Abstract The influence of Al2O3 content in refining slag on the cleanliness and fatigue property of ultra-low-carbon (ULC) automotive steel were investigated based on the industrial experiments. The inclusion-adsorption capacity of the refining slag was calculated and the total [O] (T.O) content of ULC automotive steel was measured. The number density, size distribution and morphology of inclusions were analyzed and their effects on the cleanliness and fatigue property of ultra-low-carbon (ULC) automotive steel were investigated. The results showed that as the Al2O3 content in refining slag increased from 19.92% to 39.73%, the inclusion-adsorption capacity of ULC automotive steel decreased from 210.30 down to 57.12, and the fatigue life from 1.4x104 down to 0.9x104 cycles, while the T.O content of steel increased from 12 up to18 ppm and the inclusion number density from 4 up to 9 per mm2.

Abstract Background: To analyze the relative expression of PELI3 and its mechanistic involvement in the non-small cell lung cancer (NSCLC). Methods: PELI3 expression in NSCLC tissue samples was determined by the immunohistochemistry. The transcripts abundance of PELI3 was measured with real-time PCR. The protein intensity was analyzed by western blot. The overall survival in respect to PELI3 or miR-365a-5p expression was plotted by the Kaplan–Meier's analysis. Cell growth was determined by colony formation assay. Cell viability was measured by MTT assay. The migration and invasion were evaluated by wound healing and transwell assay respectively. The regulatory effect of miR-365a-5p on PELI3 was interrogated with luciferase reporter assay. The direct binding between miR-365a-5p and PELI3 was analyzed by pulldown assay. Results: PELI3 was aberrantly up-regulated in NSCLC both in vivo and in vitro. High level of PELI3 associated with poor prognosis. PELI3-deficiency significantly inhibited cell viability, colony formation, migration and invasion. We further identified that miR-365a-5p negatively regulated PELI3 in this disease. Ectopic expression of miR-365a-5p in both A549 and H1299 phenocopied PELI3-deficiency. Meanwhile, PELI3-silencing significantly abolished the pro-tumoral effect elicited by miR-365a-5p inhibition. Conclusion: Our results highlighted the importance of dysregulated miR-365a-5p-PELI3 signaling axis in NSCLC.