ObjectiveTo investigate the therapeutic effects and mechanisms of Qinlian Hongqutang （QLHQT） on nonalcoholic steatohepatitis （NASH）. MethodsC57BL/6J mice were randomly divided into normal and modeling groups. The NASH model was established by feeding a high-fat diet for 12 weeks. After successful modeling， mice were randomly assigned to the model group， low-， medium-， and high-dose QLHQT groups （0.51， 1.02， and 2.04 g·kg^-1）， and a positive control metformin group， with six mice in each group. The mice were treated for 8 weeks. Body weight was recorded before and after treatment. Serum levels of total cholesterol （TC）， triglycerides （TG）， and low-density lipoprotein cholesterol （LDL-C）， as well as hepatic TC， TG， and LDL-C contents， were determined by biochemical assays. Hematoxylin-eosin （HE） staining and oil red O staining were used to evaluate liver histopathology and lipid deposition， respectively. Flow cytometry， enzyme-linked immunosorbent assay （ELISA）， and Real-time polymerase chain reaction （Real-time PCR） were used to assess hepatic macrophage expression and related markers. Western blot and immunofluorescence were used to investigate the potential mechanisms of QLHQT in regulating macrophage polarization. ResultsCompared with the normal group， body weight and serum and hepatic levels of TC， TG， and LDL-C were significantly increased in the model group （P<0.01）. Liver histopathology showed unevenly distributed round lipid droplets in the hepatocyte cytoplasm， accompanied by inflammatory cell aggregation. Flow cytometry showed that the proportion of CD86-positive cells was significantly increased， whereas the proportion of CD206-positive cells was markedly decreased （P<0.05）. Hepatic inducible nitric oxide synthase （iNOS） levels and tumor necrosis factor-α （TNF-α） mRNA expression were significantly increased， while hepatic IL-10 levels and IL-4 mRNA expression were significantly decreased （P<0.01）. The protein expression levels of Toll-like receptor 4 （TLR4）， tumor necrosis factor receptor-associated factor 6 （TRAF6）， and myeloid differentiation factor 88 （MyD88） in the liver were significantly increased （P<0.01）. Compared with the model group， body weight was reduced in the high-， medium-， and low-dose QLHQT groups and in the metformin group. Serum and hepatic TC， TG， and LDL-C levels were significantly decreased （P<0.01）. Liver histopathology showed alleviated hepatic lipid deposition， with markedly reduced lipid droplets and inflammation. Immunofluorescence and flow cytometry showed that the proportions of CD86-positive cells were significantly decreased， whereas the proportions of CD206-positive cells were significantly increased in the high-， medium-， and low-dose QLHQT groups （P<0.05）. Hepatic iNOS levels and TNF-α mRNA expression were significantly decreased （P<0.01）， whereas hepatic IL-10 levels and IL-4 mRNA expression were significantly increased （P<0.01）. The hepatic protein expression levels of TLR4， TRAF6， and MyD88 were significantly decreased， while signal transducer and activator of transcription 6 （STAT6） phosphorylation was significantly increased （P<0.05， P<0.01）. There was no statistically significant difference in total STAT6 protein expression. ConclusionQLHQT effectively ameliorates hepatic inflammation in NASH mice， and the mechanism may involve STAT6- and TLR4-mediated signaling pathways driving polarization of M1 macrophages toward the M2 phenotype.

