Objective To explore the relationship between oxidative stress inducing neuronal apoptosis and the protein expressions of c-Myc, Fas-FasL and nuclear factor ?B (NF-?B) in neurons. Methods The primarily cultured neurons of SD rat in vitro were divided into 5 groups: Group A (control), Group B (treated with hypoxia), Group C (treated with small dose of H 2O 2), Group D (treated with hypoxia and SOD) and Group E (treated with H 2O 2 and SOD). Then, the neuronal apoptosis was elevated with TUNEL,Gel electrophoresis and flow cytometry. The protein expressions of c-Myc, Fas-FasL and NF-?B were detected with immunohistochemistry. Results Apoptosis rates of the Groups B and C were 6 and 8 times than that of the Group A respectively ( P

Objective To develop a new impact device that can cause different levels of spinal cord injury in adult rats so as to provide a scientific means for standard spinal cord injury model in adult rats. Methods First, two laser heads were installed beside the impacting hammer in order to define the dropping point of imparting hammer through the focus of the two tracts of lasers. A height controlled electrocircuit was designed to control the rotation of the minitype dynamo that regulated the height of impacting hammer precisely via the worm gear. Meanwhile, a time controlled electrocircuit was made so as to secure that the process of injury could be finished within 10 millionseconds constantly according to the technique of weight dropping and the principle of electromagnetic electromagnetism respectively. Results The present impact device could produce different levels of spinal cord injury in adult rats within special times, heights and dropping points. Conclusion We have successfully produced an electro-circuit controlled impact device with laser defining position that is simple and easy to use for making controllable and precise injury models.

Objective To investigate the effect of endovascular cooling on perioperative brain injury in patients undergoing intracranial aneurysm resection.Methods Sixteen Hunt-Hess Ⅱ -Ⅳ patients of both sexes aged 18-64 yr undergoing intracranial aneurysm resection were randomly divided into 2 groups(n = 8 each): mild hypothermia group(group MHT)and nonnothermia group(group NT).A CL-2295AE catheter was placed in the femoral vein after anesthesia induction to perform endovascular cooling.Bladder temperature was reduced to 34 ℃ and maintained for 24 h.The hemodynamic parameters were recorded during and after operation.Coagulantion function and electrolyte levels were determined at 24 h before operation and at 12 and 24 h after operation.The serum neuron-specific enolase(NSE)and S100B concentrations were determined at 1 d before operation and at 1,3and 7 d after operation by ELISA.Neurological function was assessed with GOS grade at 1 and 3 months after operation.Results There was no significant difference in hemodynamic parameters,electrolyte levels(Na+ ,K+ ,Ca2+)and coagulantion function(PT,APTT,Plt)between the two groups(P ＞ 0.05).The GOS grade was significantly higher,while serum NSE and S100B concentrations were significantly lower after operation in group MHT than in group NT(P ＜ 0.05).Conclusion Endovascular cooling(34℃,24 h)can reduce the brain injury safely and effectively during the perioperative period in patients undergoing intracranial aneurysm resection and improve the prognosis.

Objective: To explore the expression of hypoxia inducible factor-1α (HIF-1~) and the correlation between HIF-1α and apoptosis after traumatic brain injury.Methods: Using experimental traumatic brain injury in the rats, the expression of HIF-1α was studied by immunohisto-chemistry in cerebral tissue, apoptotic cell death was evaluated with TUNEL (transferase-mediated XdUTP nick end labeling ), and double-labeled immunohistochemistry and TUNEL methods were used to investigate the relationship between HIF-1α and apoptosis.Results: There was remarkable difference in the expression of HIF-1α between the experimental groups and the control groups (P ＜ 0.01), in the experimental groups,the expression of HIF-1α at 48 hours was highest; the evidence of apoptotic cell death after experimental traumatic brain injury was found by TUNEL; the apoptotic percentage increased or decreased according to the changes of the positive expression of HIF-1α (r = 0.99).Conclusions: The results suggest that secondary brain ischemia plays a crucial role in apoptotic cell death after traumatic brain injury; HIF-1α can prompt apoptotic cell death after experimental traumatic brain injury.

OBJECTIVE: To explore the relationship between neuronal apoptosis and hypoxia or traumatic injury. METHODS: Rat neurons primarily cultured in vitro were treated w ith hypoxia (the hypoxia group) or traumatic injury (the trauma group). The neur onal apoptosis was evaluated with microscope, TUNEL (terminal deoxynucleotidyl t ransferase mediated X-dUTPnick end labeling) staining, flow cytometry, agarose gel electrophoresis and immunohistochemistry RESULTS: Morphological changes of apoptosis appeared in the t reated neurons and the DNA fragmentation showed "ladder" break. The apoptotic index was 10.8% in the hypoxia group and 4.8% in the trauma group, while it was only 1.6% in the control group. The expression of apoptosis-associated genes (c-myc, fas and fasL) increased. CONCLUSIONS: Hypoxia or traumatic injury can induce neuronal ap optosis, and its molecular mechanism is probably related to the expressions of a poptosis-associated genes.

