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With the development of power switches and processor performance in recent years, the control frequency of inverters has been significantly improved. However, limited by technology and price, the sensor sampling frequency in large-scale industrial applications is much lower than the inverter control frequency that can be realized. This frequency mismatch limits the performance improvement of the inverter. In this article, the current and voltage at the non-sampling time are reconstructed using the current prediction control principle and the input observer theory, allowing a single-phase inverter to implement multi-sampling rate control with a low sampling frequency and high control frequency. In addition, an improved adaptive controller is designed to solve the effect of incorrect model parameters, which realizes adaptive control when the sampling frequency and control frequency are mismatched. Finally, the effectiveness of the method is verified through a simulation and experiments. The proposed method can solve the problem of high-speed switching for inverters under low-sampling-frequency conditions, improving the inverter’s adaptive performance and robustness.

Crystallin zeta (CRYZ) is a phylogenetically restricted water-soluble protein and provides cytoprotection against oxidative stress via multiple mechanisms. Increasing evidence suggests that CRYZ is high abundantly expressed in the kidney where it acts as a transacting factor in increasing glutaminolysis and the Na+/K+/2Cl- cotransporter (BSC1/NKCC2) expression to help maintain acid-base balance and medullary hyperosmotic gradient. However, the mechanism by which CRYZ is regulated in the kidney remains largely uncharacterized. Here, we show that CRYZ is a direct target of farnesoid X receptor (FXR), a nuclear receptor important for renal physiology. We found that CRYZ was ubiquitously expressed in mouse kidney and constitutively expressed in the cytoplasm of medullary collecting duct cells (MCDs). In primary cultured mouse MCDs, CRYZ expression was significantly upregulated by the activation and overexpression of FXR. FXR-induced CRYZ expression was almost completely abolished in the MCD cells with siRNA-mediated FXR knockdown. Consistently, treatment with FXR agonists failed to induce CRYZ expression in the MCDs isolated from mice with global and collecting duct-specific FXR deficiency. We identified a putative FXR response element (FXRE) on the CRYZ gene promoter. The luciferase reporter and ChIP assays revealed that FXR can bind directly to the FXRE site, which was further markedly enhanced by FXR activation. Furthermore, we found CRYZ overexpression in MCDs significantly attenuated hypertonicity-induced cell death possibly via increasing Bcl-2 expression. Collectively, our findings demonstrate that CRYZ is constitutively expressed in renal medullary collecting duct cells, where it is transcriptionally controlled by FXR. Given a critical role of FXR in MCDs, CRYZ may be responsible for protective effect of FXR on the survival of MCDs under hypertonic condition during dehydration.