Objective : To explore the mechanism of isorhamnetin (Iso) in the treatment of oral squamous cell carcinoma (OSCC) using network pharmacology and molecular docking methods and to verify it in vitro. Methods : The key targets were obtained by constructing the PPI protein interaction network based on the common intersection targets of Iso-OSCC. At the same time, gene ontology (GO) and Kyoto encyclopedia of genes and genomes (KEGG) were used to analyze the related signaling pathways of the intersection targets. Iso and core targets were also analyzed through molecular docking and visualization. Colony formation assay and Transwell assay were used to identify the effect of Iso on the proliferation and invasion of Cal-27 cells. Western blot was used to analyze the regulatory effects of different concentrations of Iso on estrogen receptor-1 (ESR1), phosphoinositide-3-kinase regulatory subunit-1 (PIK3R1), Src tyrosine kinase (SRC), and phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signaling pathway proteins. Results: A total of 269 potential intersection targets of Iso-regulated OSCC were obtained. According to the degree obtained by topological analysis, PIK3R1, AKT1, SRC, ESR1, and other core targets were screened out. KEGG analysis showed that 165 signaling pathways were enriched in the intersection targets of Iso-OSCC, among which the PI3K/AKT signaling pathway played an important role in the treatment of OSCC with Iso. Molecular docking results showed that the absolute value of binding energy between target proteins PIK3R1, AKT1, SRC, ESR1, and Iso was high. After Cal-27 cells were treated with Iso, the number of cell colony formations, the number of transmembrane cells, and the expression of PIK3R1, ESR1, SRC, p-PI3K, and p-AKT were negatively correlated with the increase in Iso concentration (P < 0.05). Conclusion Iso can inhibit PI3K/AKT signal transduction and influence the expression of PIK3R1, AKT1, SRC, and ESR1 proteins, thereby inhibiting the occurrence and development of OSCC.

Objective: To investigate the occupational health status of medical radiation workers in Hangzhou City, so as to provide the basis for their occupational health risk assessment. Methods: Data on medical radiological workers who underwent occupational health examinations from 2021 to 2022 were collected through the Physical Examination Information Management System of the Hangzhou Occupational Disease Prevention and Control Hospital. The physical examination data including blood routine, eye lens, thyroid ultrasound, thyroid function, liver function, renal function and blood lipid were collected, and the abnormal rates of occupational health examinations among workers with different genders, working years and occupational exposure types were analyzed. Results: A total of 3 968 medical radiation workers were investigated, including 2 310 males (58.22%) and 1 658 females (41.78%). There were 2 039 (51.39%), 821 (20.69%) and 1 108 (27.92%) workers with 1-<6, 6-<10 years and 10 years and above of work, respectively. Diagnostic radiology was the predomenant type of exposure, with 2 240 workers accounting for 56.45%. The abnormal rates of thyroid ultrasound and blood lipid were 47.73% and 45.21%, respectively, which were relatively higher than other items. The abnormal rates of micronucleus rate, thyroid ultrasound, thyroid function and renal function were higher in females than in males, while the abnormal rates of lymphocyte count, liver function and blood lipid in males were higher in males than in females (all P<0.05). With the increase of working years, the abnormal rates of micronucleus rate and blood lipid showed upward trends (both P<0.05). There were statistically significant differences in the abnormal rates of thyroid ultrasound, liver function and blood lipid among different occupational exposure types (all P<0.05). Conclusion Long-term low-dose ionizing radiation environment affects the thyroid, micronucleus rate and blood lipid of medical radiation workers in Hangzhou City, with differences observed among workers with different genders and occupational exposure types.