Chromosomal region maintenance 1 (CRM1) is associated with an adverse prognosis in glioma. We previously reported that CRM1 inhibition suppressed glioma cell proliferation both in vitro and in vivo. In this study, we investigated the role of CRM1 in the migration and invasion of glioma cells. S109, a novel reversible selective inhibitor of CRM1, was used to treat Human glioma U87 and U251 cells. Cell migration and invasion were evaluated by wound-healing and transwell invasion assays. The results showed that S109 significantly inhibited the migration and invasion of U87 and U251 cells. However, mutation of Cys528 in CRM1 abolished the inhibitory activity of S109 in glioma cells. Furthermore, we found that S109 treatment decreased the expression level and activity of MMP2 and reduced the level of phosphorylated STAT3 but not total STAT3. Therefore, the inhibition of migration and invasion induced by S109 may be associated with the downregulation of MMP2 activity and expression, and inactivation of the STAT3 signaling pathway. These results support our previous conclusion that inhibition of CRM1 is an attractive strategy for the treatment of glioma.

Chromosomal region maintenance 1 (CRM1) is associated with an adverse prognosis in glioma. We previously reported that CRM1 inhibition suppressed glioma cell proliferation both in vitro and in vivo. In this study, we investigated the role of CRM1 in the migration and invasion of glioma cells. S109, a novel reversible selective inhibitor of CRM1, was used to treat Human glioma U87 and U251 cells. Cell migration and invasion were evaluated by wound-healing and transwell invasion assays. The results showed that S109 significantly inhibited the migration and invasion of U87 and U251 cells. However, mutation of Cys528 in CRM1 abolished the inhibitory activity of S109 in glioma cells. Furthermore, we found that S109 treatment decreased the expression level and activity of MMP2 and reduced the level of phosphorylated STAT3 but not total STAT3. Therefore, the inhibition of migration and invasion induced by S109 may be associated with the downregulation of MMP2 activity and expression, and inactivation of the STAT3 signaling pathway. These results support our previous conclusion that inhibition of CRM1 is an attractive strategy for the treatment of glioma.

Objective To explore the expression level and clinical significance of α-Arrestin domain-containing protein 3(ARRDC3)gene in human brain glioma tissues.Methods Clinical data and gene expression of patients with brain glioma were analyzed using the Chinese Glioma Genome Atlas(CGGA)database and the Cancer Genome Atlas(TCGA)database.Brain glioma specimens were collected from 9 patients with primary brain gliomas treated in the Department of Neurosurgery,the Affiliated Hospital of Xuzhou Medical University from January 2018 to December 2021.The expression levels of ARRDC3 in gliomas of different grades were detected through immunohistochemical experiments.The expression levels of ARRDC3 in gliomas with different molecular types and grades were analyzed by using thenon-parametrictest.The effect of ARRDC3 expression on the survival time of brain glioma patients was analyzed by using the Kaplan-Meier survival curve,while the effect of ARRDC3 expression on prognosis of glioma patients was analyzed by using univariate and multivariate Cox regression models.Results Data in the CGGA and TCGA databases showed that the expression of ARRDC3 in the grade Ⅱ,Ⅲ and Ⅳhuman brain gliomas increased gradually(P＜0.05).The results of immunohistochemical staining experiments were consistent with the above results(P＜0.05).The ARRDC3 expression in isocitrate dehydrogenase(IDH)wild type glioma patients was significantly higher than that in IDH mutant glioma patients(P＜0.05).The overall survival of the patients with high ARRDC3 expression was significantly shorter than that of the patients with low ARRDC3 expression(P＜0.05).Multivariate Cox regression analysis revealed that age,IDH mutation state,radiotherapy and ARRDC3 expression were risk factors for prognosis of human brain glioma patients(P＜0.05).Conclusion With the pathological grade rising gradually,the relative expression level of ARRDC3 in human brain glioma tissues increases gradually.The prognosis of brain glioma patients with low expression of ARRDC3 is significantly better than that of patients with high expression of ARRDC3.ARRDC3 can be used as a prognostic factor for glioma patients.

Traumatic supraorbital fissure syndrome (TSOFS) is a symptom complex caused by nerve entrapment in the supraorbital fissure after skull base trauma. If the compressed cranial nerve in the supraorbital fissure is not decompressed surgically, ptosis, diplopia and eye movement disorder may exist for a long time and seriously affect the patients′ quality of life. Since its overall incidence is not high, it is not familiarized with the majority of neurosurgeons and some TSOFS may be complicated with skull base vascular injury. If the supraorbital fissure surgery is performed without treatment of vascular injury, it may cause massive hemorrhage, and disability and even life-threatening in severe cases. At present, there is no consensus or guideline on the diagnosis and treatment of TSOFS that can be referred to both domestically and internationally. To improve the understanding of TSOFS among clinical physicians and establish standardized diagnosis and treatment plans, the Skull Base Trauma Group of the Neurorepair Professional Committee of the Chinese Medical Doctor Association, Neurotrauma Group of the Neurosurgery Branch of the Chinese Medical Association, Neurotrauma Group of the Traumatology Branch of the Chinese Medical Association, and Editorial Committee of Chinese Journal of Trauma organized relevant experts to formulate Chinese expert consensus on the diagnosis and treatment of traumatic supraorbital fissure syndrome ( version 2024) based on evidence of evidence-based medicine and clinical experience of diagnosis and treatment. This consensus puts forward 12 recommendations on the diagnosis, classification, treatment, efficacy evaluation and follow-up of TSOFS, aiming to provide references for neurosurgeons from hospitals of all levels to standardize the diagnosis and treatment of TSOFS.