Objective:To investigate therapeutic effect of cisplatin sequential recombinant human vascular endostatin thoracic perfusion in treatment of malignant pleural effusion.Methods:A total of 80 patients with malignant pleural effusion in Maoming People's Hospital from January 2018 to February 2021 were enrolled, and all patients were divided into 2 groups according to the random number table methods, each group with 40 cases. The control group was treated with small-bore catheter minimally invasive drainage combined with cisplatin thoracic perfusion, and the study group was treated with small-bore catheter minimally invasive drainage combined with cisplatin sequential recombinant human vascular endostatin thoracic perfusion. And then the clinical efficacy, expressions of vascular endothelial growth factor (VEGF) expression, pain degree and adverse reactions were compared of both groups.Results:The treatment efficacy rate of the study group was higher than that of the control group [90% (36/40) vs. 75% (30/40)], and the difference was statistically significant ( χ2 = 5.04, P < 0.05). After treatment, the level of VEGF in pleural fluid and serum of the study group was lower than that of the control group [(304±106) pg/ml vs. (598±159) pg/ml,(103±43) pg/ml vs. (189±49) pg/ml], and the difference was statistically significant ( t = 6.62, P < 0.001; t = 6.23, P < 0.001). After treatment, the visual analogue scale (VAS) score of the study group was lower than that of the control group [(3.7±0.3) scores vs. (4.4±0.7) scores], and the difference was statistically significant ( t = 2.10, P < 0.05). The incidence of adverse reactions including stethalgia, fever, nausea and vomiting in both groups had no statistically significant differences (all P > 0.05). Conclusions:Cisplatin sequential recombinant human vascular endostatin thoracic perfusion combined with small-bore catheter minimally invasive drainage can effectively ameliorate clinical symptoms, inhibit the expression of VEGF, and alleviate pain degree with no serious adverse reactions in patients with malignant pleural effusion.

Objective:To investigate the expression changes at the transcriptional level in normal lung tissues of mice after exposure to heavy ion radiation for different durations at different doses, aiming to provide evidence for exploring sensitive genes of heavy ion radiation, heavy ion radiation effect and the damage mechanism.Methods:Experiments on the temporal kinetics: the whole thorax of mice was irradiated with 14.5Gy carbon-ions and the total RNA of lung tissue was extracted at 3days, 7days, 3 weeks and 24 weeks. In dose-dependent experiment, the total RNA of lung tissue was extracted at 1 week after irradiated with a growing thoracic dose of 0, 7.5, 10.5, 12.5, 14.5, 17.5 and 20Gy. Protein-to-protein interaction (PPI) analysis and gene-ontology biological process enrichment analysis were performed on significant differentially expressed genes (DEGs).Results:A clearly differential expression patterns were observed at 3-day (acute stage), 1-week (subacute stage), 3-week (inflammatory stage) and 24-week (fibrosis stage) following 14.5Gy carbon-ions irradiation. Among those, the 3-day time point was found to be the mostly different from the other time points, whereas the 7-day time point had the highest uniformity with the other time points. Cellular apoptosis was the main type of cell death in normal lung tissues following carbon-ions exposure. The interactive genes of Phlda3, GDF15, Mgmt and Bax were identified as the radiosensitive genes, and Phlda3 was the center ( R=0.76, P<0.001). Conclusion:The findings in this study provide transcriptional insights into the biological mechanism underlying normal lung tissue toxicity induced by carbon-ions.