Objective: To explore the association of vegetables and fruits intake with depressive symptoms among multi ethnic first year junior high school students in Yunnan Province, so as to provide data support for preventing and reducing depressive symptoms among first year junior high school students. Methods: From October to December 2022, a cluster random sampling method was used to select 8 500 first year junior high school students from 11 ethnic minority areas in Yunnan Province (Fugong County, Longling County, Longyang District, Luchun County, Mojiang County, Nanjian County, Qiaojia County, Shuangjiang County, Tengchong City, Yuanmou County, Zhenyuan County), to investigate with a questionnaire. The Dietary Frequency Questionnaire was used to collect dietary behavior datas, and the Chinese version of Depression Anxiety Stress Scale-21 (DASS-21) was used to assess depressive symptoms. The generalized linear model was used to analyze the association of vegetable and fruit intake with depressive symptoms in students, and stratified analysis was performed according to ethnicity. Results: The detection rate of depressive symptoms among first year junior high school students in Yunnan Province was 29.5%. The detection rates of depressive symptoms in Han and minority first year junior high school students were 26.9% and 31.6%. After controlling for demographic variables such as gender, age, family residence and other confounding factors, the generalized linear model analysis results showed that the intake of leafy vegetables ( β= -0.07 , 95%CI =-0.12 to -0.01), flat fruits ( β=-0.06, 95%CI =-0.12 to -0.00) and hot natured fruits ( β=0.11, 95%CI = 0.04- 0.17) were associated with depressive symptoms in Han first year junior high school students (all P <0.05). The intake of melon and fruit vegetables ( β=-0.06, 95%CI =-0.11 to -0.01) and hot natured fruits ( β=0.06, 95%CI =0.01-0.12) were associated with depressive symptoms in ethnic minority first year junior high school students (both P <0.05). Conclusions The intake of vegetables and fruits among multi ethnic first year junior high school students in Yunnan Province is related to the risk of depressive symptoms. It is suggested to strengthen the consumption guidance and education of vegetables and fruits to prevent depressive symptoms among first year junior high school students.

Objective To investigate the association between the Chinese visceral adiposity index (CVAI) and diabetes mellitus, hypertension, diabetes mellitus or hypertension, and diabetes with hypertension among elderly people in Hebei Province. Methods In 2020, a stratified multi-stage random sampling was used to conduct questionnaire survey, physical examination and laboratory detection among permanent residents of 10 monitoring sites in Hebei Province. Logistic regression was used to analyze the association between CVAI and diabetes mellitus, hypertension, diabetes mellitus or hypertension, and diabetes with hypertension. The area under the ROC curve (AUC) was used to evaluate the predictive value of CVAI for diabetes mellitus, hypertension, diabetes mellitus or hypertension, and diabetes with hypertension. Results The detection rates of diabetes mellitus, hypertension, diabetes mellitus or hypertension, and diabetes with hypertension were 19.8%, 74.6%, 78.2%, and 16.2%, respectively. Multivariate logistic regression analysis showed that compared with the lowest quartile of CVAI group Q1, the OR (95% CI) of diabetes mellitus, hypertension, diabetes mellitus or hypertension, and diabetes with hypertension in the highest quartile Q4 group were 3.55 (2.58~4.89), 2.52 (1.92~3.31), 3.09 (2.31~4.12), and 4.92 (3.40~7.12), respectively. The ROC curve results showed that CVAI had the best predictive value in the diagnosis of diabetes with hypertension, and the optimized critical values in males and females were 128.54 and 141.88, respectively. Conclusion The detection rates of diabetes mellitus and hypertension are high in the elderly population in Hebei Province. CVAI is positively associated with the risk of diabetes mellitus, hypertension, diabetes mellitus or hypertension, and diabetes with hypertension among the elderly in Hebei. CVAI has the strongest prediction ability for diabetes with hypertension.

