Objective To investigate the antibacterial performance and biocompatibility of silver nanoparticles-coated root canal nickel titanium instruments(AgNPs-NiTi).Methods AgNPs-NiTi was prepared using pulse electrochemical deposition.The morphol-ogy of AgNPs-NiTi was observed using field emission scanning electron microscopy(FE-SEM),and the elemental composition and con-tent were analyzed using X-ray diffraction(XRD)and energy dispersive spectroscopy(EDS).The mechanical properties of AgNPs-NiTi were tested.After Co-culturing AgNPs-NiTi with E.faecalis,the antibacterial effect was detected by colony-forming units method.By constructing an in vitro model of E.faecalis biofilm in the root canal of teeth,the antibacterial effect of AgNPs-NiTi was observed using FE-SEM and live/dead bacterial staining.In addition,AgNPs-NiTi was co-cultured with Raw 264.7 cells,and its cytotoxicity was de-tected by CCK-8.Results The pulse electrochemical deposition was used to construct a silver nanoparticle(AgNPs)coating on NiTi instruments with no significant change in the mechanical properties.AgNPs-NiTi significantly inhibited the proliferation of E.faecalis and damaged E.faecalis biofilm in the root canal.AgNPs-NiTi had no significant influence on the proliferation of Raw264.7 cells and had no cytotoxicity.Conclusion The mechanical properties of AgNPs-NiTi are similar to those of nickel titanium instruments.AgNPs-NiTi inhibits E.faecalis proliferation with good biocompatibility.

Via an insufficient coat protein complex I (COPI) retrieval signal, the majority of SARS-CoV-2 spike (S) is resident in host early secretory organelles and a tiny amount is leaked out in cell surface. Only surface-exposed S can be recognized by B cell receptor (BCR) or anti-S therapeutic monoclonal antibodies (mAbs) that is the trigger step for B cell activation after S mRNA vaccination or infected cell clearance by S mAbs. Now, a drug strategy to promote S host surface exposure is absent. Here, we first combined structural and biochemical analysis to characterize S COPI sorting signals. A potent S COPI sorting inhibitor was then invented, evidently capable of promoting S surface exposure and facilitating infected cell clearance by S antibody-dependent cellular cytotoxicity (ADCC). Importantly, with the inhibitor as a probe, we revealed Omicron BA.1 S is less cell surface exposed than prototypes because of a constellation of S folding mutations, possibly corresponding to its ER chaperone association. Our findings not only suggest COPI is a druggable target against COVID-19, but also highlight SARS-CoV-2 evolution mechanism driven by S folding and trafficking mutations.