ObjectiveTo investigate the therapeutic effects and mechanisms of Qinlian Hongqutang （QLHQT） on nonalcoholic steatohepatitis （NASH）. MethodsC57BL/6J mice were randomly divided into normal and modeling groups. The NASH model was established by feeding a high-fat diet for 12 weeks. After successful modeling， mice were randomly assigned to the model group， low-， medium-， and high-dose QLHQT groups （0.51， 1.02， and 2.04 g·kg^-1）， and a positive control metformin group， with six mice in each group. The mice were treated for 8 weeks. Body weight was recorded before and after treatment. Serum levels of total cholesterol （TC）， triglycerides （TG）， and low-density lipoprotein cholesterol （LDL-C）， as well as hepatic TC， TG， and LDL-C contents， were determined by biochemical assays. Hematoxylin-eosin （HE） staining and oil red O staining were used to evaluate liver histopathology and lipid deposition， respectively. Flow cytometry， enzyme-linked immunosorbent assay （ELISA）， and Real-time polymerase chain reaction （Real-time PCR） were used to assess hepatic macrophage expression and related markers. Western blot and immunofluorescence were used to investigate the potential mechanisms of QLHQT in regulating macrophage polarization. ResultsCompared with the normal group， body weight and serum and hepatic levels of TC， TG， and LDL-C were significantly increased in the model group （P<0.01）. Liver histopathology showed unevenly distributed round lipid droplets in the hepatocyte cytoplasm， accompanied by inflammatory cell aggregation. Flow cytometry showed that the proportion of CD86-positive cells was significantly increased， whereas the proportion of CD206-positive cells was markedly decreased （P<0.05）. Hepatic inducible nitric oxide synthase （iNOS） levels and tumor necrosis factor-α （TNF-α） mRNA expression were significantly increased， while hepatic IL-10 levels and IL-4 mRNA expression were significantly decreased （P<0.01）. The protein expression levels of Toll-like receptor 4 （TLR4）， tumor necrosis factor receptor-associated factor 6 （TRAF6）， and myeloid differentiation factor 88 （MyD88） in the liver were significantly increased （P<0.01）. Compared with the model group， body weight was reduced in the high-， medium-， and low-dose QLHQT groups and in the metformin group. Serum and hepatic TC， TG， and LDL-C levels were significantly decreased （P<0.01）. Liver histopathology showed alleviated hepatic lipid deposition， with markedly reduced lipid droplets and inflammation. Immunofluorescence and flow cytometry showed that the proportions of CD86-positive cells were significantly decreased， whereas the proportions of CD206-positive cells were significantly increased in the high-， medium-， and low-dose QLHQT groups （P<0.05）. Hepatic iNOS levels and TNF-α mRNA expression were significantly decreased （P<0.01）， whereas hepatic IL-10 levels and IL-4 mRNA expression were significantly increased （P<0.01）. The hepatic protein expression levels of TLR4， TRAF6， and MyD88 were significantly decreased， while signal transducer and activator of transcription 6 （STAT6） phosphorylation was significantly increased （P<0.05， P<0.01）. There was no statistically significant difference in total STAT6 protein expression. ConclusionQLHQT effectively ameliorates hepatic inflammation in NASH mice， and the mechanism may involve STAT6- and TLR4-mediated signaling pathways driving polarization of M1 macrophages toward the M2 phenotype.

Objective: To explore the relationship between school sports environment and physical activity levels of middle school students, so as to provide theoretical and empirical support for optimizing school sports environment and enhance adolescent physical activity. Methods: Using multi-stage random cluster sampling, from September to December 2023, 1 329 junior and senior high school students from Xuancheng City of Anhui Province, Lianyungang City of Jiangsu Province, Wuhan City of Hubei Province, Qiqihar City and Suihua City of Heilongjiang Province, and Shenzhen City of Guangdong Province were selected. The International Physical Activity Questionnaire-Short Form (IPAQ-SF) assessed students physical activity levels, and the questionnaire on the characteristics of school sports environment was developed to evaluate the factors of school sports environment. Multivariate ordered Logistic regression was performed to analyze the correlation between school sports environment factors and physical activity levels, and the analytic hierarchy process determined the weight of key influencing factors. Results: The results showed that weekly vigorous physical activity time was [60 (25, 90)] minutes, moderate physical activity time was [60 (30, 90)] minutes, light physical activity time was [105 (40, 200)] minutes, and sedentary behavior time was [ 3 300 (2 100, 4 500)] minutes, only 10.53% of the students met World Health Organization physical activity recommendations, and 89.69% of the students averaged >8 h daily sedentary time. Multivariate ordered Logistic regression showed that adequate sports equipment significantly promoted physical activity across all intensities and reduced sedentary time ( OR = 4.97, 11.54, 4.03, 0.11); diverse sports activities improved vigorous and moderate physical activity while reducing sedentary time ( OR =4.20, 14.06, 0.17); and peer encouragement was associated with increased low-intensity physical activities and decreased sedentary time ( OR =10.40, 0.15)( P <0.05). The analytic hierarchy process weighting analysis identified the top three influential factors related to physical activity among middle school students: sufficient sports equipment, varied physical education activities, frequent peer encouragement, the influence weight accounts for 23.55% , 14.18% and 11.77% of the total, respectively. Conclusion Key school sports environmental factors for adolescent physical activity level include ensuring adequate sports equipment and class availability, diversifying activity content, fostering peer support, and cultivating an active sports culture and a comprehensive approach encourage students participation in extracurricular physical activities.

