ABSTRACT
Objective To investigate the influencing factors and predictors for radiation encephalic necrosis after CyberKnife radiotherapy.Methods Ninety-four patients (104 targets) with primary or metastatic intracranial tumors who were treated with CyberKnife radiotherapy from 2006 to 2011 were retrospectively analyzed.All surgeries adopted skull tracking modes with a dose of 12-45 Gy in 1-8 fractions prescribed to 60％-87％ isodose line.Radiation encephalic necrosis was determined by imaging or pathological examination.Logistic regression analysis was used to analyze the relationship between radiation encephalic necrosis and factors including diabetes,cardio-cerebrovascular diseases,target volume,isodose line,prescribed dose,number of fractions,combination with whole-brain irradiation (WBI),and biologically equivalent dose (BED).Predictability and critical threshold of all influencing factors for radiation encephalic necrosis were determined by the receiver operating characteristic (ROC) curve.Results Twelve targets (11.54％) had radiation encephalic necrosis.According to the result of logistic regression analysis,BED,combination with WBI,and number of fractions were influencing factors for radiation encephalic necrosis.In the ROC curves,the areas under curves for the above three factors were 0.892 ± 0.034,0.650± 0.072,and 0.712 ± 0.064,respectively,indicating that only BED can well predict radiation encephalic necrosis after CyberKnife radiotherapy with a dose threshold of ＞ 7410 cGy.Conclusions BED,combination with WBI,and number of fractions are influencing factors for radiation encephalic necrosis.BED is the best predictor of radiation encephalic necrosis with a dose threshold of ＞ 7 410 cGy.
ABSTRACT
Objective:To investigate the effects and underlying mechanisms of XRCC3 on esophageal squamous-cell carcinoma (ESCC) radiotherapy response. Methods:Expression levels of XRCC3 were detected by reverse transcription PCR, Western blot, and immunohistochemistry. We knocked down XRCC3 with lentiviral infection in ESCC cells. Cell apoptosis was examined by flow cytom-etry. DNA damage and telomere dysfunction-induced foci were determined by immunofluorescence. Results:The expression levels of XRCC3 in ESCC cells and tissues were higher than those in normal esophageal epithelial cells and corresponding adjacent noncancer-ous esophageal tissues. Knockdown of XRCC3 in ESCC cells substantially increased the therapeutic efficacy of radiation. We demon-strated that the radiation resistance of XRCC3 was attributed to the XRCC3-maintaining telomere stability, which reduced ESCC cell death through radiation-induced apoptosis. Conclusion: Our data suggested that XRCC3 protects ESCC cells from ionizing radia-tion-induced DNA damage and death by enhancing telomere stability. Thus, XRCC3 can be used as a promising therapeutic target for ESCCs.
ABSTRACT
Objective To investigate the change of gamma-aminobutyric acid A (GABAA) receptor α1 subunit mRNA expression in nitroglycerin induced migraine rat model,thus suggesting the relationship between GABAA receptor and migraine.Methods Thirty adult female Sprague-Dawley (SD) rats were randomly divided into control group,migraine model group,sodium valproate-treated group,each of the last 2 groups was divided into the attacking group and intermission group.The model of migraine was established using Cristina method,once a week for 5 weeks.After the second injection,rats in sodium valproate-treated group were given sodium valproate(0.5 g/L,10 ml/kg) everyday,and those in control group and model group were given normal saline solution(10 ml/kg).After the fifth injection,at the second hour(attacking groups) or the fourth day(intermission groups and control group),reverse transcription-polymerase chain reaction was used to detect the expression level of GABAA receptor α1 mRNA in brainstem and trigeminal ganglion.Results The expression level of GABAA receptor α1 mRNA in modeling attacking group(1.50 ±0.13) was higher than any other group(control group:1.01 ±0.24,modeling intermission group:1.04 ±0.10,sodium valproate-treated attacking group:0.99 ± 0.22,sodium valproate-treated intermission group:0.72 ± 0.03),and it was significantly higher than modeling intermission group(x2 =9.490,P =0.009).There was no statistical difference between modeling group and any other group,and compared with control group,there was no statistical difference in sodium valproate-treated attacking group or intermission group.Conclusion The pathogenesis of migraine may be related to the expression level of GABAA receptor α1 mRNA.