0 05). In PCI group,the balloon inflation time, the highest inflation pressure and the number of placed stents in the patients with the increased level of cTnI had not significant difference compared with those in the patients without the increased level of cTnI. There were 2 patients with side branch occlusion, whose cTnI level obviously elevated. Conclusion PCI could lead to minor myocardial injury in some patients, the reason of which might be side branch occlusion. The number of placed stents and balloon inflation time were not associated with the minor myocardial injury.

Objective:To screen the interaction proteins of WW domain containing protein 1 (WWP1), and explore the effects of WWP1 and etoposide induced 24 (EI24) on cell proliferation in hepatocellular carcinoma (HCC).Methods:Yeast two-hybrid screening system was used to identify the interaction proteins of WWP1. The interaction was further validated by co-immunoprecipitation. WWP1 and EI24 stably over-expressing or deleted HepG2 cells were established by using the lentivirus transduction method. Colony forming assay and cell counting kit-8 (CCK8) assay were performed to identify the effects of WWP1 and EI24 on cell proliferation. In addition, the role of WWP1 in the tumorigenicity of liver cancer in vivo was examined by subcutaneous injection of different level of WWP1 expressed HepG2 into nude mice. Results:WWP1 can interact with EI24 and ubiquitin-degrade EI24 protein. The WWP1 and EI24 over-expressing or deleted HepG2 cell lines were successfully generated. Overexpression of WWP1 decreased while knockdown of WWP1 increased the protein level of EI24. The results of CCK-8 assay showed that the relative proliferation activities of WWP1 overexpressed (WWP1-OE) group and WWP1 knockdown (shWWP1) group on 36 hours were (347.00±8.15)% and (187.08±4.86)%, respectively, significantly different from (270.33±15.01)% of control group (both P<0.05). The relative proliferation activities of EI24 overexpressed (EI24-OE) group and EI24 knockdown (shEI24) group on 36 hours were (183.75±8.11)% and (317.33±9.60)%, respectively, significantly different from (270.33±15.01) % of control group (both P<0.05). The results of colony formation assay showed that the colony numbers of control group, WWP1-OE group and shWWP1 group were (52±7)/visual field (VF), (76±4)/VF, (19±3)/VF, respectively. Overexpression of WWP1 significantly increased while knockdown of WWP1 significantly decreased the colon formation ability of HepG2 cells (both P<0.05). The colon number of control group, EI24-OE group and shEI24 group were (38±4)/VF, (10±3)/VF, (69±7)/VF, respectively. Overexpression of EI24 significantly decreased while knockdown of EI24 significantly increased the colony formation ability of HepG2 cells (both P<0.05). The results of xenograft mice model showed that the tumor volumes of control, WWP1-OE, and shWWP1 group were (1 400.00±43.71)mm 3, (2 636.67±290.45) mm 3 and (642.17±36.00)mm 3, respectively, with significant differences ( P<0.05). The tumor weight for these three groups were (1.23±0.08)g, (2.05±0.17)g, and (0.88±0.09)g, respectively, with significant differences ( P<0.05). The tumor volumes of control, EI24-OE, and shEI24 group were (1 245.17±93.10)mm 3, (662.17±60.88)mm 3 and (1 986.67±226.75)mm 3 respectively, with significant differences ( P<0.05). The tumor weight for these three groups were (1.15±0.04)g, (0.85±0.02)g and (1.73±0.05)g respectively, with significant difference ( P<0.05). Conclusion:WWP1 promote the cell proliferation of liver cancer through ubiquitin-degradation of EI24.

