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When wind generation systems operate under weak grid conditions, synchronization stability issues may arise, restricting the wind farms' power transfer capacity. This paper aims to address these challenges on the grid side. Firstly, a clear exposition of the coupling mechanism between the grid-connected inverters (GCI) of wind generations and the weak grid is provided. Then, an equivalent parallel compensation method integrated into the PLL to enhance synchronization stability is proposed. The method changes the reference of the PLL and equivalently parallels the virtual resistance with the grid impedance, which alters the strength of the grid. It reshapes the inverter qq-axis impedance at the impedance level. And the proper design of the virtual resistance will enhance the system's stability without compromising the dynamic performance of PLL. In addition, the proposed method is robust to the parameter changes of the grid-connected system and the grid impedance measurement error. Experimental results are presented to validate the effectiveness of the compensation method. [ABSTRACT FROM AUTHOR]

The article presents the discussion on tongue squamous cell carcinoma being a common type of cancer of the oral cavity. Topics include lncRNAs in cancer initiation and progression, dysregulation serving as a promising indicators of tumor characteristic; and considering the vital role of HPV infection contributed to the initiation and progression of TSCC.

Prostate cancer (PRAD) is associated with abnormal cholesterol metabolism and low-density lipoprotein (LDL) receptor-related protein (LRP) family is essential for the homeostasis of cholesterol. Immune check points like PD-L1 are vital for tumour cells to evade immune attack. However, the potential cross-talk between these two pathways has not been explored before in PRAD. Insight from the regulation mechanism of PD-L1 in PRAD may help to optimise PD-L1 based immunotherapy. In this study, we investigated a regulation network of LRP11/β-catenin/PD-L1 in PRAD. We showed that the expression of LRP11 and PD-L1 was up-regulated in PRAD compared to paired normal tissues. LRP11 expression was positively correlated to PD-L1 expression in PRAD tissues. Further experiments in two PRAD cell lines with LRP11 over-expression and knockdown showed that LRP11 induced PD-L1 expression through β-catenin signalling. In addition, LRP11 over-expression in PRAD cell line induced immunosuppression of Jurkat cell in in-vitro co-culture system. The effects of LRP11 could be blocked by neutralising LRP11 or PD-L1 antibody. Our results provide evidence for a novel regulation mechanism of PD-L1 expression in PRAD and LRP11 may be a potential therapeutic target in PRAD. [ABSTRACT FROM AUTHOR]

Porcine epidemic diarrhea virus (PEDV) is an enteric coronavirus that causes acute enteric disease in piglets and severely threatens the pig industry all over the world. Death domain-associated protein (DAXX) is a classical chaperone protein involved in multiple biological processes, such as cell apoptosis, transcriptional regulation, DNA damage repair, and host innate immunity. However, whether DAXX functions in the anti-PEDV innate immune responses remains unclear. In this study, we found that PEDV infection upregulated DAXX expression and induced its nucleocytoplasmic translocation in IPEC-J2 cells. Furthermore, we found that DAXX overexpression was inhibitory to PEDV replication, while downregulation of DAXX by RNA interference facilitated PEDV replication. The antiviral activity of DAXX was due to its positive effect on IFN-λ3-STAT1 signaling, as DAXX positively regulated STAT1 activation through their interaction in cytoplasm and enhancing the downstream ISG15 expression. Mutation of tryptophan at 621 to alanine in DAXX increased its abundance in the cytoplasm, leading to the upregulation of STAT1 phosphorylation and ISG15 expression. It indicated that cytoplasmic fraction of DAXX was advantageous for the STAT1-ISG15 signaling axis and PEDV inhibition. In summary, these results show that DAXX inhibits PEDV infection by increasing IFN-λ3-induced STAT1 phosphorylation and the downstream ISG15 expression. • DAXX suppresses PEDV infection in IPEC-J2 cells accompanied with its elevated expression and nuclear export. • DAXX interacts with host transcription factor STAT1. • The cytoplasmic fraction of DAXX exerts the efficient antiviral function by positively regulating STAT1-ISG15 signaling. [ABSTRACT FROM AUTHOR]

Fixed appliances used in orthodontic treatment make oral hygiene difficult to maintain, leading to bacterial adhesion around brackets and consequently resulting in white spot lesions (WSLs). After the bracket debonding, the residual adhesive is difficult to remove precisely due to its appearance similar to tooth enamel. In this study, we successfully synthesized small-sized and highly active PL-CDs by one-pot pyrolysis using ε-poly-l-lysine as a precursor. It was incorporated into orthodontic adhesives for multi-function modification. Based on our experimental results, the 3 wt% PL-CDs modified orthodontic adhesive exhibited excellent antibacterial properties and color identifiability. The addition of 3 wt% PL-CDs did not affect the biocompatibility and mechanical properties of the adhesive, and the cell survival rate was up to 80%. Therefore, this study provides a new strategy to solve the two major problems of enamel white spot and adhesive removal in the process of fixed orthodontics, and has important clinical application., Competing Interests: The authors declare no competing financial interest., (This journal is © The Royal Society of Chemistry.)