RESUMEN
In this work, the anisotropic microstructure and mechanical properties of selective laser melted (SLMed) Ti-5Al-5Mo-5V-1Cr-1Fe (Ti-55511) alloy before and after aging treatment are investigated. Owing to the unique thermal gradient, the prior columnar ß grains with {001} texture component grow in the building direction, and the mechanical properties of the as-fabricated Ti-55511 alloy exhibit slight anisotropy. Aging treatment creates uniform precipitation of the α phase at the boundaries as well as the interior of ß grains. Due to the microstructure of the aged samples with a weak texture, the mechanical properties exhibit almost isotropic characteristics with an ultimate tensile strength of 1133 to 1166 MPa, yield strength of 1093 to 1123 MPa, and elongation from 13 to 16%, which meet the aerospace allowable specification very well. By XRD and EBSD analyses, the total dislocation density of the aged samples (~134.8 × 1013 m-2) is significantly lower than that of the as-fabricated samples (~259.4 × 1013 m-2); however, the aged samples exhibit a higher geometrically necessary dislocation (GND) density (~28.5 × 1013 m-2) compared with the as-fabricated samples GND density (~2.9 × 1013 m-2). Thus, a new approach to strengthening theory for estimating the anisotropic mechanical properties of AM alloys is proposed.
RESUMEN
OBJECTIVE: To observe the direct regulation of miR-127 on Bcl-6 and the effect of Bcl-6 in rescuing miR-127-induced cell cycle and cell growth inhibition. METHODS: The 3'UTR and coding region of human bcl-6 gene were amplified by PCR and cloned into pcDNA3.0-Luc and pcDNA3.0-Flag vectors, respectively. Mutations were introduced into the seed sequences of the predicted miR-127 target sites within the Bcl-6 3'UTR using recombinant PCR. Luciferase assay was used to verify the direct targeted regulation of miR-127 on Bcl-6. In HepG2 cell models with overexpression or knockdown of miR-12, the changes of cell cycle and cell growth were investigated after transfection with the constructed vectors. RESULTS: The recombinant plasmids were successfully obtained as confirmed by double digestion and sequence identification. Luciferase assay showed that in 293T and HepG2 cells, miR-127 inhibited the activation of wild-type Bcl-6 3'UTR reporter vector but not mutated Bcl-6 3'UTR vector. Overexpression of miR-127 induced cell cycle arrest at G(2)/M phase and suppressed the growth of HepG2 cells, and these effects were reversed by Bcl-6 overexpression. CONCLUSION: We successfully cloned wild-type and mutated 3'UTR reporter vectors and expression vector of bcl-6 gene and confirmed their biological functions.