Search

ObjectivesVirtual power plant is usually composed of distributed generator (DG). When the system lacks power grid support, practical and reasonable comprehensive operation strategies and accurate control methods are needed to ensure the smooth operation of virtual power plant.MethodsAn operation strategy based on system fluctuation value was proposed. Then, aiming at the problem of generation control of distributed generators in the system, a distributed finite-time controller was designed. The amplitudes of voltage and frequency were adjusted to nominal values within a finite time, and the active power was distributed among each DG unit. Different from the traditional centralized control strategy, the proposed control method is based on distributed junction, which only requires information exchange between adjacent DG units through sparse communication network.ResultsThe feasibility of the proposed control method and its robustness to the uncertainty of model parameters and load variation were verified by simulation experiments.ConclusionsCompared with previous studies, the proposed operation strategy divides the system operating conditions in more detail, effectively improving the stability and security of the system.

The O-GlcNAc transferase (OGT) is an essential enzyme that mediates protein O-GlcNAcylation, a unique form of posttranslational modification of many nuclear and cytosolic proteins. Recent studies observed increased OGT and O-GlcNAcylation levels in a broad range of human cancer tissues compared to adjacent normal tissues, indicating a universal effect of OGT in promoting tumorigenesis. Here, we show that OGT is essential for tumor growth in immunocompetent mice by repressing the cyclic GMP-AMP synthase (cGAS)-dependent DNA sensing pathway. We found that deletion of OGT (Ogt−/−) caused a marked reduction in tumor growth in both syngeneic mice tumor models and a genetic mice colorectal cancer (CRC) model induced by mutation of the Apc gene (Apcmin). Pharmacological inhibition or genetic deletion of OGT induced a robust genomic instability (GIN), leading to cGAS-dependent production of the type I interferon (IFN-I) and IFN-stimulated genes (ISGs). As a result, deletion of Cgas or Sting from Ogt−/− cancer cells restored tumor growth, and this correlated with impaired CD8+ T-cell-mediated antitumor immunity. Mechanistically, we found that OGT-dependent cleavage of host cell factor C1 (HCF-1) is required for the avoidance of GIN and IFN-I production in tumors. In summary, our results identify OGT-mediated genomic stability and activate cGAS-STING pathway as an important tumor-cell-intrinsic mechanism to repress antitumor immunity.

Background: Dysregulation of long non-coding RNAs (lncRNAs) is an important component of tumorigenesis. Aberrant expression of lncRNA taurine upregulated gene 1 (lncTUG1) has been reported in various tumors; however, its precise role and key targets critically involved in osteosarcoma (OS) progression remain unclear. Methods: The expression profiles of lncRNAs and their regulated miRNAs related to OS progression were assessed by bioinformatics analysis and confirmed by qRT-PCR of OS cells. The miRNA targets were identified by transcriptome sequencing and verified by luciferase reporter and RNA pull-down assays. Several in vivo and in vitro approaches, including CCK8 assay, western blot, qRT-PCR, lentiviral transduction and OS cell xenograft mouse model were established to validate the effects of lncTUG1 regulation of miRNA and the downstream target genes on OS cell growth, apoptosis and progression. Results: We found that lncTUG1 and miR-26a-5p were inversely up or down-regulated in OS cells, and siRNA-mediated lncTUG1 knockdown reversed the miR-26a-5p down-regulation and suppressed proliferation and enhanced apoptosis of OS cells. Further, we identified that an oncoprotein ZBTB7C was also upregulated in OS cells that were subjected to lncTUG1/miR-26a-5p regulation. More importantly, ZBTB7C knockdown reduced the ZBTB7C upregulation and ZBTB7C overexpression diminished the anti-OS effects of lncTUG1 knockdown in the OS xenograft model. Conclusions: Our data suggest that lncTUG1 acts as a miR-26a-5p sponge and promotes OS progression via up-regulating ZBTB7C, and targeting lncTUG1 might be an effective strategy to treat OS.

Abstract The severity of osteoarthritis (OA) and cartilage degeneration is highly associated with synovial inflammation. Although recent investigations have revealed a dysregulated crosstalk between fibroblast‐like synoviocytes (FLSs) and macrophages in the pathogenesis of synovitis, limited knowledge is available regarding the involvement of exosomes. Here, increased exosome secretion is observed in FLSs from OA patients. Notably, internalization of inflammatory FLS‐derived exosomes (inf‐exo) can enhance the M1 polarization of macrophages, which further induces an OA‐like phenotype in co‐cultured chondrocytes. Intra‐articular injection of inf‐exo induces synovitis and exacerbates OA progression in murine models. In addition, it is demonstrated that inf‐exo stimulation triggers the activation of glycolysis. Inhibition of glycolysis using 2‐DG successfully attenuates excessive M1 polarization triggered by inf‐exo. Mechanistically, HIF1A is identified as the determinant transcription factor, inhibition of which, both pharmacologically or genetically, relieves macrophage inflammation triggered by inf‐exo‐induced hyperglycolysis. Furthermore, in vivo administration of an HIF1A inhibitor alleviates experimental OA. The results provide novel insights into the involvement of FLS‐derived exosomes in OA pathogenesis, suggesting that inf‐exo‐induced macrophage dysfunction represents an attractive target for OA therapy.

Bi2212 high-temperature superconducting films (HTSFs) have garnered significant interest as a potential material for the development of high-Tc microwave and terahertz (THz) devices due to their intrinsic Josephson effect. This work presents the utilization of the polyvinyl pyrrolidone (PVP) -assisted sol-gel dip coating (PSGDC) method for the large-scale production of Bi2212 HTSFs. Initially, Bi2212 HTSFs were prepared on a small-scale single crystal (001)-oriented SrTiO3 substrates, and comprehensive characterization of their phase purity, crystal structure, surface morphology, microstructure, stress state, and transport properties was conducted as a foundation for further analysis. By optimizing the crystallization conditions and PVP content, the Bi2212 HTSF achieved improved performance, including a higher onset superconducting transition temperature (Tc, onset) of 94 K, zero-resistance temperature (Tc, zero) of 86 K, and a critical current density (Jc) of 6.8 × 104 A/cm2 under a zero magnetic field at 2 K. Subsequently, the optimized process was applied to successfully prepare a large-scale Bi2212 HTSF with a diameter of 50 mm, exhibiting uniform phase composition, surface morphology, and superconducting properties, expanding the potential applications of Bi2212 HTSFs.