miR-15a regulates oxygen glucose deprivation/reperfusion (OGD/R)-induced neuronal injury by targeting BDNF.

Multiple microRNAs (miRs) have also been implicated in ischemic brain injury. This research intended to probe the regulatory function and the mechanism of miR-15a on the ischemic brain injury induced by oxygen-glucose deprivation/reoxygenation (OGD/R) in neurons of rats. The OGD/R model was established with the cortical neurons separated from rats. After transfection with miR-15a mimic negative control (NC), miR-15a mimic, miR-15a inhibitor NC and miR-15a inhibitor, the OGD/R-induced apoptosis were detected. Using bioinformatic softwares including TargetScan, miRanda, and miRWalk to predict the underlying targets of miR-15a, and the binding of miR-15a with brain-derived neurotrophic factor (BDNF) were validated with double-fluorescein reporter assay system. The expression levels of BDNF mRNA and protein were detected with qRT-PCR and western blot. The effect of miR-15a on PI3K/AKT pathway in neurons submitted to OGD/R was also investigated. The findings showed that miR-15a may mediate the apoptosis of neurons submitted to OGD/R, and lower expression of Bcl-2 and higher expression of Bax and cleaved caspase-3 were observed. BDNF was screened as the candidate target, and the direct binding of miR-15a with 3'-UTR of BDNF were verified. Further research showed that miR-15a downregulated the expression of BDNF mRNA and protein, thus exerted negative regulatory effect on the OGD/R injury. PI3K/AKT pathway may be related to the regulatory effect of miR-15a. Our findings contribute to uncovering novel pathogenesis for ischemic brain injury.

Cerebral inoculation of human A53T α-synuclein reduces spatial memory decline and amyloid-ß aggregation in APP/PS1 transgenic mice of Alzheimer's disease.

Amyloid-ß (Aß) peptide and α-synuclein (α-syn) are major components of senile plaques in Alzheimer's disease (AD) and Lewy bodies in Parkinson's disease (PD), respectively. Co-occurrence of Aß and α-syn in the senile brains of AD and LB diseases suggests interactions between the two proteins. However, the significance of the overlapping deposition, especially the effects of α-syn on the Aß aggregation, still remains to be clarified. In the present study, we investigated the effects of α-syn pre-formed fibrils (PFFs) injection on the cognitive behaviors and Aß deposition in the brain of APP/PS1 transgenic AD mice by using Morris water maze (MWM) test, immunohistochemistry and western blot techniques. We found that APP/PS1 transgenic mice exhibited an obvious elevation in the α-syn load, as well as Aß deposition in the brain compared with wild type of C57 BL littermates. 5 months after cerebral injection of exogenous α-syn, MWM tests showed an alleviation in cognitive impairments in APP/PS1 mice; western blot and immunohistochemistry experiments also exhibited a significant reduction in Aß level in the brain of APP/PS1 mice injected with α-syn. These results suggest that α-syn aggregated in the brain of AD may act as a protective factor and defend the brain tissue from early Aß deposition and cognitive deficits.

The relationship between exposure to hepatitis B virus and increased atherosclerosis-associated morbidity - a meta-analysis.

BACKGROUND AND AIM: The relationship between exposure to hepatitis B virus (HBV) and atherosclerosis-associated disease morbidity has not been clearly elucidated. We performed a meta-analysis to explore whether exposure to HBV is a risk factor for atherosclerosis-associated diseases. METHODS: We searched the PubMed, Web of Science, Cochrane Library, Embase, and Scopus databases for related studies. We then chose the eligible studies for meta-analysis and assessed quality assessment and risk of bias. RESULTS: The meta-analysis of the included studies showed that exposure to HBV tends to increase atherosclerosis-associated disease morbidity, but this increase was not statistically significant. CONCLUSIONS: Hepatitis B virus may not be a risk factor for atherosclerosis-associated diseases, but further studies that employ more sensitive clinical parameters are needed to verify this result.

Association between the MMP-9-1562 C>T polymorphism and the risk of stroke: a meta-analysis.

Matrix metalloproteinase (MMP)-9 so far is identified as extremely large and complicated MMP family member. Recently, dozens of studies have explored the association between a promoter polymorphism (-1562 C>T) in MMP-9 and stroke susceptibility. However, the conclusions of these studies still remain equivocal. Therefore, our current meta-analysis was conducted to investigate whether or not the MMP-9 promoter polymorphism is related to the risk of stroke. Electronic databases (PubMed, EMBASE, Web of Science, Cochrane Library and the Chinese Biomedical Literature Database) were searched to obtain all the available studies investigating this polymorphism and stroke from inception to October 2013. Overall and subgroup analyses were rigorously conducted after data extraction. Pooled odds ratio (OR) corresponding to 95 % confidence interval (CI) were estimated. The statistical analysis was performed using Review Manager 5.2. Totally, seven studies involving 1,624 cases and 1,525 controls were identified. The overall results suggested that there was no association of the C-1562T variant on stroke risk under the T allele versus C allele [OR T vs. C 0.98, 95 % CI (0.84, 1.15), P = 0.84], the dominant model [OR TT+TC vs. CC 0.95, 95 % CI (0.81, 1.13), P = 0.59], the recessive model [OR TT vs. TC+CC 1.55, 95 % CI (0.86, 2.81), P = 0.15], the homozygote comparison [OR TT vs. CC 1.48, 95 % CI (0.82, 2.68), P = 0.20] and the heterozygote comparison [OR TC vs. CC 0.93, 95 % CI (0.78, 1.10), P = 0.38]. In the subgroup analyses by ethnicity, age, stroke type and source of controls, no significant relations were observed in any genetic models. Our results indicated that MMP-9-1562 C>T polymorphism was not a risk factor for stroke. Further studies should focus on gene-gene and gene-environment interactions, and provide a more convincing explanation for this association.

[Prevalence of trachoma in rural primary school children in Tengzhou City of Shandong Province in China].

OBJECTIVE: To investigate the prevalence of trachoma and its risk factors in rural primary school children in Tengzhou City of Shandong Province. METHODS: In this cross-sectional population-based study, children aged 5 to 14 years old in primary school were randomly selected by a cluster sampling in which school shift was the sampling unit. Out of 2742 students, 2676 were eligible. The examination rate was 97.60%. All selected students were assessed for trachoma using the simplified grading scheme proposed by the World Health Organization (WHO). Statistical significance was calculated using Chi-square tests. RESULTS: Out of 2676 eligible children, 593 cases of active trachoma were found, the prevalence of trachoma was 22.16% (95% CI:20.59%-23.73%). In 1606 boys, the prevalence of active trachoma was 19.74%, compared with 25.79% for girls. Girls were affected by active trachoma higher than boys (25.79% versus 19.74%, P=0.000). There was no significant difference among different age groups in term of the prevalence of trachoma (P=0.052). The prevalence of trachomatous follicle (TF), trachomatous inflammation (TI), and trachomatous scarring (TS) was 5.68% (152/2676), 19.21% (514/2676), 0.56% (15/2676), respectively. TI was more prevalent in girls than in boys (22.90% versus 16.75%, P=0.000). CONCLUSIONS: Trachoma is still endemic in children of primary schools in Tengzhou rural areas. Some interventions including mass treatment with antibiotics, improvement of hygienic conditions, and improvement of primary eye care are needed.