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Objective Few studies are reported on the clinical characteristics of glioma-related epilepsy (GRE).Postoperative recurrence of epilepsy in some patients seriously affects their recovery.We aimed to explore the duration, frequency and type of the epileptic seizure as well as possible factors for postoperative recurrence of epilepsy.Methods We recorded the frequency and duration of epileptic seizures, analyzed the recurrence-related factors using the Cox regression model, and investigated the risk factors of recurrent epilepsy.Results The postoperative recurrence of epilepsy was found in 24 (26.97%) of the 89 cases, which, compared with the 65 non-recurrence cases, had a significantly longer seizure duration (7[3-10] vs 5[2-9] min, P2 cm) (HR=2.867, 95% CI: 1.210-6.795), brain wave type (HR=2.501, 95% CI: 1.058-5.914), and preoperative frequency of epileptic seizure (>6 times/mo) (HR=5.100, 95% CI: 2.437-10.677).Conclusion Postoperative recurrence of epilepsy is associated with the clinical pathological parameters, and the changes of the frequency and duration of epileptic seizures before and after surgery may provide some new theoretical reference for the treatment and prognosis of the disease.
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Objective To explore expression of HMGB1 and TLR4 in epileptogenic focus brain tissue of temporal lobe intractable epilepsy patients, and analyze its significance in epileptic seizures. Methods 85 tempo-ral lobe intractable epilepsy patients were included in the research. Patients underwent resection of epileptogenic focus in Neurosurgery Department of The Fifth Affiliated Hospital of Zhengzhou University during January 2011 to January 2012. Epileptogenic focus brain tissue during operation were studied. 20 patients underwent intracranial decompression were selected as control group. Normal brain tissue during operation were studied. Immunohisto-chemical method was applied to detect HMGB1 and TLR4 expression level in epileptogenic focus brain tissue of ex-perimental group patients and normal brain tissue of control group patients. Correlation of HMGB1 and TLR4 expres-sion level and epileptic seizures was analyzed. Results Positive expression rate of HMGB1 (χ2= 74.375, P =0.000) and TLR4(χ2= 57.495, P = 0.000) in epileptogenic focus brain tissue of experimental group patients are both higher than that in normal brain tissue of control group patients. Expression of HMGB1 and TLR4 in epilepto-genic focus brain tissue is correlated with course of epilepsy (χ2= 25.798, P = 0.000), (χ2= 10.548, P = 0.001) preoperative epileptic seizure duration(χ2=8.403, P=0.004),(χ2=10.564, P= 0.001) and preoperative epilep-tic seizure frequency (χ2=4.912, P=0.027), (χ2=5.567, P=0.018). Conclusions HMGB1-TLR4 passageway may become new direction to study pathogenesis, diagnosis, and treatment of intractable epilepsy.
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Objective To explore expression of HMGB1 in glioma tissue of glioma-related epilepsy patients. Methods Immunohistochemistry was used to detect the expression of HMGB1 in the tissues from 82 glioma-related epi?lepsy patients (glioma-related epilepsy group), 80 glioma patients (glioma without epilepsy group), 80 intractable epilepsy patients (epilepsy control group) epileptogenic foci tissue and 20 normal controls (negative control group). Results HMGB1 in glioma tissue of glioma-related epilepsy group was significantly higher than that in glioma tissue of glioma without epilepsy grou p (χ2=16.944, P<0.001), especially in low pathological grade glioma tissue. HMGB1 was higher in glioma tissue of glioma-related epilepsy group than in epileptogenic foci tissue of epilepsy control group (χ2=26.094, P<0.001). Expression of HMGB1 in glioma tissue of glioma without epilepsy group (χ2=32.273, P<0.001) and epileptogenic foci tissue of epilepsy control group ( χ2=22.236,P<0.001) was higher than in normal brain tissue of negative control group. In glioma-related epilepsy group, HMGB1 was positively correlated with seizures duration(r=0.365,P=0.001), sei? zures frequency (r=0.531,P=0.000) and pathological grade of glioma tissue (r=0.265,P=0.016). Conclusions HMGB1 is highly expressed in glioma tissues of glioma-related epilepsy; HMGB1 expression is closely related with seizures; and HMGB1 in glioma tissue may contribute to the formation of glioma-related epilepsy.
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Objective:To detect the functional role of Fascin1 and its related molecular mechanisms in migration and invasion capacity of glioma cells,we utilized gene specific small interference RNA of Fascin1 in cell line U87 MG. Methods:Fascin1-siRNA or negative siRNA was transfected into U87 MG cells of control group or experiment group. Transwell method was employed to assess the migration and invasion capacity of glioma cells. Western blot analysis was used to detect the protein expression of Fascin1,pAKT and pSTAT3. The impact of PI3K/AKT pathway and STAT3 pathway on migration and invasion of U87 MG cells was verified,via applying LY294002 and LY294002,which was inhibitor of the two pathways respectively. Results:As compared to control groups,the migration and invasion capacity of transfected glioma cells were attenuated about 52% or 43%(P<0. 05),accompanied with the decreased phos-phorylation of AKT and STAT3. As utilizing the inhibitors of AKT and STAT3,attenuated migration and invasion capacity of U87 MG cells were observed. Conclusion:Down-regulated expression of Fascin1 could suppress the migration and invasion capacity of U87 MG cells by inhibiting the phosphorylation of PI3K/AKT pathway and STAT3 pathway.
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Objective To investigate the protective effect of allopurinol in kainic acid-induced epileptic rats and to explore new ideas and methods for the clinical treatment of epilepsy. Methods 120 Wistar rats were randomly divided into sham group, KA epilepsy group and allopurinol groups. Six rats of each group were randomly selected and were given electrodes into their left frontal and hippocampal regions. After injection, behavior changes were observed in all rates without electrodes. 24 h later, MDA level and SOD enzymatic activity of the left hippocampi were measured. One week later, the EEGs were recorded in rates with electrode, as well as total time of seizures /30 min and numbers of seizures / 30 min. Results Compared with the KA model group, latency period of the epilepsy in the allopurinol group was longer (P < 0.05) and the extent was lighter (P < 0.05); the MDA level was significantly lower (P < 0.01), the SOD enzymatic activity was significantly higher (P < 0.01). The total time of seizures / 30min and numbers of seizures / 30 min in allopurinol group reduced significantly (P < 0.01). Conclusion Allopurinol has potential antiepileptic and antioxidative activities in kainic acid-induced epileptic rats.