore the mechanism of total saponins of Dioscoreae Nipponicae Rhizoma （TSDN） in treating gouty arthritis （GA） by regulating cyclooxygenase-2 （COX-2）-mediated M1 macrophage reprogramming by in vivo and in vitro experiments. MethodsIn vivo experiment： 24 male SD rats were randomly allocated into blank， model （GA）， TSDN， and celecoxib groups， with 6 rats in each group. After 7 days of administration， pathological changes in the ankle synovial tissue were observed via hematoxylin-eosin （HE） staining. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was used to quantify the mRNA levels of NOD-like receptor protein 3 （NLRP3） inflammasome， apoptosis-associated speck-like protein （ASC）， Caspase-1， COX-2， interleukin-1β （IL-1β）， and tumor necrosis factor-α （TNF-α） in the synovial tissue. Enzyme-linked immunosorbent assay （ELISA） was employed to measure the serum levels of inducible nitric oxide synthase （iNOS）， IL-1β， CD86， CD80， CD206， and arginase-1 （Arg-1）. In vitro experiment： The GA model was established by lipopolysaccharide （LPS） + MSU induction， and the inhibitor concentration was screened by the methyl thiazolyl tetrazolium （MTT） assay. RAW264.7 cells were allocated into blank， model， TSDN， dexamethasone， COX-2 inhibitor （celecoxib）， and TSDN + COX-2 inhibitor groups. The levels of iNOS， IL-1β， CD86， CD80， CD206， and Arg-1 in the cell supernatant of each group were determined by enzyme-linked immunosorbent assay （ELISA）. The mRNA and protein levels of NLRP3 inflammasome， COX-2， IL-1β， and TNF-α in each group were determined by Real-time PCR and Western blot， respectively. ResultsIn vivo experiment： compared with the model group， TSDN reduced the mRNA levels of NLRP3 inflammasome， COX-2， IL-1β， and TNF-α in the synovial tissue （P<0.05， P<0.01）. ELISA results showed that TSDN lowered the serum levels of iNOS， IL-1β， CD86， and CD80 （P<0.01） while increasing the serum levels of CD206 and Arg-1 （P<0.01）. In vitro experiment： compared with the model group， TSDN and inhibitor down-regulated the mRNA levels of NLRP3 inflammasome， COX-2， IL-1β， and TNF-α and the protein levels of NLRP3 inflammasome， COX-2， cleaved IL-1β， and TNF-α （P<0.01）. Compared with TSDN alone， TSDN + COX-2 inhibitor further reduced the mRNA and protein levels of the markers above （P<0.01）. Compared with the model group， TSDN and COX-2 inhibitor decreased the levels of IL-1β， iNOS， CD80， and CD86 （P<0.01） and increased the levels of CD206 and Arg-1 （P<0.01） in cells. Compared with TSDN alone， TSDN + COX-2 inhibitor reduced IL-1β， iNOS， CD80， and CD86 levels （P<0.05， P<0.01） and elevated CD206 and Arg-1 levels （P<0.01） in cells. ConclusionTSDN can alleviate GA by downregulating COX-2-mediated M1 macrophage reprogramming and suppressing the inflammatory factors.

