ObjectiveInfections are frequent after stroke and lead to increased mortality and neurological disability. Antibiotic prophylaxis has potential of decreasing the risk of infections and mortality and improving poor functional outcome. Several studies evaluated antibiotic prophylaxis for infections in acute stroke patients have generated conflicting results. The systematic review of randomized clinical trials (RCTs) aimed at comprehensively assessing the evidence of antibiotic prophylaxis for the treatment of acute stroke patients.Materials and MethodsPubMed, EMBASE, the Cochrane library and the reference lists of eligible articles were searched to identify all potential studies. We included the studies that investigated the efficacy and safety of antibiotic prophylaxis for the treatment of acute stroke patients. The primary outcome included mortality and infection rate. The secondary outcomes included poor functional outcome and adverse events.ResultsSeven trials randomizing 4,261 patients were included. Pooled analyses showed that antibiotic prophylaxis did not improve the mortality (risk ratio (RR) = 1.03, 95% confidence interval (CI) 0.84 to 1.26, p = 0.78, I2 = 25%) and poor functional outcome (RR = 0.93, 95% CI 0.80 to 1.08, p = 0.32, I2 = 80%), but reduced the incidence of infection (RR = 0.67, 95% CI 0.53 to 0.84, p = 0.0007, I2 = 49%). No major side effects were reported. Sensitivity analyses confirmed the results of infection rate and poor functional outcome.ConclusionsAntibiotic prophylaxis can be used to treat the infectious events of acute stroke patients although it has no potential of decreased mortality and improved functional outcome.

Objective. Casein kinase 2 interacting protein-1 (CKIP-1) has exhibited multiple functions in regulating cell proliferation, apoptosis, differentiation, and cytoskeleton. CKIP-1 also plays an important role as a critical regulator in tumorigenesis. The aim of this study is to further examine the function of CKIP-1 in glioma cells. Methods. The expression level of CKIP-1 protein was determined in gliomas tissues and cell lines by immunohistochemistry stain and western blotting while the association of CKIP-1 expression with prognosis was analyzed by Kaplan-Meier method and compared by log-rank test. CKIP-1 was overexpressed or silenced in gliomas cell lines. CCK-8, colony formation assay, and BrdU incorporation assay were used to determine cell proliferation and DNA synthesis. Cell cycle and apoptosis rate were determined with fluorescence-activated cell sorting (FACS) method. Then, expression of key members in AKT/GSK3β/β-catenin pathway was detected by western blot analysis. Results. In the present study, we reported new evidence that CKIP-1 was reversely associated with the proliferation of glioma cells and survival in glioma patients. Additionally, the overexpressed CKIP-1 significantly inhibited glioma cell proliferation. Further experiments revealed that CKIP-1 functioned through its antiproliferative and proapoptotic activity in glioma cells. Importantly, mechanistic investigations suggested that CKIP-1 sharply suppressed the activity of AKT by inhibiting the phosphorylation, markedly downregulated the phosphorylated GSK3β at Ser9, and promoted β-catenin degradation. Conclusions. Overall, our results provided new insights into the clinical significance and molecular mechanism of CKIP-1 in glioma, which indicated CKIP1 might function as a therapeutic target for clinical treatment of glioma.

ObjectiveLong non-coding RNA breast cancer anti-estrogen resistance 4 (BCAR4) has been recognized as a proto-oncogene in various malignancies. It has been reported to be highly expressed and promote cell proliferation in glioma. However, its additional roles in gliomagenesis remain largely unclear. This research intends to investigate the impact and internal molecular mechanism of BCAR4 on glioma cell growth, invasion and tumorigenesis.MethodsBCAR4 expression was examined by qPCR in 30 cases of graded glioma specimens and 7 glioblastoma (GBM) cell lines compared with respective controls. Its potential prognostic value was evaluated by Kaplan–Meier survival analysis. The biological roles of BCAR4 in gliomagenesis were verified by CCK-8, transwell and intracranial xenograft assays successively. qPCR and RNA pull-down assays were applied to study the relationship between BCAR4 and miR-2276. Then, qPCR, Western blot and luciferase reporter assays were used to validate the targeting of matrix metallopeptidase 7 (MMP7) by miR-2276 and the regulation of MMP7 by BCAR4. Finally, MMP7 was restored in BCAR4-silenced GBM cells and the rescue effects were determined by CCK-8 and transwell assays.ResultsBCAR4 expression was increased in glioma tissues and GBM cell lines, and its high expression positively correlated with advanced grades and worse prognosis. Functional assays verified that knockdown of BCAR4-inhibited cell growth and invasion in vitro, and impaired tumor formation in vivo. Mechanistically, we found that BCAR4 could act as a competing endogenous RNA (ceRNA) by targeting miR-2276 to upregulate MMP7 expression. Importantly, MMP7 restoration effectively rescued the inhibitory modulations on GBM cell growth and invasion caused by BCAR4 knockdown.ConclusionOur findings identified the essential roles of the BCAR4/miR-2276/MMP7 axis in gliomagenesis and provided novel insights on glioma therapy.

No abstract