High-frequency-link (HFL) power conversion systems (PCSs) are attracting more and more attentions in academia and industry for high power density, reduced weight, and low noise without compromising efficiency, cost, and reliability. In HFL PCSs, dual-active-bridge (DAB) isolated bidirectional dcdc converter (IBDC) serves as the core circuit. This paper gives an overview of DAB-IBDC for HFL PCSs. First, the research necessity and development history are introduced. Second, the research subjects about basic characterization, control strategy, soft-switching solution and variant, as well as hardware design and optimization are reviewed and analyzed. On this basis, several typical application schemes of DAB-IBDC for HPL PCSs are presented in a worldwide scope. Finally, design recommendations and future trends are presented. As the core circuit of HFL PCSs, DAB-IBDC has wide prospects. The large-scale practical application of DAB-IBDC for HFL PCSs is expected with the recent advances in solid-state semiconductors, magnetic and capacitive materials, and microelectronic technologies.

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Rejection is still a critical barrier to the long-term survival of graft after liver transplantation, requiring clinicians to unveil the underlying mechanism of liver transplant rejection. The cellular diversity and the interplay between immune cells in the liver graft microenvironment remain unclear. Herein, we performed single-cell RNA sequencing analysis to delineate the landscape of immune cells heterogeneity in liver transplantation. T cells, NK cells, B cells, and myeloid cell subsets in human liver and blood were enriched to characterize their tissue distribution, gene expression, and functional modules. The proportion of CCR6+CD4+ T cells increased within an allograft, suggesting that there are more memory CD4+ T cells after transplantation, in parallel with exhausted CTLA4+CD8+ T and actively proliferating MKI67+CD8+ T cells increased significantly, where they manifested heterogeneity, distinct function, and homeostatic proliferation. Remarkably, the changes of CD1c+ DC, CADM+ DC, MDSC, and FOLR3+ Kupffer cells increase significantly, but the proportion of CD163+ Kupffer, APOE+ Kupffer, and GZMA+ Kupffer decreased. Furthermore, we identified LDLR as a novel marker of activated MDSC to prevent liver transplant rejection. Intriguingly, a subset of CD4+CD8+FOXP3+ T cells included in CTLA4+CD8+ T cells was first detected in human liver transplantation. Furthermore, intercellular communication and gene regulatory analysis implicated the LDLR+ MDSC and CTLA4+CD8+ T cells interact through TIGIT-NECTIN2 signaling pathway. Taken together, these findings have gained novel mechanistic insights for understanding the immune landscape in liver transplantation, and it outlines the characteristics of immune cells and provides potential therapeutic targets in liver transplant rejection.

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