BACKGROUNDTo investigate the efficacy of combined hyperfractionated radiation therapy (HFX RT) plus accelerated HFX RT and concomitant chemotherapy (CHT) in stage IIIA or IIIB non-small-cell lung cancer (NSCLC) compared with HFX RT alone.

METHODSFrom August 1998 to December 2001, 56 patients with NSCLC were randomized into the following groups: HFX RT alone group (group I, n=28), HFX RT with 1.2 Gy twice daily to a total dose of 45.6 Gy, followed by accelerated HFX RT with 1.6 Gy twice daily, the total planned radiation dose was 68.0 Gy in tumour; HFX RT/CHT concomitant group (group II, n=28), same RT with CHT consisting of 20 mg/m² of cisplatin (DDP) on days 1 to 3 and 50 mg/m² of etoposide (VP 16) on days 1 to 3, repeated every two weeks during the RT course.

RESULTSThe overall response rate was 78.6% in group II, including 10 patients with complete response and 12 with partial response; 39.3% in group I, including 11 patients with partial response. Group II had a higher overall response rate compared to Group I (P=0.003). The median survival time was 16 months for group II, 13 months for group I. There was a significant difference in the median survival time between two groups (P= 0.000 3 ). Group II (57.1%) had a lower distant metastasis rate compared with group I (85.7%) (P= 0.018 ). Patients in group II showed a higher incidence of acute and/or late high-grade toxicity (hematologic toxicity, esophagitis, late lung toxicity) compared with group I patients, but no significant difference was observed between the two groups.

CONCLUSIONSThe HFX RT plus accelerated HFX RT and concomitant PDD/VP-16 CHT is tolerable and substantially increases the response rate and prolongs survival in IIIA/IIIB NSCLC patients.

Objective To investigate the protective effect and mechanism of apigenin on the liver of hyperlipidemic mice based on metabolomics methods.Methods C57BL/6 mice were randomly divided into four groups including blank,model,fenofibrate(26.0 mg·kg-1),and apigenin(12.5 mg·kg-1)groups,with six mice in each group.Each group was treated with corresponding drug by gavage once a day for five days.On the third day of administration,the mouse model of acute hyperlipidemia was induced by a single intramuscular injection of Triton WR-1339(5 mL·kg-1)at a concentration of 0.12 g·mL-1.Biochemical indexes such as TC and TG in mice serum were measured by using a fully automatic microplate reader.HE staining was used to observe pathological changes in liver tissue.UPLC-Q-TOF-MS/MS technology was applied to analyze liver tissue samples.Differential metabolites were screened by using multivariate statistical analysis methods such as PCA,PLS-DA,and OPLS-DA.Then we ran the mass spectrometry information of these metabolites through online databases including HMDB,METLIN and KEGG,as well as combined with relevant literature to obtain the potential differential metabolites.The identified potential differential compounds were imported into the MetaboAnalyst platform for metabolic pathway analysis.Results Compared with the blank group,TC and TG levels in mice serum of model group increased obviously(P＜0.01).Irregular arrangement of liver cells,fat vacuoles and infiltration of inflammatory cells were found.Compared with the model group,TC and TG levels in mice serum of apigenin group decreased(P＞0.05).Fatty lesions in liver tissue were significantly improved,and fat vacuoles and inflammatory cell infiltration were significantly reduced.A total of 35 differential metabolites were screened.Twenty-six differential metabolites showed callback trend after apigenin treatment.Eight metabolic pathways were obviously affected,among which pantothenate and CoA biosynthesis,as well as arachidonic acid metabolism are two main metabolic pathways(P＜0.05).Conclusion Apigenin exhibits a certain protective effect on liver of hyperlipidemic mice,and its mechanism may be related to regulating liver inflammatory response and lipid metabolism-related pathways.