A cascaded converter interfacing long distance HVDC and back-to-back HVDC systems

This paper proposes a cascaded converter dedicated to long-distance HVDC infeed and asynchronous back-to-back interconnection of receiving grids. The cascaded converter is consisted of MMCs in series and parallel connection, meeting the high DC voltage and power demand of HVDC system. It realizes hierarchical feeding and asynchronous interconnection of receiving grids, optimizing the multi-infeed short circuit ratio and improving the flexibility of the receiving grids. The topology and operating characteristics of the cascaded converter are introduced in detail. The multi-infeed short-circuits ratio (MISCR) and the maximum power infeed of the cascaded converter based HVDC systems are analyzed. Various feasible operating modes with online switching strategies of the cascaded converter are studied to improve the operational flexibility of the system. The simulation results verify the effectiveness of the control strategy of the HVDC system embedding the cascaded converter. The DC faults clearing strategy and operating modes switching strategies are also validated

Active current-limiting control to handle DC line fault of overhead DC grid

To handle with the DC line faults in a DC grid, this paper proposed an active current-limiting controller for hybrid MMC. With this active current-limiting control strategy, the requirement of interruption current of DCCB will be significantly decreased, and the investment of DC grid will be reduced obviously. Firstly, the control architecture of active current-limiting controller is disclosed. To avoid the overvoltage of submodule capacitors during DC fault, a dynamic limiter for the reference value of the DC current controller is proposed. To decrease the peak of fault current, the feedforward controller of DC voltage is put forward. The decoupling controllability of the AC/DC voltage of hybrid MMC is disclosed. The current-limiting mechanism of the active current-limiting controller is analysis. Then, the validity of the active current-limiting control strategy is verified by RTDS

Epigenetic silencing of SALL2 confers tamoxifen resistance in breast cancer

Abstract Resistance to tamoxifen is a clinically major challenge in breast cancer treatment. Although downregulation of estrogen receptor‐alpha (ERα) is the dominant mechanism of tamoxifen resistance, the reason for ERα decrease during tamoxifen therapy remains elusive. Herein, we reported that Spalt‐like transcription factor 2 (SALL2) expression was significantly reduced during tamoxifen therapy through transcription profiling analysis of 9 paired primary pre‐tamoxifen‐treated and relapsed tamoxifen‐resistant breast cancer tissues. SALL2 transcriptionally upregulated ESR1 and PTEN through directly binding to the DNA promoters. By contrast, silencing SALL2 induced downregulation of ERα and PTEN and activated the Akt/mTOR signaling, resulting in estrogen‐independent growth and tamoxifen resistance in ERα‐positive breast cancer. Furthermore, hypermethylation of SALL2 promoter was found in tamoxifen‐resistant breast cancer. Importantly, in vivo experiments showed that DNA methyltransferase inhibitor‐mediated SALL2 restoration resensitized tamoxifen‐resistant breast cancer to tamoxifen therapy. These findings shed light on the mechanism of SALL2 in regulation of ER and represent a potential clinical signature that can be used to categorize breast cancer patients who may benefit from co‐therapy with tamoxifen and DNMT inhibitor