Composite ADRC Speed Control Method Based on LTDRO Feedforward Compensation

The performance of the extended state observer (ESO) in an Active Disturbance Rejection Control (ADRC) is limited by the operational load in stepper motor control, which has high real-time requirements and may cause delays. Additionally, the complexity of parameter tuning, especially in high-order systems, further limits the ESO’s performance. This paper proposes a composite ADRC (LTDRO-ADRC) based on a load torque dimensionality reduction observer (LTDRO). Firstly, the LTDRO is designed to estimate abrupt load disturbances that are difficult to compensate for using the ESO. Secondly, the transfer function under the double-closed loop is deduced. Additionally, the LTDRO uses a magnetic encoder to gather the system state and calculate the load torque. It then outputs a compensating current feedforward to the current loop input. This method reduces the delay and complexity of the ESO, improving the response speed of the ADRC speed ring and the overall response of the system to load changes. Simulation and experimental results demonstrate that it significantly enhances dynamic control performance and steady-state errors. LTDRO-ADRC can stabilize the speed again within 49 ms and 17 ms, respectively, in the face of sudden load increase and sudden load removal. At the same time, in terms of steady-state error, compared with ADRC and CADRC, they have increased by 94% and 88%, respectively. In terms of zero-speed starting motors, the response speed is increased by 58% compared to a traditional ADRC

Primate‐Specific DAZ Regulates Translation of Cell Proliferation‐Related mRNAs and is Essential for Maintenance of Spermatogonia

Abstract Primate‐specific DAZ (deleted in azoospermia) has evolved in the azoospermia factor c (AZFc) locus on the Y chromosome. Loss of DAZ is associated with azoospermia in patients with deletion of the AZFc region (AZFc_del). However, the molecular mechanisms of DAZ in spermatogenesis remain uncertain. In this study, the molecular mechanism of DAZ is identified, which is unknown since it is identified 40 years ago because of the lack of a suitable model. Using clinical samples and cell models, it is shown that DAZ plays an important role in spermatogenesis and that loss of DAZ is associated with defective proliferation of c‐KIT‐positive spermatogonia in patients with AZFc_del. Mechanistically, it is shown that knockdown of DAZ significantly downregulated global translation and subsequently decreased cell proliferation. Furthermore, DAZ interacted with PABPC1 via the DAZ repeat domain to regulate global translation. DAZ targeted mRNAs that are involved in cell proliferation and cell cycle phase transition. These findings indicate that DAZ is a master translational regulator and essential for the maintenance of spermatogonia. Loss of DAZ may result in defective proliferation of c‐KIT‐positive spermatogonia and spermatogenic failure