The incomplete degradation of tumour cells by macrophages (Mϕ) is a contributing factor to tumour progression and metastasis, and the degradation function of Mϕ is mediated through phagosomes and lysosomes. In our preliminary experiments, we found that overactivation of NADPH oxidase 2 (NOX2) reduced the ability of Mϕ to degrade engulfed tumour cells. Above this, we screened out liquiritin from Glycyrrhiza uralensis Fisch, which can significantly inhibit NOX2 activity and inhibit tumours, to elucidate that suppressing NOX2 can enhance the ability of Mϕ to degrade tumour cells. We found that the tumour environment could activate the NOX2 activity in Mϕ phagosomes, causing Mϕ to produce excessive reactive oxygen species (ROS), thus prohibiting the formation of phagolysosomes before degradation. Conversely, inhibiting NOX2 in Mϕ by liquiritin can reduce ROS and promote phagosome-lysosome fusion, therefore improving the enzymatic degradation of tumour cells after phagocytosis, and subsequently promote T cell activity by presenting antigens. We further confirmed that liquiritin down-regulated the expression of the NOX2 specific membrane component protein gp91 phox, blocking its binding to the NOX2 cytoplasmic component proteins p67 phox and p47 phox, thereby inhibiting the activity of NOX2. This study elucidates the specific mechanism by which Mϕ cannot degrade tumour cells after phagocytosis, and indicates that liquiritin can promote the ability of Mϕ to degrade tumour cells by suppressing NOX2.

The incomplete degradation of tumour cells by macrophages(Mφ)is a contributing factor to tumour progression and metastasis,and the degradation function of Mφ is mediated through phagosomes and lysosomes.In our preliminary experiments,we found that overactivation of NADPH oxidase 2(NOX2)reduced the ability of Mφ to degrade engulfed tumour cells.Above this,we screened out liquiritin from Glycyrrhiza uralensis Fisch,which can significantly inhibit NOX2 activity and inhibit tumours,to elucidate that suppressing NOX2 can enhance the ability of Mφ to degrade tumour cells.We found that the tumour environment could activate the NOX2 activity in Mφ phagosomes,causing Mφ to produce excessive reactive oxygen species(ROS),thus prohibiting the formation of phagolysosomes before degradation.Conversely,inhibiting NOX2 in Mφ by liquiritin can reduce ROS and promote phagosome-lysosome fusion,therefore improving the enzymatic degradation of tumour cells after phagocytosis,and subse-quently promote T cell activity by presenting antigens.We further confirmed that liquiritin down-regulated the expression of the NOX2 specific membrane component protein gp91 phox,blocking its binding to the NOX2 cytoplasmic component proteins p67 phox and p47 phox,thereby inhibiting the activity of NOX2.This study elucidates the specific mechanism by which Mφ cannot degrade tumour cells after phagocytosis,and indicates that liquiritin can promote the ability of Mφ to degrade tumour cells by suppressing NOX2.

Objective:To investigate the effectiveness and safety of domestic upper gastrointestinal endoscopic ultrasound (EUS).Methods:A total of 160 patients undergoing EUS at Shengjing Hospital of China Medical University (Center1) and Shenzhen People's Hospital (Center 2) from March to July 2021 were randomly selected by stratified blocked randomization, and were treated with SonoScape EG-UG5T (the test group) or Fujifilm EG-580UT (the control group). The primary outcome was the ultrasound image quality excellence rate, and the comparison was verified by non-inferiority. The secondary outcomes were the endoscopic image quality excellence rate, the operational performance excellence rate, and the system stability evaluation. The safety evaluation was based on the occurrence of intraoperative and postoperative adverse events in the subjects.Results:In the intention-to-treat analysis set (ITT), the excellence rate of ultrasound image quality in the test group and the control group was 100.0% (78/78) and 100.0% (77/77), respectively. The rate difference between the two groups was 0.0% (95% CI: -4.7%-4.8%). In the per protocol analysis set (PPS), the excellence rate of ultrasound image quality in the test group and the control group was 100.0% (78/78) and 100.0% (75/75), respectively. The rate difference between the two groups was 0.0% (95% CI: -4.7%-4.9%). The lower limit of the confidence interval of ultrasound image quality excellence rate of both data sets was greater than the non-inferiority threshold value of -8%, which inferred that the non-inferiority hypothesis of the test machine non-inferior to the control machine was valid. The endoscopic image quality excellence rate and the operational performance excellence rate of the test group and the control group was 100.0% in both the ITT and PPS analyses, and there was no statistically significant difference between the two groups ( P=1.000). The system instability event rate was 0.0% (0/78) in the test group and 3.9% (3/77) in the control group ( P=0.120). No adverse event occurred in either group. Conclusion:The domestic upper gastrointestinal endoscopic ultrasound is standard-compliant for clinical application under normal conditions in terms of effectiveness, safety, and stability.