ObjectiveTo explore the mechanism of total saponins of Dioscoreae Nipponicae Rhizoma （TSDN） in treating gouty arthritis （GA） by regulating cyclooxygenase-2 （COX-2）-mediated M1 macrophage reprogramming by in vivo and in vitro experiments. MethodsIn vivo experiment： 24 male SD rats were randomly allocated into blank， model （GA）， TSDN， and celecoxib groups， with 6 rats in each group. After 7 days of administration， pathological changes in the ankle synovial tissue were observed via hematoxylin-eosin （HE） staining. Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） was used to quantify the mRNA levels of NOD-like receptor protein 3 （NLRP3） inflammasome， apoptosis-associated speck-like protein （ASC）， Caspase-1， COX-2， interleukin-1β （IL-1β）， and tumor necrosis factor-α （TNF-α） in the synovial tissue. Enzyme-linked immunosorbent assay （ELISA） was employed to measure the serum levels of inducible nitric oxide synthase （iNOS）， IL-1β， CD86， CD80， CD206， and arginase-1 （Arg-1）. In vitro experiment： The GA model was established by lipopolysaccharide （LPS） + MSU induction， and the inhibitor concentration was screened by the methyl thiazolyl tetrazolium （MTT） assay. RAW264.7 cells were allocated into blank， model， TSDN， dexamethasone， COX-2 inhibitor （celecoxib）， and TSDN + COX-2 inhibitor groups. The levels of iNOS， IL-1β， CD86， CD80， CD206， and Arg-1 in the cell supernatant of each group were determined by enzyme-linked immunosorbent assay （ELISA）. The mRNA and protein levels of NLRP3 inflammasome， COX-2， IL-1β， and TNF-α in each group were determined by Real-time PCR and Western blot， respectively. ResultsIn vivo experiment： compared with the model group， TSDN reduced the mRNA levels of NLRP3 inflammasome， COX-2， IL-1β， and TNF-α in the synovial tissue （P<0.05， P<0.01）. ELISA results showed that TSDN lowered the serum levels of iNOS， IL-1β， CD86， and CD80 （P<0.01） while increasing the serum levels of CD206 and Arg-1 （P<0.01）. In vitro experiment： compared with the model group， TSDN and inhibitor down-regulated the mRNA levels of NLRP3 inflammasome， COX-2， IL-1β， and TNF-α and the protein levels of NLRP3 inflammasome， COX-2， cleaved IL-1β， and TNF-α （P<0.01）. Compared with TSDN alone， TSDN + COX-2 inhibitor further reduced the mRNA and protein levels of the markers above （P<0.01）. Compared with the model group， TSDN and COX-2 inhibitor decreased the levels of IL-1β， iNOS， CD80， and CD86 （P<0.01） and increased the levels of CD206 and Arg-1 （P<0.01） in cells. Compared with TSDN alone， TSDN + COX-2 inhibitor reduced IL-1β， iNOS， CD80， and CD86 levels （P<0.05， P<0.01） and elevated CD206 and Arg-1 levels （P<0.01） in cells. ConclusionTSDN can alleviate GA by downregulating COX-2-mediated M1 macrophage reprogramming and suppressing the inflammatory factors.

Objective:To analyze the incidence of adverse treatment outcome of rifampicin-resistant tuberculosis (RR-TB) patients and influencing factors in 9 provinces in China.Methods:The information about the basic characteristics, diagnosis and treatment of RR-TB patients registered from January 1, 2017 to December 31, 2021 in 9 provinces (Beijing, Jilin, Shanghai, Jiangsu, Zhejiang, Hubei, Henan, Yunnan and Guizhou) were collected from the tuberculosis information management sub-system of China Disease Control and Prevention Information System for a descriptive analysis, and the influencing factors of adverse treatment outcome were identified by binary logistic regression analysis.Results:In 18 204 RR-TB patients in this study a total of 6 852 had adverse treatment outcomes (37.64%). Treatment failure occurred in 1 031 patients, 1 272 patients died, 2 284 patients were lost to follow-up, and 2 265 patients were not evaluated. The results of multivariate logistic regression analysis showed that being man (a OR=1.54, 95% CI: 1.43-1.66), age ≥65 years (a OR=2.42, 95% CI: 2.20-2.67), being from other ethnic groups (a OR=1.18, 95% CI: 1.03-1.35), being farmer (a OR=1.22, 95% CI: 1.13-1.32), being retired with honours or being retired (a OR=1.16, 95% CI: 1.00-1.35) and being floating population (a OR=1.23, 95% CI: 1.13-1.34), re-treatment (a OR=1.33, 95% CI: 1.24-1.42), long-term treatment therapy (a OR=3.26, 95% CI: 2.52-4.23), living in central provinces (a OR=2.76, 95% CI: 2.55-2.99), living in western provinces (a OR=2.31, 95% CI: 2.08-2.57) were the influencing factors for adverse treatment outcome of RR-TB. Conclusions:The incidence of adverse outcomes in RR-TB patients in 9 provinces in China was higher from 2017 to 2021. There were many influencing factors associated with adverse treatment outcome in RR-TB patients, especially the area specific factors. The national tuberculosis control program should strengthen the follow-up and treatment management of RR-TB in men, the elderly, floating population, people in central and western provinces and other key groups, actively promote the short-term treatment program and improve the allocation of medical resources to reduce the influencing for adverse treatment outcomes in RR-TB patient.