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 explore the correlation between cardiac remodeling and the occurrence of contrast-associated acute kidney injury(CA-AKI)assessed by echocardiography.Methods A retrospective analysis was conducted on the clinical data of 100 patients with coronary artery disease(CAD)who underwent coronary angiography(CAG)and percutaneous coronary intervention(PCI)from March 2021 to March 2024.The patients were divided into CA-AKI group and non-CA-AKI group according to whether CA-AKI occurred.Baseline data and echocardiographic parameters,inclu-ding left ventricular end-diastolic internal diameter index(LVIDDI),left ventricular end-systolic in-ternal diameter index(LVIDSI),and left ventricular mass index(LVMI),were collected and com-pared between the two groups.Logistic regression analysis was used to screen for independent influen-cing factors of CA-AKI occurrence.Results The level of N-terminal pro-B-type natriuretic peptide(NT-proBNP)in the CA-AKI group was higher than that in the non-CA-AKI group,and the difference was statistically significant(P＜0.001).Compared with the non-CA-AKI group,the CA-AKI group had higher levels of C-reactive protein and glycosylated hemoglobin(HbA1c),as well as a higher proportion of patients with diabetes and anemia,and the differences were statistically significant(P＜0.05).Echocardiographic data showed that LVMI,LVIDDI,and LVIDSI in the CA-AKI group were all higher than those in the non-CA-AKI group,and the differences were statistically sig-nificant(t=2.057,3.429,2.975;P＜0.05).The left ventricular ejection fraction(LVEF)level in the CA-AKI group was lower than that in the non-CA-AKI group,and the difference was statisti-cally significant(t=3.005,P=0.003).Univariate Logistic regression analysis showed that diabe-tes,anemia,inflammation,NT-proBNP,HbA1c,LVMI,LVIDDI,LVIDSI,LVEF,ventricular hy-pertrophy,and ventricular dilation were significantly associated with the occurrence of CA-AKI(P＜0.05).Multivariate Logistic regression analysis results showed that LVMI(OR=3.81;95％CI,1.04 to 8.50;P=0.045),LVIDDI(OR=4.21;95％CI,2.02 to 6.08;P＜0.001),LVIDSI(OR=1.61;95％CI,1.27 to 2.03;P=0.024),ventricular hypertrophy(OR=3.42;95％CI,1.83 to 4.44;P=0.001),and ventricular dilation(OR=2.93;95％CI,1.43 to 3.74;P=0.033)were independent influencing factors for the occurrence of CA-AKI.Conclusion Cardiac remodeling is significantly correlated with the risk of CA-AKI in CAD patients.Clinicians should take protective measures timely for patients with abnormal cardiac structure to prevent the occurrence of CA-AKI.

Objective: To investigate the role of murine double minute 2(MDM2) in dihydroartemisinin′s(DHA) inhibition of lung adenocarcinoma cell proliferation and migration. Methods: CCK8 assay was used to detect the inhibitory effect of gradient concentrations of DHA(0, 5, 10, 25, 50 and 100 μmol/L) and time gradients(0, 24, 48, and 72 h) on the proliferation of lung adenocarcinoma A549 and PC9 cells, and the half maximal inhibitory concentrate(IC50) were calculated respectively. Colony formation and scratch assays were used to detect the inhibitory effects of DHA on colony formation and migration of A549 and PC9 cells. Western blot was used to detect the inhibitory effects of DHA on MDM2 expression and epithelial-mesenchymal transition(EMT)-related proteins E-cadherin and N-cadherin. The promoting effects of MDM2 on proliferation, migration and EMT of lung adenocarcinoma cells were verified by small interfering RNA-mediated knockdown of MDM2(si-MDM2). The reversal effects of MDM2 overexpression on DHA′s inhibition on the proliferation and migration of A549 and PC9 cells were observed. Results: DHA inhibited the proliferation of A549 and PC9 cells in a dose⁃ and time⁃dependent manner,with IC50 values of 30. 57 and 78. 61 μmol/L , respectively. Compared with the Control group , A549 and PC9 cells had significantly decreased colony formation (both P < 0. 01) and migration (both P < 0. 01) upon treatment with DHA. Moreover, DHA significantly inhibited the protein expression levels of MDM2 and N ⁃cadherin in A549 and PC9 cells , and upregulated the expression of E ⁃cadherin protein (both P < 0. 05) . Compared with si⁃Control ,si⁃MDM2 significantly inhibited the protein levels of MDM2 and N ⁃cadherin in A549 and PC9 cells , and upregulat⁃(both P < 0. 01) of both cells. After overexpression of MDM2 in A549 and PC9 cells , the proliferation and migra⁃ tion ability were significantly enhanced (both P < 0. 05) , and the inhibitory effects of DHA were partially reversed by MDM2 overexpression (both P < 0. 05) . Conclusion DHA effectively inhibits the proliferation and migration of lung adenocarcinoma cells , and its mechanism is associated with the suppression of MDM2.

Nonalcoholic fatty liver disease （NAFLD） is a multisystem disease associated with obesity， insulin resistance， and dyslipidemia and has a complex pathogenesis. Studies have shown that gut microbiota dysbiosis is closely associated with the onset of NAFLD， and traditional Chinese medicine treatment can improve the laboratory markers and clinical symptoms of NAFLD patients by regulating intestinal microbiota and its metabolites. This article elaborates on the association between NAFLD and gut microbiota， the involvement of gut microbiota dysbiosis in the pathogenesis of NAFLD， and the possible mechanism of traditional Chinese medicine treatment in improving NAFLD from the perspective of gut microbiota， in order to provide new ideas for the treatment of NAFLD.