Objective To explore the clinical efficacy of marginal liver from elderly donors in liver transplantation. Methods According to the inclusion and exclusion criteria, the clinical data of 127 donors and recipients were retrospectively analyzed. According to the age of donors, 127 donors were divided into the elderly group (n=27) and control group (n=100). The recovery of liver function, the occurrence of postoperative complications and survival rate of the recipients after transplantation were statistically analyzed between two groups. Results The incidence of primary nonfunction (PNF) and initial poor graft function (IPGF) did not significantly differ between the elderly and control groups (both P > 0.05). Within postoperative 2 weeks, the average levels of alanine aminotransferase (ALT) and serum total bilirubin (TB) of liver transplant recipients in the elderly group was not significantly different from those in the control group (both P > 0.05). There was no significant difference in the incidence of postoperative complications in the postoperative elderly group compared with the control group (all P > 0.05). The 1-and 3-year survival rates of the recipients in the elderly group were 84% and 78% respectively, which did not significantly differ from 89% and 79% in the control group (both P > 0.05). Conclusions Strict and sufficient quality evaluation and functional maintenance should be done for elderly donor livers. It can achieve good transplantation results by intraoperative fine operation, reducing bleeding and trauma, shortening the time of cold ischemia and operation, strengthening postoperative monitoring and implementing enhanced recovery after surgery.

Objective To assess the myocardial blood flow and reserve function by rest and stress 13 N-NH3 PET myocardial perfusion imaging ( MPI) , and evaluate the diagnostic value of PET and risk fac-tors of non-obstructive coronary microvascular disease ( CMVD) type 1. Methods A total of 56 patients (28 males, 28 females;age:(52.0±7.6) years) with clinical suspected CMVD type 1 from April 2017 to December 2018 were prospectively enrolled. The coronary CT angiography, coronary angiography and other clinical data were recorded. All patients underwent one-day rest and stress 13 N-NH3 PET MPI. Images were analyzed and the absolute myocardial blood flow ( MBF) and coronary flow reserve ( CFR) were obtained. Patients were divided into CMVD type 1 ( CMVD) group and non-CMVD group. The differences between 2 groups were analyzed by two-sample t test and logistic regression. Results Among 56 patients, 20 patients were diagnosed as CMVD type 1, and 36 patients were excluded as non-CMVD group. The proportion of smoking and diabetes in the CMVD group was significantly higher than that in the non-CMVD group (χ2 val-ues:9.433 and 4.114, both P<0.05). The stress MBF ((2.37±0.61) vs (3.83±1.25) ml·min-1·g-1;t=-4.807, P<0.001) and CFR (2.67±0.60 vs 3.81±0.96;t=-4.751, P<0.001) were lower in smokers than those in non-smokers, and the stress MBF was lower in diabetes patients than that in non-diabetes patients ((2.63±0.98) vs (3.62±1.28) ml·min-1·g-1;t=-2.758, P=0.008). Smoking might be the risk factor for lower stress MBF (odd ratio (OR)=0.310, 95％ CI:0.114-0.880) and lower CFR (OR=0.278, 95％ CI:0. 080-0.894), and diabetes might be the risk factor for lower stress MBF (OR=0.254, 95％ CI:0.073-0. 887) . Conclusions PET MPI can be used for the diagnosis of CMVD type 1. Smoking and diabetes are likely to be associated with the onset of CMVD type 1.