Objective:To evaluate the effect of exogenous short-chain fatty acids (SCFAs) preconditioning on the expression of zonula occludens-1 (ZO-1) in lung tissues of rats undergoing extracorporeal circulation (ECC).Methods:Thirty-six clean-grade healthy adult male Sprague-Dawley rats, weighing 320-420 g, were divided into sham operation group (S group), ECC group (E group) and SCFAs group, with 12 rats in each group. Seven days before the ECC, short-chain fatty acids dissolved in 2 ml of normal saline was given by gavage daily in SCFAs group, while the equal volume of normal saline was given by gavage in S group and E group. On the 8th day, E group and SCFAs group underwent arteriovenous catheterization and ECC for 1 h, while S group only underwent catheterization without ECC. Lung tissues were collected to observe the pathological results and detect the expression of ZO-1 (by Western blot), and the wet/dry lung weight ratio was calculated.Results:Compared with S group, the wet/dry lung weight ratio was significantly increased ( P<0.05), the expression of ZO-1 protein in lung tissue was down-regulated ( P<0.05), and the pathological damage of lung tissues was aggravated in E group and SCFAs group. Compared with E group, the wet/dry lung weight ratio was significantly decreased, the expression of ZO-1 protein in lung tissues was up-regulated ( P<0.05), and the pathological damage of lung tissues was significantly alleviated in SCFAs group. Conclusions:The mechanism by which SCFAs preconditioning attenuates lung injury may be related to up-regulation of ZO-1 expression in lung tissues of rats undergoing ECC.

Objective:To explore the clinical application value of serum N-glycan profiles for evaluating the severity of liver tissue inflammation in patients with chronic hepatitis B (CHB).Methods:A total of 221 CHB patients who underwent liver biopsy at Mengchao Hepatobiliary Hospital of Fujian Medical University from January 2018 to December 2020 were retrospectively enrolled. The Scheuer scoring system was used to assess the histological inflammation grade of the liver tissue. Serum N-glycan levels were measured using DNA sequencer-assisted N-glycan fingerprinting (NGFP). Using the upper limit of the alanine aminotransferase (ALT) reference value (40 U/L) as a cutoff, logistic regression models were developed to construct diagnostic models under two scenarios: normal ALT or abnormal ALT. Models based on serum N-glycan levels and serum N-glycan levels combined with routine laboratory indicators, were used to non-invasively evaluation of various pathological grades of liver tissue inflammation in CHB patients. The DeLong test was used to compare the diagnostic efficacy of the models by analyzing the areas under the receiver operating characteristic curve (AUC). Glycosylation-related gene expression differences associated with varying degrees of liver inflammation were analyzed using the Gene Expression Omnibus (GEO) database.Results:In CHB patients with normal ALT level, the relative abundances of N-glycan structure peak 1 (NGA2F) and peak 2 (NGA2FB) increased with higher liver inflammation grades, while the relative abundance of peak 5 (NA2) decreased ( P<0.05). The AUCs of the HIS-G model (HIS-G A) and its enhanced version (HIS-G A Plus) for identifying significant inflammation and necrosis (≥G2, indicating the initiation of antiviral therapy) were 0.805 (95% CI 0.690-0.899) and 0.904 (95% CI 0.821-0.960), respectively. In CHB patients with ALT>40 U/L, the relative abundances of peaks 1 (NGA2F), 2 (NGA2FB), and 3 (NG1A2F) increased with higher liver inflammation grades, while the relative abundances of peaks 8 (NA3) and 11 (NA4) decreased ( P<0.05). The AUCs of the HIS-G model (HIS-G B) and its enhanced version (HIS-G B Plus) for identifying significant inflammation (≥G2) were 0.810 (95% CI 0.727-0.889) and 0.838 (95% CI 0.754-0.901), respectively. With increasing liver inflammation grades, the expression levels of four glycosyltransferase genes (CHST4, FUT8, SLC51B, and ST8SIA4) were significantly upregulated ( P<0.05). Conclusions:Serum N-glycan biomarker models can be used to assist in evaluating the severity of liver tissue inflammation in CHB patients with both normal and abnormal ALT levels.

