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Objective:To investigate the effect of lncRNA HOTAIR on the radiosensitivity of glioma cells and its underlying mechanism.Methods:The negative control plasmid, HOTAIR silencing plasmid, miR-NC over expressing plasmid, miR-17-5p over expressing plasmid were transfected into U87R cells, and assigned intothe silencing control, HOTAIR silencing, miR-NC over expressing and miR-17-5 pover expressing groups. Cells in the the above groups were irradiated at a dose of 4Gy, and recorded as silencing control+ 4Gy group, HOTAIRsilencing+ 4Gy group, miR-NC over expressing+ 4Gy group and miR-17-5p over expressing+ 4Gy group. The HOTAIR silencing plasmid, miR-NC suppressing plasmid and miR-17-5p suppressing plasmid were co-transfected into U87R cells and recorded as the HOTAIR silencing+ miR-NC suppressing group and HOTAIR silencing+ miR-17-5p suppressing group. All procedures were transfected by the liposome method. The expression of miR-17-5p and HOTAIR was detected by qRT-PCR. The radio sensitivity of glioma cells was evaluated by cell clone formation assay. The cell apoptosis was assessed by flow cytometry. The fluorescence activity was assessed by dual luciferase reporter assay.Results:HOTAIR was highly expressed in the radiation-resistant glioma cells. Silencing HOTAIR and over-expressing miR-17-5p could increase the radiosensitivity of U87R cells and promote radiation-induced apoptosis of U87R cells. HOTAIR could target and regulate the miR-17-5p expression. Suppressing miR-17-5p reversed the effect of silencing HOTAIR on U87R cell sensitization and promoting radiation-induced U87R cell apoptosis.Conclusions:Silencing lncRNA HOTAIR yields radiation sensitization and promotes radiation-induced apoptosis in glioma cells. The mechanism may be related to the regulation of miR-17-5p.
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Objective To investigate the genotoxicity of aniline and repair dynamics in hepatocytes and lymph-cytes.Methods Aniline was administered intragastrically to SPF Kunming mice ( five mice in each group) in a single dose of 100 mg/kg body weight.The hepatocytes and peripheral blood lymphocytes were obtained at 3, 8, 16, 24, and 32 hours after aniline administration, respectively.The control mice received tap water only.The DNA damages were detected by single cell gel electrophoresis assay ( SCGE) and the time-effect relationship was analyzed.Results The results of SCGE experiment showed that both the tail lenth and tail moment of the hepatocyte DNA were increased gradually from 8 h, and reached the maximum at 16 h ( P0.05).The two DNA damage indexes of peripheral blood lymphocytes started to increase at 16 h, reached the maxi-mum at 24 h ( P<0.01) , and began to recover at 32 h after aniline administration.Conclusions Our findings suggeste that aniline may be a potential genotoxicant to hepatocytes and peripheral blood lymphocytes.There is a clear time-response relationship in terms of the two DNA damage indexes, indicating that hepatocytes and lymphocytes in mice possess an effi-cient DNA repair mechanism against aniline toxicity.
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Objective To investigate the incidence and etiological factors of hyponatremia following traumatic brain injury (TBI) and analyze the relationship between hyponatremia and the patient’s age, gender, type of injury, Glasgow coma scale (GCS), operation and computerized tomography (CT) scan of head. Methods Clinical data of 136 pa-tients with moderate or severe TBI in our hospital were analyzed retrospectively, including patient’s age, gender, type of injury, GCS, operation, brain edema and basal skull fracture. The relationship between clinical data and hyponatremia were analyzed statistically by Chi-square test and multivariate Logistic regression analysis. Results There were 56 pa-tients with hyponatremia in 136 patients (81 males) with moderate or severe TBI. Multivariate Logistic regression analysis showed that hyponatremia secondary to TBI was not associated with patient’s age, gender, type of injury and operation or not. However, there was a high correlation between hyponatremia following TBI and clinical characteristics of TBI at ear-ly stage, such as GCS, brain edema and basal skull fracture. Conclusions Patients with TBI is more likely to develop hy-ponatremia when they have the following clinical factors, such as GCS≤8, brain edema or basal skull fracture. Preven-tive measures should be given to these patients in advance.
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Objective To explore the localization of epileptogenic focus and select the appropriate surgical procedures for post-traumatic epilepsy. Methods The clinical data of 21 patients with post-traumatic epilepsy were studied retrospectively. Epileptogenic focus was located by comprehensively analyzing data of electro-neurophysiology, neurological imaging and clinical manifestation. Surgical procedures were performed in all patients, including resection of lesion and peripheral cortex in 12 patients, epileptogenie focus resection plus low power bipolar coagulation in five, anterior temporal iobectomy plus amygdalohippocampectomy in three and corpus callosotomy in one. Results All patients were followed up from 6 months to 3 years, which showed satisfactory outcome in eight patients, marked improvement in six, improvement in five and slight improvement in two. The total effective rate was 90%. Conclusions Surgical procedure is important for intractable post-traumatic epilepsy. The good efficacy depends on precise localization of epileptogenic focus and combined application of various surgical procedures.