Atherosclerosis is a chronic and multifactorial inflammatory disease and is closely associated with cardiovascular and cerebrovascular diseases. circRNAs can act as competing endogenous RNAs to mRNAs and function in various diseases. However, there is little known about the function of circRNAs in atherosclerosis. In this study, three rabbits in the case group were fed a high-fat diet to induce atherosclerosis and another three rabbits were fed a normal diet. To explore the biological functions of circRNAs in atherosclerosis, we analyzed the circRNA, miRNA and mRNA expression profiles using RNA-seq. Many miRNAs, mRNAs and circRNAs were identified as significantly changed in atherosclerosis. We next predicted miRNA-target interactions with the miRanda tool and constructed a differentially expressed circRNA-miRNA-mRNA triple network. A gene ontology enrichment analysis showed that genes in the network were involved in cell adhesion, cell activation and the immune response. Furthermore, we generated a dysregulated circRNA-related ceRNAs network and found seven circRNAs (ocu-cirR-novel-18038, -18298, -15993, -17934, -17879, -18036 and -14389) were related to atherosclerosis. We found these circRNAs also functioned in cell adhesion, cell activation and the immune response. These results show that the crosstalk between circRNAs and their competing mRNAs might play crucial roles in the development of atherosclerosis.

MicroRNAs are single-stranded small non-coding RNA molecules which regulate mammalian cell growth, differentiation, and apoptosis by altering the expression of other genes and play a role in tumor genesis and progression. MiR-106a is upregulated in several types of malignancies and provides a pro-tumorigenic effect. However, its role in glioma is largely unknown. Our findings demonstrate that the low expression of miR-106a in human glioma specimens is significantly correlated with high levels of E2F1 protein and high-grade glioma. Here, we present the first evidence that miR-106a provides a tumor-suppressive effect via suppressing proliferation of and inducing apoptosis in human glioma cells. We further show that E2F1 is a direct functional target of miR-106a, suggesting that the effect of miR-106a on the glioma suppressive effect may result from inhibition of E2F1 via post-transcriptional regulation. In addition, our results reveal that miR-106a can increase p53 expression via E2F1 inhibition, whereas the effect of miR-106a on the proliferation of glioma cells is independent of p53 status. Further investigations will focus on the therapeutic use of miR-106a-mediated antitumor effects in glioma.

Previous studies proposed that isocitrate dehydrogenase 1 (IDH1) mutation was associated with improved survival in patients with glioblastoma, but those studies reported varying estimates and yielded inconclusive results. The purpose of the present study was to determine the effect of IDH1 mutation on the prognosis of patients with glioblastoma by performing a meta-analysis. Pubmed and Embase databases were searched for eligible studies. Studies reporting overall survival by IDH1 mutation in patients with glioblastoma were considered potentially eligible for the meta-analysis. For the quantitative aggregation of the survival results, the IDH mutation effect was measured by the pooled hazard ratio (HR) with its 95% confidence interval (95%CI). Nine studies with a total of 1,669 patients with glioblastoma were finally included into this meta-analysis. Overall, the IDH1 mutation was associated with improved survival in patients with glioblastoma (random effects model HR = 0.45, 95%CI 0.29-0.69, P < 0.001). Sensitivity analysis further showed that the pooled estimates were stable in this meta-analysis. Therefore, the findings from this meta-analysis suggest that IDH1 mutation is associated with improved overall survival in patients with glioblastoma.

Ischemic stroke is a leading cause of death and adult disability worldwide. Recent research suggests that renalase is strongly associated with heart disease and hypertension and may play a role in ischemic stroke. In this study, we investigate the genetic association between renalase and ischemic stroke in a northern Chinese Han population. We genotyped single-nucleotide polymorphisms of the renalase gene in 507 ischemic stroke patients and 503 gender-matched controls from a northern Chinese Han population, and we classified these case samples in depth by complications with diabetes or hypertension and by ischemic stroke subtypes. We undertook allele, genotype, and haplotype association studies in all the cases and in the subgroups, as well as multiple factor analysis by logistic regression. rs10887800 and rs2576178 were significantly associated with ischemic stroke with hypertension by logistic regression (p = 0.041 and p = 0.038, respectively). The recessive model showed a strong association of rs2296545 with ischemic stroke patients in hypertension subgroups (OR = 1.927, 95 % CI = 1.012-3.669, p = 0.046). The renalase gene is closely related to ischemic stroke in this northern Chinese Han population, suggesting that renalase may be mechanistically involved in stroke pathology.

OBJECTIVE ：the main purpose of this experiment was to study the change of C6 glioma cells' ultrastructure treated by photodynamic therapy(PDT), observe the change of morphology METHOD ：Make the model of rat glioma by transplanted C6 glioma cells into caudate nucleus，treated the glioma rat by PDT after two weeks. Observed the difference of subcellular structure before and after PDT by electron microscope. RESULT ： Apoptosis and necrosis can be seen after treated by PDT in the C6 glioma, basal membrance damaged ，number of cellular organ of endothelial cell of blood capillary declined，tight junction of endothelial cell lengthen and the gap enlarge. The PDT has slightly effect on the nomorl rat's subcellular structue. CONCLUSION: PDT can induce the apoptosis and necrosis of C6 glioma cell. The damage of the ultramicrostructure of mitochondria and endoplasmic reticulum was the foundmentol of the change. PDT initiate the damage of BBB of the C6 glioma cell and weeken the function、 and makes it a useful way of treating the glioma combained with chemotherapy.KEY WORDS : photodynamic therapy; glioma; mitochondria; blood brain barrier; blood brain tumor barrier; electron microscope; apoptosis; subcellular structue; chemotherapy 1. MATERIAL AND METHOD 1.1 Cell the C6 glioma cell purchase from shanghai cell library medical science of china.