Objective To investigate the protective effects of (-)-epigallocatechin gallate ( EGCG ) on daunorubicin ( DNR)-induced cardiotoxicity in mice. Methods The qualified mice were randomly divided into four groups:normal control group, myocardial injured model control group,high dose group (80 mg·kg-1 ) and low dose group (40 mg·kg-1 ) of EGCG. EGCG was administered intragastrically once daily for 7 days,followed by a single intraperitoneal injection of DNR (15 mg·kg-1 ) except in the normal control group. The electrocardiogram,myocardial enzymes and TNT-Hs in serum,cardiac ultrastructure of mice were detected after 48 h. Results In DNR model control group,the incidence of arrhythmia was 64. 7%. The activity of serum cardic enzymes including CK,CK-MB,LDH,α-HBDH and ALT,AST, level of TNT-Hs were significantly higher than those in the normal control group(P<0. 01),and myocardial ultrastructure was injured remarkably. The incidence of arrhythmia was 44. 4% in mice treated with high dose of EGCG and 31. 6% in mice with low dose of EGCG. Compared to the model control group, the activity of CK,CK-MB,LDH,α-HBDH and ALT,AST, level of TNT-Hs in serum decreased remarkably in EGCG groups( P<0. 05 or P<0. 01). Low can EGCG alleviated the injury to the ultrastructure of myocardium compared to the model control group. Conclusion EGCG can prevent the cardiac toxicity induced by DNR in mice.

Objective:To investigate the effects of Bcl3 gene knockout on the composition of spleen immune cells and antitumor ability of mice.Methods:Bcl3 gene knockout mice (Bcl3 -/-) were established by CRISPR/Cas9 genome editing technology. Blood routine test and flow cytometry were used to detect the immune cell composition in Bcl3 -/- mice. Lung metastasis models were established by injecting mice with B16F10 melanoma cells. The number of tumor nodules in lung and the survival time of mice were used to assess the antitumor ability of wild-type (WT) and Bcl3 -/- mice. Results:Bcl3 -/- mice were successfully bred to a strain with normal growth rate and normal breeding performance. Furthermore, no embryonic death occurred. Compared with WT mice, Bcl3 -/- mice showed splenomegaly and a significant increase in the number of spleen immune cells ( P<0.05). The counts and percentages of platelets and neutrophils in Bcl3 -/- mice were significantly lower than those in WT mice. The proportion of CD19 + B cells showed no significant change, while the proportions of CD3 + T cells and T cell subsets (CD4 + , CD8 + , Treg) increased significantly ( P<0.05). The proportions of NK cells (NK1.1 + ) and neutrophils (Gr1 + ) decreased ( P<0.05), while no significant change in the proportion of DC (CD11b + ) was observed. There were a large number of tumor nodules formed by melanoma cells in the lung of Bcl3 -/- tumor bearing mice, and their survival time was shortened dramatically. Conclusions:Knockout of Bcl3 gene affected the development, differentiation and function of immune cells, thereby reducing the antitumor ability of mice.

Objective:The aim of this study was to design and perform "Tap-hammer"system that can be used to elicit vestibular evoked myogenic potentials (VEMP) in normal adults and to report the preliminary results of this system.Methods:A triggered Tap-hammer was designed, made and connected with an electric recording system, to form as a system for Tap-VEMP recording. Twenty healthy adult volunteers (7 males and 13 females, aged 20 to 37 years, 40 ears in total) were recruited for air-conducted sound VEMP (ACS-VEMP) and Tap-VEMP examinations. Waveforms and parameters of both VEMPs were recorded and analyzed. SPSS 22.0 software was used for statistical analysis.Results:The response rates of ACS-, Tap-ocular VEMP (oVEMP) and ACS-, Tap-cervical VEMP (cVEMP) were both 100% (40/40). The mean±SD n1 latency, p1 latency, n1-p1 interval, amplitude, and asymmetry ratio (AR%) of Tap-oVEMP were (9.80±2.51)ms, (13.90±3.26)ms, (4.09±1.43)ms, (16.43±9.61)μV, (22.68±17.35)% respectively. The mean±SD p1 latency, n1 latency, p1-n1 interval, amplitude, and asymmetry ratio (AR%) of Tap-cVEMP were (13.26±2.07)ms, (21.84±2.89)ms, (8.58±2.10)ms, (457.65±274.94)μV, (20.42±13.46)% respectively. Both n1 latency and p1 latency of Tap-VEMPs were shorter than those in ACS-VEMPs ( P<0.05). No statistical difference could be found between the two stimulation methods in the parameters of n1-p1 interval, amplitude, and asymmetry ratio( P>0.05). Conclusion:The Tap-hammer system can elicit VEMP responses in healthy young people. This system can be used as an alternative stimulation method for bone conduction VEMP.

Objective: To detect the expression of NRAGE protein in esophageal squamous cell carcinoma and investigate the relationship between NRAGE and therapeutic effect of radiotherapy. Methods: The expression level of NRAGE in 44 patients with esophageal squamous cell carcinoma was evaluated by immunohistochemistry and statistically analyzed along with clinical data by using multivariate analysis using Cox regression model. Results: The overall expression level of NRAGE protein in esophageal squamous cell carcinoma (P=0.025) and the expression level of NRAGE nuclear protein (P=0.008) were negatively correlated with short-term efficacy. In terms of the overall expression level of NRAGE protein, the 3-year survival rates in the strongly positive group and the positive weakly positive group were 16% and 36%(P=0.198). As for the expression of NRAGE nuclear protein, the 3-year survival rates in the strongly positive group and the positive+ weakly positive group were 0% and 41%(P<0.001). Multivariate analysis using Cox regression model demonstrated that as for the expression of NRAGE nuclear protein, the risk of death in the strongly positive group was significantly higher than those in the positive+ weakly positive group (P=0.002). Conclusion The overall expression level of NRAGE protein in the esophageal cancer is negatively correlated with the short-term efficacy of radiotherapy, whereas it is not correlated with long-term survival rate. The strongly positive expression level of NRAGE nuclear protein is negatively correlated with the short-term efficacy of radiotherapy and the long-term survival rate, prompting that NRAGE may be a molecular indicator for predicting radiation resistance and even the efficacy of radiotherapy for esophageal squamous cell carcinoma

Objective: To investigate the effects of human adult T lymphoblastic leukemia virus typeⅠ (HTLV-1) infection on the production of reactive oxygen species (ROS) and mitochondrial damage in host cells. Methods: A cell model of HTLV-1 infection was established by co-culturing HTLV-1-positive cell line MT2 with HeLa cells. ROS, mitochondrial membrane potential (MMP) and total mitochondria were detected using specific fluorescence probe labeling method. Cell apoptosis was detected by Annexin V-FITC/PI method. Western blot was performed to detect viral proteins Tax and p19, as well as mitochondrial proteins TIM23 and TOM20. After the treatment of MT2 cells with different concentrations of reverse transcription inhibitors (ZDV), relative viral loads were detected by quantitative real-time PCR and Western blot, and the mass of mitochondria was analyzed by flow cytometry. Results: After co-culturing HeLa cells with MT2 cells for 24 h, the ROS level in host cells increased without obvious cell apoptosis, while the mitochondrial membrane potential, mitochondrial protein expression and total mitochondria decreased significantly. When the replication of HTLV-1 in MT2 cells was inhibited by ZDV, the ROS level and total mitochondria increased. Conclusions HTLV-1 infection can cause oxidative stress in host cells, resulting in mitochondrial damage. Autophagy might be activated to degrade mitochondrial damage and maintain cell homeostasis during the infection.