BACKGROUND:Studies have found that massage can reduce blood sugar,promote myogenic factor expression,and increase skeletal muscle content.The extracellular matrix is an important component of skeletal muscle,and association between massage and extracellular matrix and their mechanism of action are still unclear.OBJECTIVE:To explore the effect of massage on extracellular matrix collagen deposition in type 2 diabetic sarcopenia rats.METHODS:Totally 24 Wistar male rats were randomly divided into blank group,model group,and massage group.High-fat diet combined with the streptozotocin method was used to establish a type 2 diabetes mellitus and sarcopenia model.After successful model establishment,the massage group used abdominal massage combined with hind limbs.After 8 weeks of treatment,the fasting blood glucose and serum insulin levels of the rats were measured.The skeletal muscle mass was detected by dual-energy X-ray.The exhaustion time was measured by small animal treadmill.The sliding angle was measured by inclined board test.The pathological changes of skeletal muscle tissue were observed by hematoxylin-eosin staining.The skeletal muscle collagen deposition was observed by Masson staining.The mRNA and protein expressions of type Ⅰ and type Ⅲ collagen in skeletal muscle were detected by qPCR and western blot assay.RESULTS AND CONCLUSION:(1)Compared with the model group,the blood glucose(P＜0.05)and serum insulin(P＜0.01)decreased in the massage group.(2)Compared with the model group,the skeletal muscle mass,running exhaustion time,and the angle of inclined plate experiment were increased in massage group(P＜0.05).(3)Compared with the model group,the skeletal muscles of the massage group were arranged neatly,muscle atrophy was improved,and collagen fiber deposition was reduced.(4)Compared with the model group,the expression levels of type Ⅰ and type Ⅲ collagen mRNA and protein in skeletal muscle were decreased in the massage group(P＜0.05).(5)The results suggest that massage can enhance insulin sensitivity,lower blood sugar,improve skeletal muscle mass,strength and function,and diminish collagen deposition in rats with type 2 diabetes,and may be a potential target for massage to exert its therapeutic effects.

OBJECTIVES: This study aimed to explore the therapeutic effect and mechanism of ginsenoside Rb3 on experimental periodontitis and bone resorption in rats. METHODS: Male SD rats were randomly divided into a control group, a ligation group, an Rb3 group, and a doxycycline (Dox) group for in vivo experiments. A periodontitis model was established by ligating the maxillary second molar, and samples were collected after 3 weeks of drug treatment. Micro-CT assessment of alveolar bone resorption was performed, and hematoxylin-eosin (HE) staining was used to observe pathological changes in periodontal and visceral tissues. Tartrate resistant acid phosphatase (TRAP) staining was applied to detect the formation of osteoclasts in periodontal tissues, and enzyme-linked immunosorbent assay (ELISA) was adopted to detect the serum levels of interleukin (IL)-6, IL-8, immunoglobulin (Ig)M, and IgG. Quantitative polymerase chain reaction (qPCR) was employed to detect the expression of factors related to gingival inflammation and osteoclast formation. Immunofluorescence staining was used to detect phospho-extracellular signal-regulated kinase (p-ERK) expression. In vitro experiments were conducted by pretreating RAW264.7 cells with drugs and adding lipopolysaccharides (LPS) stimulation from Porphyromonas gingivalis (P. gingivalis). IL-1β and IL-6 mRNA expression was detected by qPCR, and Western blot was used to detect the effect of Rb3 on the mitogen-activated protein kinases (MAPKs) signaling pathway. RESULTS: Compared with the control group, the ligation group showed significant periodontitis and bone resorption. Compared with the ligation group, the Rb3 group showed a decrease in alveolar bone resorption and osteoclast formation; p-ERK/ERK ratio, IL-1β, IL-6, and nuclear factor of activated T cells (NFATc1) mRNA levels and downstream gene expression in periodontal tissues; serum IL-6, IL-8, IgG, and IgM levels. Rb3 reduced IL-8 and IL-1β mRNA expression levels and p-ERK/ERK and p-p38 MAPK/p38 MAPK ratios in RAW264.7 cells induced by P. gingivalis LPS stimulation. CONCLUSIONS Rb3 inhibits inflammation and bone resorption in experimental periodontitis in rats. Compared with Dox, Rb3 has better effects in inhibiting pro-inflammatory factors and osteoclast gene expression and may exert anti-inflammatory effects by activating the MAPK signaling pathway.
Animals ; Ginsenosides/therapeutic use* ; Rats, Sprague-Dawley ; Male ; Periodontitis/pathology* ; Rats ; Osteoclasts/drug effects* ; Interleukin-1beta/metabolism* ; Interleukin-6/blood* ; Mice ; Alveolar Bone Loss ; Interleukin-8/blood* ; Immunoglobulin G/blood* ; RAW 264.7 Cells ; Transcription Factors