Andrographolide sulfonate (AS) is a sulfonated derivative of andrographolide extracted from Andrographis paniculata (Burm.f.) Nees, and has been approved for several decades in China. The present study aimed to investigate the novel therapeutic application and possible mechanisms of AS in the treatment of rheumatoid arthritis. Results indicated that administration of AS by injection or gavage significantly reduced the paw swelling, improved body weights, and attenuated pathological changes in joints of rats with adjuvant-induced arthritis. Additionally, the levels of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and IL-1β in the serum and ankle joints were reduced. Bioinformatics analysis, along with the spleen index and measurements of IL-17 and IL-10 levels, suggested a potential relationship between AS and Th17 cells under arthritic conditions. In vitro, AS was shown to block Th17 cell differentiation, as evidenced by the reduced percentages of CD4⁺ IL-17A⁺ T cells and decreased expression levels of RORγt, IL-17A, IL-17F, IL-21, and IL-22, without affecting the cell viability and apoptosis. This effect was attributed to the limited glycolysis, as indicated by metabolomics analysis, reduced glucose uptake, and pH measurements. Further investigation revealed that AS might bind to hexokinase2 (HK2) to down-regulate the protein levels of HK2 but not glyceraldehyde-3-phosphate dehydrogenase (GAPDH) or pyruvate kinase M2 (PKM2), and overexpression of HK2 reversed the inhibition of AS on Th17 cell differentiation. Furthermore, AS impaired the activation of phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signals in vivo and in vitro, which was abolished by the addition of lactate. In conclusion, AS significantly improved adjuvant-induced arthritis (AIA) in rats by inhibiting glycolysis-mediated activation of PI3K/AKT to restrain Th17 cell differentiation.
Animals ; Th17 Cells/immunology* ; Diterpenes/pharmacology* ; Arthritis, Rheumatoid/metabolism* ; Proto-Oncogene Proteins c-akt/immunology* ; Glycolysis/drug effects* ; Cell Differentiation/drug effects* ; Phosphatidylinositol 3-Kinases/genetics* ; Rats ; Male ; Rats, Sprague-Dawley ; Humans ; Andrographis paniculata/chemistry* ; Arthritis, Experimental/drug therapy* ; Interleukin-17/immunology* ; Signal Transduction/drug effects*

Objective To investigate the association between antenatal white blood cell count(WBC)and the risk of histological chorioamnionitis(HCA)in pregnant women with late pregnancy premature rupture of membranes(PROM).Methods A retrospective analysis was performed on totally 118 pregnant women with PROM in late pregnancy from March 2018 to August 2021 in the hospital.They were divided into HCA group and non-HCA group according to the presence or absence of HCA.The general clinical data,laboratory indica-tors and delivery outcomes of the two groups were compared.Univariate and multivariate Logistic regression were used to analyze the association between prenatal WBC and HCA risk.Generalized additive models were used for curve fitting,and segmented regression models were used to further explain the nonlinear relationship between maternal prenatal WBC and HCA risk.Results The prenatal WBC of the HCA group was signifi-cantly higher than that of the non-HCA group(P＜0.001).After adjusting for covariates,elevated prenatal WBC increased the risk of HCA,with an OR of 1.190(95％CI:1.006-1.406,P=0.042).Curve fitting showed that there was a nonlinear relationship between prenatal WBC and HCA risk,and the log-likelihood ratio test of WBC at the inflection point 13.5×109/L(95％CI:11.75-14.56)was statistically significant(P=0.029).For the three groups of prenatal WBC,the risk of HCA in pregnant women gradually increased with the increase of WBC level,which was 0.314(95％CI:0.200-0.456)in the normal group,0.439(95％CI:0.252-0.645)in the high group,and 0.682(95％CI:0.354-0.893)in the elevated group.Conclusion The higher the prenatal WBC of pregnant women with PROM in late pregnancy,the greater the risk of HCA,but there is no simple linear relationship between the two,and there is a threshold effect.

Objective: To construct and validate a prognostic model for lung cancer based on acrolein-related genes using bioinformatics methods . Methods: Lung cancer datasets GSE30219 and GSE68465 were obtained from the GEO database , and acrolein-related gene sets were retrieved from the CTD database . Differentially expressed genes (DEGs) between cancer and adjacent tissues were identified in the GSE30219 dataset. The intersection of these DEGs and acrolein-related genes was then used to identify candidate genes . Gene set variation analysis ( GSVA) was performed to assess functional alterations based on the intersection genes . A protein-protein interaction (PPI) network was constructed based on the STRING database to identify core hub genes . Subsequently , support vector machine recursive feature elimination (SVM-RFE) and LASSO-Cox regression analyses were employed to develop a prognostic model based on acrolein-related genes , which was independently validated using the GSE68465 dataset. The CIBERSORT algorithm was applied to evaluate the immune cell infiltration characteristics between high- and low-risk groups , and functional enrichment analysis of DEGs between the two groups was conducted to further ex- plore the potential molecular mechanisms underlying the prognostic model . Results : A total of 361 acrolein-related DEGs were identified in lung cancer , and 7 key genes were selected for model construction . Kaplan-Meier survival analysis revealed that patients in the high-risk group had significantly lower survival rates compared to those in the low-risk group (P < 0. 000 1) . Receiver operating characteristic (ROC) curve analysis demonstrated that the mod- el possessed good predictive performance . Moreover , immune infiltration analysis indicated that the risk score was closely associated with multiple immune cell subsets , suggesting a potential role of acrolein-related genes in modula- ting the lung cancer immune microenvironment. Conclusion The prognostic model for lung cancer based on acro- lein-related genes demonstrates significant application value in predicting the prognosis of lung cancer , providing new insights into the potential mechanisms of acrolein in the onset and progression of lung cancer.