Objective:To screen the interaction proteins of WW domain containing protein 1 (WWP1), and explore the effects of WWP1 and etoposide induced 24 (EI24) on cell proliferation in hepatocellular carcinoma (HCC).Methods:Yeast two-hybrid screening system was used to identify the interaction proteins of WWP1. The interaction was further validated by co-immunoprecipitation. WWP1 and EI24 stably over-expressing or deleted HepG2 cells were established by using the lentivirus transduction method. Colony forming assay and cell counting kit-8 (CCK8) assay were performed to identify the effects of WWP1 and EI24 on cell proliferation. In addition, the role of WWP1 in the tumorigenicity of liver cancer in vivo was examined by subcutaneous injection of different level of WWP1 expressed HepG2 into nude mice. Results:WWP1 can interact with EI24 and ubiquitin-degrade EI24 protein. The WWP1 and EI24 over-expressing or deleted HepG2 cell lines were successfully generated. Overexpression of WWP1 decreased while knockdown of WWP1 increased the protein level of EI24. The results of CCK-8 assay showed that the relative proliferation activities of WWP1 overexpressed (WWP1-OE) group and WWP1 knockdown (shWWP1) group on 36 hours were (347.00±8.15)% and (187.08±4.86)%, respectively, significantly different from (270.33±15.01)% of control group (both P<0.05). The relative proliferation activities of EI24 overexpressed (EI24-OE) group and EI24 knockdown (shEI24) group on 36 hours were (183.75±8.11)% and (317.33±9.60)%, respectively, significantly different from (270.33±15.01) % of control group (both P<0.05). The results of colony formation assay showed that the colony numbers of control group, WWP1-OE group and shWWP1 group were (52±7)/visual field (VF), (76±4)/VF, (19±3)/VF, respectively. Overexpression of WWP1 significantly increased while knockdown of WWP1 significantly decreased the colon formation ability of HepG2 cells (both P<0.05). The colon number of control group, EI24-OE group and shEI24 group were (38±4)/VF, (10±3)/VF, (69±7)/VF, respectively. Overexpression of EI24 significantly decreased while knockdown of EI24 significantly increased the colony formation ability of HepG2 cells (both P<0.05). The results of xenograft mice model showed that the tumor volumes of control, WWP1-OE, and shWWP1 group were (1 400.00±43.71)mm 3, (2 636.67±290.45) mm 3 and (642.17±36.00)mm 3, respectively, with significant differences ( P<0.05). The tumor weight for these three groups were (1.23±0.08)g, (2.05±0.17)g, and (0.88±0.09)g, respectively, with significant differences ( P<0.05). The tumor volumes of control, EI24-OE, and shEI24 group were (1 245.17±93.10)mm 3, (662.17±60.88)mm 3 and (1 986.67±226.75)mm 3 respectively, with significant differences ( P<0.05). The tumor weight for these three groups were (1.15±0.04)g, (0.85±0.02)g and (1.73±0.05)g respectively, with significant difference ( P<0.05). Conclusion:WWP1 promote the cell proliferation of liver cancer through ubiquitin-degradation of EI24.

Objective: To analyze the correlation between refractive errors and physical development indicators among primary school students aged 6 to 9, so as to provide a scientific basis for the development of effective prevention and control measures. Methods: A stratified cluster random sampling method was used to recruit 2 833 elementary school students aged 6 to 9 from Guangdong Province for vision screening, ocular biometry, and physical examinations in Octorber, 2020. The Chi square test, t-test, and ANOVA were employed to compare myopia rates and indicator values across different groups. Multiple linear regression models were used to analyze the correlations between height, weight, and body mass index (BMI) with refractive development indicators. Results: The screening myopia rate among primary school students aged 6 to 9 was 16.7%, and the myopia rate increased with age ( χ 2= 51.58 , P <0.01). The height and weight of the myopic group [(126.96±7.41)cm, (26.59±6.45)kg] were higher than those of the non myopic group [(124.76±7.77)cm, (25.42±5.87)kg] ( t =5.84, 3.65, P <0.01). The mean values of spherical equivalent (SE), axial length (AL), anterior chamber depth (ACD), and AL/corneal curvature radius (CR) ratio for students aged 6 to 9 were (-0.17±1.04)D, (22.96±0.78)mm, (3.38±0.24)mm, and (2.95±0.08), respectively, with statistically significant differences across different age and myopia severity groups ( t =37.08, 119.20, 41.54, 133.60; 935.30, 184.10, 73.95, 498.50, P < 0.01). After adjusting for gender, age, and residence, the multiple linear regression model showed that height was positively correlated with AL and CR, weight was positively correlated with ACD, and BMI was positively correlated with AL and ACD ( β = 0.191 , 0.070, 0.035, 0.013, 0.007, P <0.05). When stratified by myopia status, results for the non-myopic group were similar to the overall results, whereas in the myopic group, the correlations between height, BMI, and AL were not statistically significant ( P > 0.05). Conclusions Among primary school students aged 6 to 9, height and BMI are positively correlated with AL in the non myopic group but no similar correlation is observed in the myopic group, indicating that factors other than physical development, such as environmental and behavioral factors, should be considered for their impact on refractive development.