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Objective To explore the relationship between single nucleotide polymorphism (SNP) of pharmacokinetic genes and postoperative disease-free survival in patients with esophageal squamous cell carcinoma, and to evaluate the prognosis of patients undergoing surgery. Methods Seventy-seven patients with esophageal squamous cell carcinoma were selected in the study. Seven SNPs-ATP binding cassette subfamily B member 1 (ABCB1) rs1045642, rs2032582, rs3213619, ATP binding cassette subfamily G member 2 (ABCG2) rs2231137, rs2231142, ATP binding cassette subfamily C member 1 (ABCC1) rs246221 and ATP binding cassette subfamily C member 2 (ABCC2) rs3740066 were sequenced, and the relationship between genetic variation and disease-free survival was evaluated by Cox regression model. Semi-Bayesian shrinkage method was applied to correct for multiple comparison and small sample size issues. Results With the dominant genetic model, the minor allele of ABCC2 rs3740066 was significantly associated with shorter disease-free survival [crude hazard ratio (cHR) 95%CI= 4.623 (1.111-19.241), P=0.035, adjusted hazard ratio (aHR) 95% CI= 4.290 (1.010-18.215), P= 0.048]. Conclusion The SNP rs3740066 of pharmacokinetic gene ABCC2 is associated with postoperative disease-free survival in patients with esophageal squamous cell carcinoma. [ABSTRACT FROM AUTHOR]

Objective To investigate the toxic effects and mechanisms of silica nanoparticles on myocardial mitochondrial. Methods The Balb/c mice were intratracheally instilled with silica nanoparticles (40 nm) at three doses of 7, 21 and 35 mg/kg every three days for a total of 5 times. Control group was given the same volume of normal saline. The transmission electron microscope was used to observe the ultrastructure of myocardial mitochondria. By measuring the concentration of ATP，the effect of silica nanoparticles on the function of myocardial mitochondria was evaluated. Through the detection of the ability of anti O2-·in the myocardial tissue, the antioxidant capacity of mitochondria in cardiac muscle was evaluated. The expression levels of cytochrome coxidase subunit 1 (COX1) and succinate dehydrogenase subunit a (SDHA) were detected by Western blot assay. Results The results showed that silica nanoparticles at high dose can damage the structure of myocardial mitochondrial, which induced swelling of mitochondria，mitochondrial cristae disorder disappeared and even mitochondrial fusion. Silica nanoparticles (21 and 35 mg/kg) can induced the decrease in functions of mitochondria. Silica nanoparticles (7 and 21 mg/kg) can enhance the myocardial antioxidant capacity. But high dose of silica nanoparticles can induce the decrease in the myocardial antioxidant capacity. Silica nanoparticles (21 mg/kg) induced mitochondrial biosynthesis, but high dose of silica nanoparticles (35 mg/kg) inhibited mitochondrial biosynthesis. Conclusion Silica nanoparticles (35 mg/kg) can induce the production of O2-· and decrease the antioxidant capacity of mitochondria, which leads to the damage of the function and structure of the mitochondria and inhibits the mitochondria biosynthesis. [ABSTRACT FROM AUTHOR]