Previous studies had shown that CXC chemokine ligand-12 (CXCL12) plays a significant role in animal models of ischemic stroke, but its role in human stroke is unclear. The aim of this study was to test the relationship between elevated serum circulating CXCL12 levels and the 1-year stroke recurrence in Chinese patients with acute ischemic stroke (AIS). All consecutive patients with first-ever acute ischemic stroke from January 2011 to September 2013 were recruited to participate in the study. Serum levels of CXCL12 and National Institute of Health Stroke Scale (NIHSS) were measured at the time of admission. Logistic regression analysis was used to evaluate the stroke recurrence according to serum CXCL12 levels. Receiver operating characteristic (ROC) curve was used to evaluate the accuracy of serum CXCL12 in predicting stroke recurrence. Clinical follow-up was performed at 1 year. In our study, 248 patients finished the 1-year follow-up. At 1-year follow-up, 31 patients had a recurrence ischemic stroke. The median CXCL12 levels were significantly higher in those who sustained a recurrence ischemic stroke compared with those who did not [24.2 ng/mL (IQR 15.4-33.7) vs 6.5 ng/mL (IQR 3.4-10.2); Z = 8.258, P < 0.0001]. In multivariate analysis, there was an increased risk of stroke recurrence associated with serum CXCL12 levels ≥12.15 ng/mL (OR 9.122, 95 % CI 6.103-15.104) after adjusting for above possible confounders. The time to recurrence stroke distribution between patients with baseline CXCL12 levels ≥12.15 ng/mL and those with baseline CXCL12 levels <12.15 ng/mL were significantly different (P < 0.0001, log-rank test). Elevated circulating CXCL12 levels at admission are strongly associated with the future recurrence of ischemic stroke in Chinese patients with AIS. Further studies are warranted to confirm this association and define the role for CXCL12 as a novel predictor biomarker for stroke recurrence.

Abstract. The aim of the present study was to investigate the effects of microRNA-18a (miR-18a) on the invasiveness and metastasis of invasive meningiomas and the underlying mechanism. A total of 69 patients with meningiomas (30 patients in the invasive meningioma group and 39 patients in the non-invasive meningioma group) and 48 cases in the control group were enrolled. Samples of meningioma tissues, serum and cerebrospinal fluid were collected. Reverse transcription-quantitative polymerase chain reaction was performed to quantify the expression levels of hypoxia-inducible factor-1α (HIF-1α) mRNA and miR-18a. Western blot analysis was used to determine protein expression levels of HIF-1α. The expression levels of HIF-1α mRNA and protein in all three types of sample from the invasive meningioma group were significantly higher compared with those in the control and non-invasive meningioma groups (P<0.05), and the expression levels of HIF-1α mRNA in the serum and cerebrospinal fluid of the non-invasive meningioma group were significantly higher compared with those in the control group (P<0.05). The expression levels of miR-18a in the invasive meningioma group were significantly reduced compared with those in the control and non-invasive meningioma groups (P<0.05), whereas the levels of miR-18a in the non-invasive meningioma group were significantly lower compared with those in the control group (P<0.05). The expression of HIF-1α is significantly upregulated in patients with invasive meningiomas, possibly due to the downregulation of miR-18a expression. Therefore, miR-18a may regulate invasive meningiomas via HIF-1α.

The present study aimed to investigate the roles of the vascular endothelial cell growth factor (VEGF) and micro (mi)RNA-210 in the metastasis of primary medulloblastoma (MB) tumors. A total of 86 adult patients diagnosed with cerebellar MB were enrolled in the present study, of which 11 patients had metastatic MB in the subarachnoid space. The following samples were collected: MB primary tumor tissue, MB secondary tumor tissue, tumor adjacent tissues and cerebrospinal fluid (CSF). Immunohistochemical analyses of the tissue samples were conducted in order to detect patterns of VEGF expression. In addition, the expression levels of VEGF mRNA and miRNA-210 were analyzed using reverse transcription-quantititative polymerase chain reaction, and western blot analyses were used to investigate VEGF protein expression levels. The positive expression rate of VEGF was significantly higher in MB tumor tissue, as compared with adjacent tissues (P<0.01). In addition, VEGF mRNA and protein expression levels in MB primary and secondary tumor tissues, and in the CSF of patients with metastatic MB, were significantly upregulated, as compared with tumor adjacent tissues and the CSF of patients with non-metastatic MB, respectively (P<0.01). miRNA-210 expression levels were significantly upregulated in MB tumor tissues, the CSF of patients with metastatic MB and in tumor tissues of metastatic MB (P<0.01). In the present study, the expression levels of VEGF and miRNA-210 were upregulated in patients with MB and metastatic MB; thus suggesting that miRNA-210 may promote the metastasis of MB primary tumors by regulating the expression of VEGF.