RESUMEN
One of the notorious problems in BiFeO3-based piezoelectric ceramics is how to limit the formation of Bi25FeO39 and Bi2Fe4O9 impurities to achieve excellent piezoelectric performance. In this study, a one-step preparation technology, namely, excluding PVA, calcining, and sintering are completed in one step, instead of three steps in the ordinary sintering method, is developed to prepare BiFeO3-xBaTiO3 (BF-xBT) ceramics. The significance of this one-step method is that the thermodynamically unstable region of BiFeO3 is successfully avoided based on the Gibbs free energy of BiFeO3, Bi25FeO39, and Bi2Fe4O9. Benefiting from preventing the formation of Bi25FeO39 and Bi2Fe4O9 impurities, the resultant ceramics show dense structures, macroscopic stripe domains, and a small number of island domains and display saturated P-E curves, sharp I-V characteristics, butterfly-shape S-E loops, and good piezoelectric properties (d33 = 174-199 pC/N; TC = 494-513 °C). By analyzing X-ray diffraction patterns of BF-xBT (0 ≤ x ≤ 1) powders at different calcination temperatures (Tcal), the different reaction mechanisms between 750 °C ≤ Tcal ≤ 900 °C and 950 °C ≤ Tcal ≤ 1000 °C are revealed. When 750 °C ≤ Tcal ≤ 900 °C, Bi3+ diffuses into Fe2O3 particles to form BiFeO3 and Bi25FeO39 and then reacts with BaTiO3; in this temperature range, the formed Bi25FeO39 is hard to eliminate. At 950 °C ≤ Tcal ≤ 1000 °C, Bi3+ and Fe ions simultaneously diffuse into BaTiO3 to form BF-xBT, which is beneficial to preventing the formation of Bi25FeO39 and the improvement of performance.
RESUMEN
The lentiviral vector is a useful tool for delivery of hairpin siRNA (shRNA) into mammalian cells. However, the efficiency of this system for carrying double-stranded siRNA (dsRNA) has not been explored. In this study we cloned the two forms of siRNA-coding sequence, a palindromic DNA with a spacer loop for shRNA and a double-stranded DNA with opposing Pol III promoters for dsRNA, into lentiviral DNA vectors, and compared their viral vector production yields. Our results indicate that sharply lower titer vector was obtained for dsRNA while much higher titer vector was produced for shRNA, posing a fundamental concern whether siRNA-carrying viral RNA itself is an inherent target of RNAi. Further experimental analyses using packaging cells that either allow or do not allow siRNA transcription indicate that the shRNA-carrying viral RNA is resistant to RNAi but the viral RNA carrier for dsRNA is not, offering a linker of RNAi bias-target secondary structure that causes shRNA vector to evade RNAi degradation. More importantly, the poor yield of dsRNA vector production was restored when a novel packaging cell line was used that blocks the antisense strand from dsRNA duplexes. This method has important implications for the RNAi field, especially for those who are using lentiviral dsRNA and dsRNA libraries for various biological discovery and therapeutic interventions.