Bone formation and deposition are initiated by sensory nerve infiltration in adaptive bone remodeling. Here, we focused on the role of Semaphorin 3A (Sema3A), expressed by sensory nerves, in mechanical loads-induced bone formation and nerve withdrawal using orthodontic tooth movement (OTM) model. Firstly, bone formation was activated after the 3rd day of OTM, coinciding with a decrease in sensory nerves and an increase in pain threshold. Sema3A, rather than nerve growth factor (NGF), highly expressed in both trigeminal ganglion and the axons of periodontal ligament following the 3rd day of OTM. Moreover, in vitro mechanical loads upregulated Sema3A in neurons instead of in human periodontal ligament cells (hPDLCs) within 24 hours. Furthermore, exogenous Sema3A restored the suppressed alveolar bone formation and the osteogenic differentiation of hPDLCs induced by mechanical overload. Mechanistically, Sema3A prevented overstretching of F-actin induced by mechanical overload through ROCK2 pathway, maintaining mitochondrial dynamics as mitochondrial fusion. Therefore, Sema3A exhibits dual therapeutic effects in mechanical loads-induced bone formation, both as a pain-sensitive analgesic and a positive regulator for bone formation.
Humans ; Bone Remodeling ; Cell Differentiation ; Osteogenesis ; Semaphorin-3A/pharmacology* ; Trigeminal Ganglion/metabolism*

Objective:Laboratory evaluation of the relationship between cerebrospinal fluid and plasma indicators and intrathecal immunoglobulin G(IgG) synthesis in patients with neurological diseases, and establishment of a new diagnostic method for intrathecal IgG synthesis.Methods:This study retrospectively analyzed the content of IgG in cerebrospinal fluid samples and blood albumin in blood samples, and other test results of 410 patients with neurological diseases who visited Beijing Tiantan Hospital from 2019 to 2022. According to the results of oligoclonal bands in cerebrospinal fluid, patients were divided into intrathecal IgG synthesis group and non-intrathecal IgG synthesis group. The Mann Whitney U test was used for inter group comparison, and a bilateral test with P<0.05 indicates a statistically significant difference. Include indicators with differences between groups in logistic regression analysis, construct a predictive model, and compare it with the established quantitative formula IgG index. Results:There were significant differences in 10 indicators, including cerebrospinal fluid leukocyte count and 24-hour intrathecal IgG synthesis rate, between the intrathecal IgG synthesis group and the non-intrathecal IgG synthesis group, with P<0.05. The area under the curve (AUC) of intrathecal IgG synthesis was higher than the IgG index (AUC=0.920, 0.809, Z=31.178, P<0.001), the sensitivity was higher than the IgG index (0.825, 0.618), and the specificity was lower than the IgG index (0.876, 0.908). Conclusion:The combination of 10 indicators such as cerebrospinal fluid white blood cell count and 24-hour intrathecal IgG synthesis rate can improve the diagnostic efficacy and sensitivity of intrathecal IgG synthesis.

