OBJECTIVE: To evaluate the effect of hyperfractionated radiation therapy and concomitant chemotherapy for inoperable stage III non-small cell lung cancer (NSCLC). METHODS: Seventy patients were randomized equally into two group. The therapy group received radiotherapy with hyperfractionated radiation therapy combined with concomitant chemotherapy, and the control group was treated with chemotherapy only. RESULT: The overall response rate, including the rate of both complete (CR) and partial responses (PR), in the therapy group was 60.0% with a CR rate of 8.6%. The overall response rate in the control group was 40.0% with a CR rate of 5.7%. The difference in overall response rate was statistically significant between the two groups (P<0.05). The median survival time, 1- and 2-years survival rate were 12.8 months, 48.6%, and 25.7%, respectively, in the hyperfractionated radiotherapy group, and 9.4 months, 34.3%, and 17.1%, respectively, in the chemotherapeutic group (P 0.031). The major toxic effects of the chemotherapy were myelosuppression and radiation esophagitis. CONCLUSION: Hyperfractionated radiation therapy plus concomitant chemotherapy with paclitaxel for inoperable stage III NSCLC improves the short-term response of the patients, but fail to raise the survival rate. 相似文献
Background: Volatile anesthetic preconditioning (APC) protects against myocardial ischemia-reperfusion (IR) injury, but the precise mechanisms underlying this phenomenon remain undefined. To investigate the molecular mechanism of APC in myocardial protection, the activation of nuclear factor (NF) [kappa]B and its regulated inflammatory mediators expression were examined in the current study.
Methods: Hearts from male rats were isolated, Langendorff perfused, and randomly assigned to one of three groups: (1) the control group: hearts were continuously perfused for 130 min; (2) the IR group: 30 min of equilibration, 15 min of baseline, 25 min of ischemia, 60 min of reperfusion; and (3) the APC + IR group: 30 min of equilibration, 10 min of sevoflurane exposure and a 5-min washout, 25 min of global ischemia, 60 min of reperfusion. Tissue samples were acquired at the end of reperfusion. NF-[kappa]B activity was determined by electrophoretic mobility shift assay. The NF-[kappa]B inhibitor, I[kappa]B-[alpha], was determined by Western blot analysis. Myocardial inflammatory mediators, including tumor necrosis factor [alpha], interleukin 1, intercellular adhesion molecule 1, and inducible nitric oxide synthase, were also assessed by Western blot analysis.
Results: Nuclear factor [kappa]B-DNA binding activity was significantly increased at the end of reperfusion in rat myocardium, and cytosolic I[kappa]B-[alpha] was decreased. Supershift assay revealed the involvement of NF-[kappa]B p65 and p50 subunits. APC with sevoflurane attenuated NF-[kappa]B activation and reduced the expression of tumor necrosis factor [alpha], interleukin 1, intercellular adhesion molecule 1, and inducible nitric oxide synthase. APC also reduced infarct size and creatine kinase release and improved myocardial left ventricular developed pressure during IR. 相似文献