Objective To study the effects of 6-week aerobic treadmill exercise on the genes expression in skeletal muscle of C57BL/6 mice.Gene array was performed and the data was analyzed to evaluate the adaptive changes at gene level caused by exercise.Methods Twenty male C57BL/6 mice were randomly divided into two groups:control group(C) and aerobic exercise group (E).The mice from group E were forced to run on treadmill for 6 weeks.After 6 weeks,all mice were fasted for 16 hours,and then sacrificed.Their flexor muscle was removed.4 samples from each group were analyzed with gene chips to dissect the differentially expressed genes between the two groups.Results Our results showed that 723 genes were differentially expressed in E group as compared with C group after the 6 weeks aerobic exercise,among which 510 genes were up-and 213 down-regulated.There were 6 differentially expressed calcium signaling genes and 2 ofwhich(Gnall and Pdgfra) were up-regulated,while the others(Phka1,Picd4,RYR1 and Ppid)were down regulated.

Objective To analyze the clinical efficacy of the laparoscopic breast-conserving surgery combined with radiofrequency ablation to treat the early-stage breast cancer.Methods We collected 55 patients diagnosed early-stage breast cancer in retrospect,which started from January 2014 to December 2016.Twenty-seven of them were performed the laparoscopic breast-conserving surgery combined with radiofrequency ablation while others went through laparoscopic breast-conserving surgery without radiofrequency ablation.Meanwhile,we adopted the student t-test and the chi-square test to compare results of two groups.More specific,the main indexes of this study are including the post-operative local recurrence,the incidence of fat liquefaction or the incision-infection,operation time,post-operative hospital stay and the hospitalization expense.Results The laparoscopic breast-conserving surgery combined with radiofrequency ablation group had low local-recurrence than the laparoscopic breastconserving surgery group (0 and 7.69％).Additionally,there were no statistical differences between two groups in the incidence of fat liquefaction.However,The laparoscopic breast-conserving surgery combined with radiofrequency ablation group had more hospitalization expense than the laparoscopic breast-conserving surgery group [(4.1 ± 0.7) ten thousand yuan and (2.3 ± 0.6) ten thousand yuan,P ＜ 0.05].Conclusions Although the laparoscopic breast-conserving surgery combined with radiofrequency ablation group remarkably increased the hospitalization expense because of the utility of the radiofrequency ablation related apparatus,it may provide the probability of shaving more residual tumor cell and may low down the recurrence,especially not rising up the incidence of the post-operative fat liquefaction.Therefore,this surgery method might be one of the potential developments in the minimal-invasive of early stage breast cancer.

AIM: To investigate the role of sorafenib in promoting ferroptosis in HCC, and whether cell death can be induced by activating mitochondrial oxidative stress and consequent mitochondrial dysfunction. METHODS: Hepatocellular carcinoma cell lines Huh7 and HCC-LM3 were treated with different concentrations of sorafenib, the cell viability was determined by CCK-8 assay; mitochondrial membrane potential (MMP) was measured by Tetramethylrhodamine (TMRM) staining; The mitochondrial oxygen consumption rate was monitored by the Seahorse XF24 Analyzer; mitochondrial superoxide indicator (Mitosox) was used to determine the level of reactive oxygen species (ROS) in mitochondria; the formation of total ROS was determined by dichlorofluorescein diacetate (DCF-DA) staning. Finally, The recovery of oxidative damage and cell death induced by sorafenib was observed after pretreated by glutathione (GSH). RESULTS: With the increasing concentration of sorafenib, the survival of the Huh7 and HCC-LM3 was significantly decreased. Sorafenib also inhibited the oxygen consumption rate and decreased oxidative phosphorylation, which results in the depolarization of MMP, ROS accumulation and eventually ferroptosis of HCC cells. However, the occurrence of oxidative stress induced by sorafenib in HCC cells can be effectively reversed by the pretreatment of GSH. CONCLUSION: The ferroptosis can be induced by sorafenib through inducing mitochondrial dysfunction and ROS accumulation in HCC cells. However, the GSH can restore oxidative damage. Therefore, induction of the GSH deficiency in HCC may be a potential therapeutic option to enhance the efficacy of sorafenib.