ObjectiveTo study the effects of Buyang Huanwutang on the skeletal muscle injuries in type 2 diabetes mellitus from mitochondrial transport， glucose metabolism， oxidative stress， and inflammation. MethodA total of 60 SPF-grade male C57BL/6J mice were selected in this study. The mouse model of type 2 diabetes mellitus was established with a high-fat diet combined with intraperitoneal injection of streptozotocin. The mice were assigned by the random number table method into blank control， model， high-， medium-， and low-dose （86.5， 43.2， 21.6 g·kg^-1， respectively） Buyang Huanwutang， and metformin （150 mg·kg^-1） groups， 10 mice in each group. During the experiment period， blood glucose and other indicators of mice were measured regularly. At the end of the experiment， skeletal muscle samples were collected and frozen in 4% paraformaldehyde and -80 ℃， respectively. Blood samples were sent for examination. The skeletal muscle was stained with hematoxylin-eosin. The levels of inflammation indicators and reactive oxygen species （ROS） were determined by enzyme-linked immunosorbent assay. The expression of mitochondrial proteins was determined by Western blot and immunohistochemistry. ResultCompared with the blank control group， the model group showcased increased fasting blood glucose， water intake， and food intake （P<0.01） and decreased body weight （P<0.01）. Compared with the model group， metformin and Buyang Huanwutang reduced the fasting blood glucose， water intake， and food intake （P<0.05， P<0.01） and increased the body weight （P<0.01）. Compared with the blank control group， the model group showed rising levels of tumor necrosis factor-alpha （TNF-α）， interleukin-6 （IL-6）， and ROS （P<0.01）， which were decreased by metformin and Buyang Huanwutang （P<0.05， P<0.01）. The skeletal muscle fibers in the model group were generally atrophic and thin， which suggested atrophy and morphological changes of the skeletal muscle， while metformin and Buyang Huanwutang alleviated the pathological changes of the skeletal muscle and restored the morphology of fiber bundles. Compared with the blank control group， the modeling down-regulated the expression of the mitofusin2 （Mfn2） （P<0.01）， which was up-regulated by metformin and Buyang Huanwutang （P<0.05， P<0.01）. Compared with the blank control group， the modeling up-regulated the expression of the dynamin-related protein （Drp1） （P<0.01）， which were down-regulated by metformin and Buyang Huanwutang （P<0.01）. ConclusionBuyang Huanwutang can improve the body weight and attenuate the pathological changes of the skeletal muscle， reduce fasting blood glucose， food intake， and water intake， lower the levels of TNF-α， IL-6， and ROS， down-regulate the expression of Drp1， and up-regulate the expression of Mfn2 in the mouse model of type 2 diabetes mellitus.

BACKGROUND:Cerebral ischemic stroke is one of the main fatal and disabling diseases in the clinic,but only a few patients benefit from vascular recanalization in time,so it is urgent to explore new and effective therapy.As one of the critical pathological changes of ischemic stroke,the glial scar formed mainly by astrocytes is one major cause that hinders axonal regeneration and neurological recovery at the late stage of stroke. OBJECTIVE:To elucidate the pathological process and crucial signal regulatory mechanism of astrocytes in the formation of glial scar after ischemic stroke,as well as the potential therapeutic targets,to provide a theoretical reference for intervening astrocytic scar formation against ischemic stroke effectively,and novel strategies for promoting post-stroke rehabilitation. METHODS:The relevant articles published in CNKI,PubMed and Web of Science databases from 2010 to 2022 were retrieved.The search terms were"Ischemic stroke,Brain ischemi*,Cerebral ischemi*,Astrocyt*,Astroglia*,Glial scar,Gliosis,Astrogliosis"in Chinese and English.Finally,78 articles were included after screening and summarized. RESULTS AND CONCLUSION:(1)Astrocytes play an important role in the maintenance of central nervous system homeostasis.After ischemic stroke,astrocytes change from a resting state to an active state.According to the different severities of cerebral ischemic injury,astrocyte activation changes dynamically from swelling and proliferation to glial scar formation.(2)Mature astrocytes are stimulated to restart the cell cycle,then proliferate and migrate to lesions,which is the main source of the glial scar.Neural stem cells in the subventricular zone,neuron-glial antigen 2 precursor cells and ependymal precursor cells in the brain parenchyma can also differentiate into astrocytes.Endothelin-1,aquaporin 4,ciliary neurotrophic factor and connexins are involved in this process.In addition,chondroitin sulfate proteoglycan,as the main component of the extracellular matrix,forms the dense glial scar barrier with proliferated astrocytes,which hinders the polarization and extension of axons.(3)Activation or inhibition of crucial signal molecules involved in astrocyte activation,proliferation,migration and pro-inflammation functions regulate the glial scar formation.Transforming growth factor beta 1/Smad and Janus kinase/signal transducer and activator of transcription 3 are classical pathways related to astrogliosis,while receptor-interacting protein 1 kinase and glycogen synthase kinase 3β are significant molecules regulating the inflammatory response.However,there are relatively few studies on Smad ubiquitination regulatory factor 2 and Interleukin-17 and their downstream signaling pathways in glial scar formation,which are worthy of further exploration.(4)Drugs targeting astrogliosis-related signaling pathways,cell proliferation regulatory proteins and inflammatory factors effectively inhibit the formation of glial scar after cerebral ischemic stroke.Among them,the role of commonly used clinical drugs such as melatonin and valproic acid in regulating glial scar formation has been verified,which makes it possible to use drugs that inhibit glial scar formation to promote the recovery of neurological function in patients with stroke.(5)Considering the protective effects of glial scar in the acute phase,how to choose the appropriate intervention chance of drugs to maintain the protective effect of the glial scar while promoting nerve regeneration and repair in the local microenvironment is the direction of future efforts.