Effect of valproic acid combined with transplantation of olfactory ensheathing cells modified by neurotrophic 3 gene on nerve protection and repair after traumatic brain injury.

BACKGROUND: Traumatic brain injury (TBI) often leads to cognitive and neurological dysfunction. Valproic acid (VPA) has a neuroprotective effect in acute central nervous system diseases; the neurotrophin 3 gene (NT-3) can maintain the survival of neurons, and olfactory ensheathing cells (OECs) can promote the growth of nerve axons. This study aimed to evaluate the restorative effect of VPA combined with NT-3 modified OECs (NT-3-OECs) on neurological function after TBI. METHODS: The neurological severity score (NSS) of rats was evaluated on the 1st, 7th, 14th, and 28th day after TBI modeling and corresponding intervention. Hematoxylin-eosin (HE) staining, p75 nerve growth factor receptor (P75), glial fibrillary acidic protein (GFAP), and neurofilament protein (NF)staining, and argyrophilic staining were used to observe the morphology of brain tissue 28 days after modeling. Moreover, TdT-mediated dUTP Nick-End Labeling (TUNEL) was used to detect the apoptosis rate of neurons. The changes in synapses and mitochondria in the injured area were observed by electron microscope. RESULTS: NT-3-OECs transplantation can increase the content of NT-3 in brain tissue, and NT-3-OECs can survive for >28 days. The NSS score of the TBI-VPA-NT-3-OECs group 28 days after cell transplantation was significantly lower than that of the other model treatment groups (P < 0.05). The morphological structure of the brain tissue was more complete, and the neurofilament fibers were neatly arranged, achieving better results than those of the other groups. The apoptosis rate of nerve cells in the TBI-VPA-NT-3-OECs group was significantly lower than in the other treatment groups (P < 0.05). Furthermore, the number of synapses in the combined intervention group was significantly higher than in the other treatment groups, and the mitochondrial structure was more complete. CONCLUSION: NT-3-OECs have good biological function, and VPA combined with NT-3-OECs transplantation can effectively improve the prognosis of TBI rats.

Role of narrative medicine-based education in cultivating empathy in residents.

OBJECTIVE: To explore the role of narrative medicine-based education in standardized empathy training for residents. METHODS: Among the 2018-2020 residents at the First Affiliated Hospital of Xinxiang Medical University, 230 receiving neurology training were enrolled in this study and randomly divided into study and control groups. The study group received narrative medicine-based education and standardized routine resident training. The Jefferson Scale of Empathy-Medical Student version (JSE-MS) was used to evaluate empathy in the study group, and the neurological professional knowledge test scores of the two groups were also compared. RESULTS: In the study group, the empathy score was higher than the preteaching score (P < 0.01). The neurological professional knowledge examination score was higher in the study group than in the control group, albeit not significantly. CONCLUSION: The addition of narrative medicine-based education in standardized training improved empathy and may have improved the professional knowledge of neurology residents.

LncRNA LINC00319 is associated with tumorigenesis and poor prognosis in glioma.

Glioma is one of the most universally diagnosed malignant tumors in the central nervous system with high mortality and morbidity in the world. Long non-coding long intergenic non-protein coding RNA 319 (LINC00319) exerts promoting function in diverse range of human carcinomas, but its detailed role in glioma remains to be investigated. This study aimed to investigate the potential role and regulatory mechanism of LINC00319 and also its clinical value in glioma. In our study, LINC00319 was expressed at high levels in glioma and closely associated with poor prognosis of patients with glioma, whose knockdown impaired cell proliferation, arrested cell cycle and induced cell apoptosis of glioma. In addition, high expression of high mobility group AT-hook 2 (HMGA2) was found in glioma which was also in positive relation to LINC00319 expression. Moreover, LINC00319 directly bound to TATA-box binding protein associated factor 1 (TAF1) and further regulated HMGA2. Finally, rescue assays verified that LIN00319 modulated the tumorigenesis of glioma by regulating HMGA2. The present research elucidated the function role and underlying mechanism of LINC00319 in glioma and exposed a new insight into the molecular-targeted therapy for glioma.

[Phosphatidylinositide 3-kinase inhibitor BKM120 suppresses proliferation and promotes apoptosis of U251 glioblastoma cells].

Objective To investigate the effect of phosphatidylinositide 3-kinase (PI3K) inhibitor BKM120 on the proliferation and apoptosis of human glioma U251 cells. Methods U251 cells were treated with different concentrations of BKM120 (final concentrations were 1, 5, 20 µmol/L) for 48 hours. The effect of BKM120 on cell proliferation was detected by CCK-8 assay. The apoptosis was detected by annexin V-FITC/PI staining. The protein expressions of Bax and Bcl-2 were detected by Western blotting. Results CCK-8 assay showed that BKM120 inhibited U251 proliferation in a concentration-dependent manner and the maximum inhibitory rate was 78.3%. Flow cytometry showed that BKM120 induced cell aopotosis in a concentration-dependent manner. Western blotting revealed that the expression of Bax was elevated by BKM120, but the expression of Bcl-2 had a reverse trend. Conclusion BKM120 can inhibit the proliferation and induce the apoptosis of U251 cells.

[Curcumin improves learning and memory function through decreasing hippocampal TNF-α and iNOS levels after subarachnoid hemorrhage in rats].

OBJECTIVE: To investigate the effect of curcumin on learning and memory function of rats with subarachnoid hemorrhage (SAH) and the possible mechanism. METHODS: A total of 30 male Sprague-Dawley rats were randomly divided into three groups: Sham group, SAH group and curcumin (Cur) therapy group. Experimental SAH rat models were established by injecting autologous blood into the cisterna magna. Neurological deficits of rats were examined at different time points. Spatial learning and memory abilities were tested by Morris water maze test. The hippocampal tumor necrosis factor-alpha (TNF-α) and inducible nitric oxide synthase (iNOS) were detected by ELISA. RESULTS Experimental SAH rat models were established successfully. Neurological scores of the SAH rats were significantly lower than those of the sham group. Curcumin therapy obviously improved the neurological deficits of rats compared with the SAH rats. Morris water maze test showed that SAH caused significant cognitive impairment with longer escape latency compared with the sham group. After treatment with curcumin for 4 weeks, the escape latency decreased significantly. The levels of TNF-α and iNOS in the curcumin-treated group were significantly lower than those of the SAH group. CONCLUSION: SAH can cause learning and memory impairment in rats. Curcumin can recover learning and memory function through down-regulating hippocampal TNF-α and iNOS levels.

Association of single-nucleotide polymorphisms in ERCC1 and ERCC2 with glioma risk.

We conducted a case-control study to assess the role of three single-nucleotide polymorphisms (SNPs) in excision repair cross-complementation group 1 (ERCC1) and two SNPs in excision repair cross-complementation group 2 (ERCC2) on the glioma risk in a Chinese population, and investigate the gene-environmental interaction for the cancer risk. A 1:2 matched case-control study was conducted. Logistic regression analysis revealed that individuals carrying ERCC1 rs2298881 CC genotype were associated with risk of glioma when compared with AA genotype carriers. The significant associations of ERCC1 rs2298881 polymorphism with glioma susceptibility were observed in both the dominant and the recessive models. In a stratification analysis, we found that ERCC1 rs2298881 variants showed an increased association with the risk of glioma in males, ever smokers, and high-grade glioma cases. In conclusion, our study suggests that ERCC1 rs2298881 polymorphism is associated with risk of glioma in codominant, dominant, and recessive models, especially in males, smokers, and high-grade glioma cases. This finding could be useful in revealing the genetic characteristics of glioma and suggests more effective strategies for prevention and treatment.