With the rapid development of optical communication, how to achieve efficient modulation (fast response speed and high modulation depth) of optical signals has attracted more and more attention from researchers. Among all electro-optical modulator (EOM) designs, the electro-optical metasurface is undoubtedly a competitive solution for optical signal modulation in free space. Although current research on electro-optical metasurfaces has realized improving response speed owing to the Pockels effect, there are still difficulties in achieving high modulation depth under CMOS-compatible voltage and developing rational designs of metasurfaces to achieve voltage application that trigger electro-optical effects. In this work, an ultrahigh-Q factor BaTiO3 (BTO) electro-optical metasurface, which consists of a periodic array of rectangular grooves, was designed to provide a feasible solution to address these shortcomings. Based on bound states in the continuum (BIC) theory, ultrahigh-Q factor (2.87 × 105) quasi-BIC (Q-BIC) was obtained around 1550 nm by breaking the in-plane symmetry of the two rectangular grooves in a unit cell, which could significantly deepen the modulation depth. The concave and continuous structure of rectangular grooves made the application of voltage more efficient. The simulation results show that an optical signal modulation in free space with a modulation depth of 100% could be achieved. Multipole decomposition indicated that toroidal dipole (TD) was dominant in this Q-BIC. Our work may further promote the development of electro-optical modulation towards faster and deeper modulation.

Phytophthora capsici is a destructive oomycete pathogen, causing huge economic losses for agricultural production. The genus Trichoderma represents one of the most extensively researched categories of biocontrol agents, encompassing a diverse array of effective strains. The commercial biocontrol agent Trichoderma harzianum strain T-22 exhibits pronounced biocontrol effects against many plant pathogens, but its activity against P. capsici is not known. T. harzianum T-22 significantly inhibited the growth of P. capsici mycelia and the culture filtrate of T-22 induced lysis of P. capsici zoospores. Electron microscopic analyses indicated that T-22 significantly modulated the ultrastructural composition of P. capsici, with a severe impact on the cell wall integrity. Dual RNA sequencing revealed multiple biological processes involved in the inhibition during the interaction between these two microorganisms. In particular, a marked upregulation of genes was identified in T. harzianum that are implicated in cell wall degradation or disruption. Concurrently, the presence of T. harzianum appeared to potentiate the susceptibility of P. capsici to cell wall biosynthesis inhibitors such as mandipropamid and dimethomorph. Further investigations showed that mandipropamid and dimethomorph could strongly inhibit the growth and development of P. capsici but had no impact on T. harzianum even at high concentrations, demonstrating the feasibility of combining T. harzianum and these cell wall synthesis inhibitors to combat P. capsici. These findings provided enhanced insights into the biocontrol mechanisms against P. capsici with T. harzianum and evidenced compatibility between specific biological and chemical control strategies. © 2024 Society of Chemical Industry.

The study aimed to study the potential roles and mechanisms of shikonin in gastric cancer by network pharmacology and biological experiments. The key genes and targets of shikonin in gastric cancer were predicted by network pharmacology and molecular docking study. The effect of shikonin on the proliferation, migration, and invasion of gastric cancer cells was detected by the CCK8 method, and wound healing and transwell assays. The expression levels of c-Myc and Yap-1 were detected via western blotting in gastric cancer cells after shikonin intervention. The results of network pharmacology revealed the key target genes of shikonin on gastric cancer cells to be c-Myc, Yap-1, AKT1, etc. GO and KEGG analysis showed regulation of cell migration, proliferation, adhesion, and other biological processes, including the PI3K-Akt signaling pathway, HIF-1 signaling pathway, necroptosis, and other cancer pathways. Molecular docking showed shikonin to be most closely combined with protooncogenes c-Myc and Yap-1. In vitro experiments showed that the proliferation rate, migration, and invasion ability of the gastric cancer cell group decreased significantly after shikonin intervention for 24h. The expression levels of c-Myc and Yap-1 in gastric cancer cells were found to be significantly decreased after shikonin intervention. This study showed protooncogenes c-Myc and Yap-1 to be the core target genes of shikonin on gastric cancer cells. Shikonin may suppress gastric cancer cells by inhibiting the protooncogenes c-Myc and Yap-1. This suggests that shikonin may be a good candidate for the treatment of gastric cancer.