Synchronous Sampling-Based Direct Current Estimation Method for Self-Sensing Active Magnetic Bearings.

Active magnetic bearings (AMBs) commonly use pulse-width modulation to reduce analogous hardware and manufacturing costs, but they experience sensing process, sensing accuracy and stability problems. To address these issues, a synchronous sampling-based direct current estimation (SS-DCE) method is proposed herein with a bistate switching power amplifier. First-considering the reluctance evolution mechanism of AMBs-a coupling relation mathematical model between rotor displacement and voltage/current is presented to acquire the rotor position from the working coil current alone. Then-assuming that the switching current was an approximately triangular signal-a DCE for the rotor position was established based on the estimation inductance of the charging/discharging phase. Finally-to decrease the phase shift caused by the self-sensing filters and position estimation algorithms-the SS-DCE method was introduced to conduct precise position detection for rotors with high velocities. The simulation and experimental results indicated that the proposed method could improve the sensing accuracy and stability. Compared to other AMB position estimation methods, the simple linearity of the SS-DCE method was greatly improved and could be controlled below 4%. Evaluation using frequency response analysis showed that the SS-DCE method had excellent dynamic accuracy and could perform at a higher phase margin, especially for the uprising/landing transient state. Moreover, there was a phase margin of 158° at the natural frequency of 19.26 HZ, and the peak sensitivity in the 50-250 µm range reached 10.7 dB.

Histone deacetylase 3 represses p15(INK4b) and p21(WAF1/cip1) transcription by interacting with Sp1.

Histone deacetylase 3 (HDAC3) has been implicated to play roles in governing cell proliferation. Here we demonstrated that the overexpression of HDAC3 repressed transcription of p15(INK4b) and p21(WAF1/cip1) genes in 293T cells, and that the recruitment of HDAC3 to the promoter regions of these genes was critical to this repression. We also showed that HDAC3 repressed GAL4-Sp1 transcriptional activity, and that Sp1 was co-immunoprecipitated with FLAG-tagged HDAC3. We conclude that HDAC3 can repress p15(INK4b) and p21(WAF1/cip1) transcription by interacting with Sp1. Furthermore, knockdown of HDAC3 by RNAi up-regulated the transcriptional expression of p15(INK4b), but not that of p21(WAF1/cip1), implicating the different roles of HDAC3 in repression of p15(INK4b) and p21(WAF1/cip1) transcription. Data from this study indicate that the inhibition of p15(INK4b) and p21(WAF1/cip1) may be one of the mechanisms by which HDAC3 participates in cell cycle regulation and oncogenesis.