MiRNA-199a-5p Protects Against Cerebral Ischemic Injury by Down-Regulating DDR1 in Rats.

OBJECTIVE: To assess the effects of miR-199a-5p on cerebral ischemic injury and its underlying mechanisms. METHODS: Infarct volume, neurologic deficit scores, and brain water content were evaluated after 24 hours of reperfusion. The histopathological damage in cortical neurons was assayed by hematoxylin and eosin staining. Neuronal apoptosis was evaluated by the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay. The regulatory effect of miR-199a-5p on discoidin domain receptor 1 (DDR1) was investigated using a dual luciferase reporter gene assay. Expression levels of miR-199a-5p and DDR1 were detected by real-time fluorogenic polymerase chain reaction and Western blot analysis. Expression levels of tumor necrosis factor (TNF)-α, interleukin (IL)-ß, and IL-6 were investigated by enzyme-linked immunosorbent assay. RESULTS: Our results suggest that DDR1 is the target gene of miR-199a-5p. The expression levels of miR-199a-5p and DDR1 were significantly down-regulated and up-regulated in the rats with cerebral ischemia compared with the control and sham groups, respectively. Moreover, infarct volume, neurologic score, brain water content, neuronal damage, and neuronal apoptosis were significantly decreased in the mimics group, siRNA DDR1 (siDDR1) group, and especially the mimics + siDDR1 group. The results also confirmed significantly weakened expression levels of proinflammatory cytokines (TNF-α, IL-6, and IL-1ß) in mimics, siDDR1, and especially mimics + siDDR1 rats. In addition, DDR1 silencing attenuated the effects of the miR-199a-5p inhibitor on neurologic function, infarct volume, brain water content, and proinflammatory cytokine expressions after middle cerebral artery occlusion in rats. CONCLUSIONS: miR-199a-5p may protect against cerebral ischemic injury by down-regulating DDR1 in rats.

Efficacies of minimally invasive puncture and small bone window craniotomy for hypertensive intracerebral hemorrhage, evaluation of motor-evoked potentials and comparison of postoperative rehemorrhage between the two methods.

Application value of the minimally invasive puncture and small bone window craniotomy in hypertensive intracerebral hemorrhage was investigated to explore the effects of the above treatment methods on motor-evoked potentials (MEPs) and postoperative rehemorrhage. Patients with hypertensive intracerebral hemorrhage who were admitted to Chengyang People's Hospital from March 2016 to December 2017 were selected and randomly divided into the minimally invasive group (n=40) and the craniotomy group (n=40). The minimally invasive group was treated with minimally invasive puncture and drainage for hematomas, while the craniotomy group received small bone window craniotomy for evacuation of hematomas. The clinical efficacy was compared between the two groups. At 28 days after operation, the Chinese scale of clinical neurological deficit of stroke patients (CSS) score in the minimally invasive group was lower than that in the craniotomy group (p<0.05). At 28 days after operation, the S-100ß level in the minimally invasive group was lower than that in the craniotomy group (p<0.05). At 1 week after operation, 35 patients in the minimally invasive group were able to elicit MEP waveforms, and only 7 patients in the craniotomy group were able to elicit positive waveforms. At 2 weeks after operation, 40 patients in the minimally invasive group and 20 patients in the craniotomy group could elicit MEP waveforms, and the incubation period, central motor conduction time and amplitude in the former were significantly better than those in the latter (p<0.05). The operation time and length of hospital stay were shorter with more total expenses of hospitalization in the minimally invasive group compared to those in the craniotomy group (p<0.05). Compared with small bone window craniotomy, minimally invasive puncture can reduce serum S-100ß level. Its advantages are obvious, so it is worthy of promotion and application.

Mining the glioma susceptibility genes in children from gene expression profiles and a methylation database.

Glioma is the most common type of primary brain tumor, which is associated with a poor prognosis due to its aggressive growth behavior and highly invasive nature. Research regarding glioma pathogenesis is expected to provide novel methods of adjuvant therapy for the treatment of glioma. The use of bioinformatics to identify candidate genes is commonly used to understand the genetic basis of disease. The present study used bioinformatics to mine the disease-related genes using gene expression profiles (GSE50021) and dual-channel DNA methylation data (GSE50022). The results identified 17 methylation sites located on 33 transcription factor binding sites, which may be responsible for downregulation of 17 target genes. glutamate metabotropic receptor 2 was one of the 17 downregulated target genes. Furthermore, inositol-trisphosphate 3-kinase A (ITPKA) was revealed to be the gene most associated with the risk of glioma in children. The protein coded by the ITPKA gene appeared in all risk sub-pathways, thus suggesting that ITPKA was the gene most associated with the risk of glioma, and inositol phosphate metabolism may be a key pathway associated with glioma in children. The identification of specific genes helps to determine the pathogenesis and possible therapeutic targets for the treatment of glioma in children.