Objective: The study aims to analyze the prevalence and associated factors of myopia among 4 to 9 grade students in Guangdong Province in 2022, so as to provide a scientific basis for targeted intervention measures for myopia in children and adolescents. Methods: From September to October 2022, stratified cluster random sampling was used to select 29 095 of 4 to 9 grade students from Guangzhou, Jiangmen, and Meizhou in Guangdong Province for myopia screening and questionnaire surveys. The Chisquare test was applied to compare the differences between groups, and multivariable Logistic stepwise regression analysis was used to analyze factors associated with myopia. Results: The myopia detection rate of 4 to 9 grade students was 61.7%, with detection rates of 51.5% for 4 to 6 grade primary school students and 71.95% for 7 to 9 grade junior high school students. Multivariable Logistic regression analysis showed that higher myopia rates were detected among girls (OR=1.39, 95%CI=1.30-1.49), students with one (OR=1.82, 95%CI=1.69-1.96) or both parents having myopia (OR=2.86, 95%CI=2.56-3.18), and indoor sedentary time >6 h(OR=1.28, 95%CI=1.17-1.39) in the 4 to 6 grade. Lower myopia rates were detected in the county (OR=0.92, 95%CI=0.86-0.99) and outdoors at recess activities (OR=0.88, 95%CI=0.81-0.95). Meanwhile, higher myopia rates were detected among girls (OR=1.84, 95%CI=1.69-1.99), students with one (OR=1.87, 95%CI=1.71-2.04) or both parents having myopia (OR=3.03, 95%CI=2.63-3.50), and indoor sedentary time >6 h/d (OR=1.11, 95%CI=1.01-1.23) in the 7 to 9 grade. Lower myopia rates were detected in the county (OR=0.74, 95%CI=0.68-0.80), outdoors at recess activities (OR=0.83, 95%CI=0.76-0.91), and outdoor activity time ≥2 h/d(OR=0.87, 95%CI=0.80-0.95)(P<0.05). Conclusions The detection rate of myopia among 4 to 9 grade students in Guangdong Province is relatively high. Place of recess activities, daily outdoor activity and indoor sedentary duration are associated with myopia. Therefore, targeted intervention measures should be adopted, such as appropriately increasing outdoor activity to reduce the occurrence of myopia among primary and middle school students.

Hyperkalemia is one of the common ion metabolism disorders in clinical practice. Hyperkalemia is defined as serum potassium higher than 5.0 mmol/L according to the guidelines at home and abroad. Acute severe hyperkalemia can cause serious consequences, such as flaccid paralysis, fatal arrhythmia, and even cardiac arrest. The use of renin-angiotensin- aldosterone system inhibitors, β-blockers and diuretics, low-sodium and high-potassium diets, and the presence of related comorbidities increase the occurrence of hyperkalemia. Hyperkalemia risk exist in all clinical departments, but there is a lack of a standardization in the management of multi- department cooperation in hospital. Therefore, a number of domestic nephrology and cardiology department experts have discussed a management model for multi-department cooperation in hyperkalemia, formulating the management standard on hospital evaluation, early warning, diagnosis and treatment, and process. This can promote each department to more effectively participate in nosocomial hyperkalemia diagnosis and treatment, as well as the long-term management of chronic hyperkalemia, improving the quality of hyperkalemia management in hospital.

Objective:To investigate the pharmacological basis and mechanism of Anti-cancer Essence Formula in the treatment of gastric cancer based on network pharmacology,and to provide bioinformatics basis for the clinical treatment of gastric cancer with traditional Chinese medicine.Methods:The active ingredients of Anti-cancer Essence Formula were searched in TCMSP database,and the targets of the active ingredients were further obtained using UniProt database.The targets of gastric cancer were obtained using GeneCards,OMIM and TTD databases.Cytoscape 3.9.1 software was used to build the"Disease-Component-Target"network.String database and Cytoscape 3.9.1 software were used to construct the PPI network.The transcript levels of the core genes were analyzed by UALCAN database,and the relationship between core gene expression and patient survival was analyzed by Kaplan-Meier plotter.GO function and KEGG pathway enrichment analyses were performed by DAVID database.Results:There were 236 active ingredients of Anti-Cancer Essence Formula,and 16 key targets were screened by PPI network.MAPK3,MAPK1,RELA,AKT1,TP53,FOS,MAPK14,RXRA,MAPK8 and EGFR were abnormally expressed in gastric cancer tissues(P＜0.05),and all of them showed correlation with the prognosis of gastric cancer patients(P＜0.05).GO analysis was mainly enriched in cell division,cell proliferation and apoptosis,and KEGG analysis was mainly enriched in cancer pathway,MAPK signaling pathway,Relaxin signaling pathway,TNF signaling pathway,T-cell receptor signaling pathway,Prolactin signaling pathway,and PI3K-Akt signaling pathway.Conclusion:Anti-cancer Essence Formula is characterized by the synergistic effect of multi-components,multi-targets,and multi-pathways.It mainly acts on the targets of MAPK3,MAPK1,RELA,AKT1,TP53,FOS,MAPK14,RXRA,MAPK8,and EGFR through the active ingredients such as quercetin,kaempferol,β-sitosterol,and racemic carvacrol.It also regulates the signaling pathways of MAPK,Relaxin,TNF,T-cell receptor,Prolactin,and PI3K-Akt.