Objective To observe the protective effect of Racecadotril combined with Succinate Injection on myocardial injury in children with rotavirus enteritis and explore its clinical significance.Methods Totally 116 cases of children with rotavirus enteritis from Huangshi Traditional Chinese Medicine ofEdong Healthcare Group were selected in this study.Patients were randomly divided into Racecadotril control group (n =58) and Racecadotril combined with Succinate Injection observation group (n =58).The levels of CK,CK-MB,LDH,IL-17,IL-6,and TNF-α were detected by ELISA analysis.The rates of clinic effects and adverse reaction were compared.Results There was no significant difference of CK,CK-MB,LDH,IL-17,IL-6,and TNF-α between two groups before treatment.After treatment,they were all decreased in two groups (P ＜ 0.05,0.01).However,they were all lower in observation group than those in control group after treatment (P＜0.05).The rate of clinic effects was 94.8％ in observation group,which was higher than 81.0％ in control group (P ＜ 0.05).The rate of adverse reaction was 8.6％ in observation group and 6.9％ in control group.There was no significant difference between two groups.Conclusion Racecadotril combined with Succinate Injection inhibits the inflammatory response to protect myocardial injury in RVE children,with significantly clinical efficacy and safety.

Objective To observe the effects of tea polyphenols (TP) on cardiac function and myocardial ultrastructure in rats after repeated +10 Gz stress. Method Twenty four male Wistar rats were randomly divided into three groups (n=8 each): group A (control), group B (+10 Gz), group C (+Gz with TP). Group B and C were repeatedly exposed to +10 Gz (each for 30 s, onset rate about 0.5 G/s, 3 times/d with +1 Gz 1 min intervals, 3 d/wk, 4 weeks in total), but group A was only submitted to +1 Gz. TP(200 mg.kg-1) was given orally to group C about 1h prior to the +Gz experiment, and distilled water was given to group A and B.Function of isolated rat working hearts and myocardial ultrastructure were observed. Result A significant decrease of left ventricular systolic pressure (LVSP) and injury of myocardial structure in rats were demonstrated after repeated +10 Gz stress. But TP could remarkably elevate the LVSP and improve myocardial ultrastructural injury in +10Gz stressed rats. Conclusion These results indicated that repeated high G exposure may produce cardiac structural and functional injuries in rats which might be partly related to free radical metabolism; and antioxidant TP had significant protective effects on the hearts of +Gz stressed rats.

Objective To observe the effects of repeated +10 Gz stress on cerebral lipid peroxidation,liver and renal function in rats and the prophylactic effects of antioxidant tea polyphenols(TP).Method Twenty-four male Wistar rats were randomly divided into three groups(n=8 each):group A(control),group B(+10 Gz),and group C(TP).Group B and C were exposed to repeated +10 Gz stress(each for 30s,onset rate about 0.5 G/s,3 times/d with +1 Gz 1 min intervals,3 d/wk,4 weeks in total),but group A was only submitted to +1 Gz.TP(200 mg/kg) was given orally in group C about 1 h prior to the +Gz experiment,while distilled water was given in group A and B.Lipid peroxidation in the brain,liver and renal functions and serum lipids were determined.Results As compared with the control,lipid peroxidation in rat cerebral homogenate,mitochondria and cytoplasm was significantly increased( P<0.05),and serum creatinine concentration was markedly elevated after repeated +10 Gz stress(P<0.01).But,TP had significant inhibitory effect on +10 Gz stress induced peroxidative injury in rat brain and reduced the serum creatinine level.There were no differences of serum triglyceride and total cholesterol concentrations and glutamic-pyruvic transaminase activity among the three groups.Conclusion These results indicated that repeated high +Gz stress could bring about peroxidative injury in brain and harmful effect on renal function,and natural antioxidant TP had signficant protective effects.

Objective To investigate the effects of modafinil,a new wake-promoting agent,on simulated flight performance during 48 h sleep deprivation(SD).Method Six male healthy young volunteers were exposed to two periods of 48 h continuous wakefulness during the crossover experiment.In one period,three 200 mg doses of modafinil were given and in the other,separated by two weeks,matching placebos were administered.The SD time started from 8:00 of the first day to 8:00 of the third day.Drug was given at 0:00,16:00 of the second day and 0:00 of the third day.Flight performance in J7-E flight simulator was tested at 21:00 of the first day and 1,3,5,7 h after each drug administration.Result The scores of simulated flight performance in the placebo group decreased with time during SD and became significant at 1:00～7:00 of the third day.Numbers of errors increased with time during SD,especially in the left ascending turn stage and the descending & landing stages.Compared with the placebo,flight performance was significantly increased after the third administration of modafinil.Numbers of errors during 48 h SD and at 1:00～7:00 of the third day in modafinil group was 19% and 40% lower than those in placebo group respectively.Conclusion Simulated flight performance during 48 h SD is significantly improved after repeated administration of modafinil,especially when the impacts of SD and the circadian trough are combined.

Objective:To explore the expression of long non-coding RNA (lncRNA) CDK5RAP3 in gastric cancer tissue and its regulatory effect on gastric cancer cell proliferation and invasion.Methods:The expression differences of CDK5RAP3 in gastric cancer tissues and adjacent tissues were analyzed by TCGA database. By transfecting the pcDNA3.1-CDK5RAP3 plasmid into Hs-746T cells, a gastric cancer cell line overexpressing CDK5RAP3 (CDK5RAP3 group) was constructed, and the pcDNA3.1 plasmid was transfected into Hs-746T cells as a control group. The changes of CDK5RAP3 expression in the two groups of cells were detected by real-time quantitative PCR (qRT-PCR). The effects of overexpression of CDK5RAP3 on the proliferation and invasion of Hs-746T cells were detected by CCK-8 assay and Transwell assay, respectively. The binding sites of CDK5RAP3 and miR-223-3p were predicted by the starBase v2.0 database. The direct binding of CDK5RAP3 and miR-223-3p was verified by dual-luciferase reporter gene experiment. The expression levels of miR-223-3p in Hs-746T cells in each group were detected by qRT-PCR. Western blot was used to detect the expression levels of proliferation proteins and invasion proteins in Hs-746T cells in each group. The experimental data were analyzed by SPSS 17.0 software, and the measurement data conforming to the normal distribution were expressed as Mean±SD. The t-test was used to compare between two groups, and the one-way analysis of variance was used to compare the means of multiple groups. Results:Compared with adjacent tissues, the expression level of CDK5RAP3 in gastric cancer tissues was significantly lower ( P<0.01). The expressions of CDK5RAP3 in Hs-746T cells in the control group and CDK5RAP3 group were (1.08±0.77) and (10.63±2.14), respectively, and the difference was statistically significant ( P<0.01). Up-regulation of CDK5RAP3 significantly decreased the proliferation activity of Hs-746T cells ( P<0.05). The number of invasive cells in the control group and CDK5RAP3 group were (137.80±28.72) and (57.76±24.95), respectively, and the difference was statistically significant ( P<0.01). CDK5RAP3 could directly bind miR-223-3p ( P<0.01). The expression of miR-223-3p in Hs-746T cells in control group and CDK5RAP3 group were (6.22±1.20) and (1.01±0.98), respectively, and the difference was statistically significant ( P<0.01). Compared with the control group, up-regulation of CDK5RAP3 significantly reduced the expression levels of proliferation and invasive proteins. Conclusion:The expression of CDK5RAP3 is low in gastric cancer tissue, and CDK5RAP3 inhibits the proliferation and invasion of gastric cancer Hs-746T cells by targeting miR-223-3p.