Although neural stem cells (NSCs) could migrate towards lesions after central nervous system (CNS) injury, the migration ability always is restricted due to the disturbed composition and density of the adhesion ligands and extracellular matrix (ECM) gradient after CNS injury. To date, various methods have been developed to enhance NSC migration and a number of factors, which are affecting NSC migration potential, have been identified. Here, primary NSCs were cultured and the expression of actin alpha 2 (ACTA2) in NSCs was determined using reverse transcription polymerase chain reaction (RT-PCR) and immunostaining. Next, the role of ACTA2 in regulating NSC migration and the potential mechanism was explored. Our results demonstrated that ACTA2 expressed in NSCs. Meanwhile, downregulated ACTA2 using siRNA inhibited NSC migration through hindering actin filament polymerization via increasing RhoA expression and decreasing Rac1 expression. The present study might enrich the basic knowledge of ACTA2 in NSC migration and open an avenue for enhancing NSC migration potential, subsequently providing an intervention target for functional recovery after CNS injury.

Intracerebral hemorrhage (ICH) has been becoming a serious public health problem. Pneumonia, occurring in 43% of all ICH patients, is a common complication heavily influencing outcome and accounting for more than 1/3 of the overall mortality in patients with ICH. Ambroxol may be an effective additional treatment for ICH patients with pneumonia. But its effect and potential mechanism on functional recovery post-ICH still remain elusive. In the present study, the results indicated that 35 mg/kg and 70 mg/kg ambroxol facilitated neuronal survival and reduced white matter fiber bundle damage due to mitigating microglial activation and reducing proinflammatory cytokine accumulation in mice with ICH. The possible mechanism might be due to suppressing endoplasmic reticulum stress involving the IRE1α/TRAF2 signaling pathway, which paves a new path for the treatment of ICH and opens a new window for the use of ambroxol in clinical practice.

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OBJECTIVETissue plasminogen activator (tPA) fibrinolysis did not improve functional outcomes of patients with intraventricular hemorrhage (IVH), largely because of the unsatisfactory clot clearance. The presence of neutrophil extracellular traps (NETs) within the clot has been confirmed to impair tPA fibrinolysis, but the mechanism has been unclear. The authors hypothesized that cell-free DNA (cfDNA), the main framework of NETs, might be the important reason for the fibrinolysis resistance, and they validated the hypothesis, hoping to provide a new target to promote intraventricular fibrinolysis.METHODSFirst, cfDNA was detected in IVH clots by immunofluorescence staining in a rat model of IVH. Second, after blood (with or without exogenous cfDNA) intraventricular injection, IVH rats were given intraventricular infusion of 2 μl of saline, tPA, or tPA + DNase1 randomly. Then, the ventricular volume, animal behavior, and reactive astrocyte proliferation were assessed. Third, the IVH clots were collected for fibrinolysis assay in vitro. Finally, the effects of exogenous cfDNA in IVH were evaluated.RESULTSThe presence of cfDNA in clots was observed as early as 1 hour after IVH. Compared with the whole-blood model, blood + cfDNA caused more severe ventricular dilation (day 7: blood 32.47 ± 2.096 mm3 vs blood + DNA 40.09 ± 2.787 mm3, p < 0.05), increased fibrinolysis resistance to tPA (day 7: tPA + DNA 26.04 ± 1.318 mm3 vs tPA 22.15 ± 1.706 mm3, p < 0.05), and further deteriorated the functional defects in rats (blood vs blood + DNA, p < 0.05). Degradation of cfDNA by DNase1 further enhanced the fibrinolysis effects on relieving the ventricular dilation (day 7: tPA + DNase1 11.67 ± 2.023 mm3 vs tPA, p < 0.05), improving the functional outcome (tPA vs tPA + DNase1, p < 0.05) and reducing periventricular astrocyte proliferation.CONCLUSIONScfDNA impaired tPA fibrinolysis for IVH, and degradation of cfDNA may be a new target to improve this condition.

Purpose The increasing number of deaths due to road traffic accidents (RTAs) has attracted global attention. However, the influence of road types is rarely considered in the study of RTAs. This study evaluates the influence of different road types in RTAs in northern Guizhou to provide a basis for the formulation of evidence-based policies and measures. Methods We obtained the data from the Zunyi Traffic Management Data Platform for the years 2009–2018. The mortality rates of RTAs were calculated. Descriptive methods and Chi-square tests were used to analyze the characteristics of road traffic collisions on different road types. We also examined the associations between the mortality rate per 10,000 vehicles and the growth of per capital gross domestic product (GDP) with Spearman’s rank correlation analysis. According to the passing volume and the infrastructure, we defined different types of roads, like administrative road, functional road, general urban road and urban expressway. Results In 2012, the traffic mortality rate of administrative roads was 8.9 per 100,000 people, and the mortality rate of functional roads was 7.4 per 100,000 people, which decreased in 2018 to 6.1 deaths per 100,000 people and 5.2 deaths per 100,000 people, respectively. The mortality rate per 10,000 vehicles reached the highest level in 2011 (28.8 per 10,000 vehicles and 22.5 per 10,000 vehicles on administrative and functional roads, respectively). The death rate of county roads was the highest among administrative roads ( χ 2 = 17.389, p < 0.05) and that of fourth-class roads was the highest among functional roads ( χ 2 = 21.785, p < 0.05). The mortality rate per 10,000 vehicles was negatively correlated with per capital GDP. Conclusion Although our research shows that RTAs in northern Guizhou have steadily declined in recent years, the range of decline is relatively small. Many measures and sustainable efforts are needed to control road traffic death and accelerate the progress in road traffic safety in northern Guizhou.