Single- and few-layer MoS2 nanoflowers are first discovered to have a piezo-catalyst effect, exhibiting an ultra-high degradation activity in the dark by introducing external mechanical strains. The degradation ratio of the Rhodamine-B dye solution reaches 93% within 60 s under ultrasonic-wave assistance in the dark.

We demonstrated a single microwire photodetector first made using a VO2 microwire that exhibted high responsivity (Rλ) and external quantum efficiency (EQE) under varying light intensities. The VO2 nanowires/microwires were grown and attached on the surface of the SiO2/Si(100) substrate. The SiO2 layer can produce extremely low densities of long VO2 microwires. An individual VO2 microwire was bonded onto the ends using silver paste to fabricate a photodetector. The high-resolution transmission electron microscopy image indicates that the nanowires grew along the [100] axis as a single crystal. The critical parameters, such as Rλ, EQE, and detectivity, are extremely high, 7069 A W(-1), 2.4 × 10(10)%, and 1.5 × 10(14) Jones, respectively, under a bias of 4 V and an illumination intensity of 1 μW cm(-2). The asymmetry in the I-V curves results from the unequal barrier heights at the two contacts. The photodetector has a linear I-V curve with a low dark current while a nonlinear curves was observed under varing light intensities. The highly efficient hole-trapping effect contributed to the high responsivity and external quantum efficiency in the metal-oxide nanomaterial photodetector. The responsivity of VO2 photodetector is 6 and 4 orders higher than that of graphene (or MoS2) and GaS, respectively. The findings demonstrate that VO2 nanowire/microwire is highly suitable for realizing a high-performance photodetector on a SiO2/Si substrate.

CD14, a multiligand pattern-recognition receptor, is involved in the activation of many TLRs. Thrombomodulin (TM), a type I transmembrane glycoprotein, originally was identified as an anticoagulant factor that activates protein C. Previously, we showed that the recombinant TM lectin-like domain binds to LPS and inhibits LPS-induced inflammation, but the function of the recombinant epidermal growth factor–like domain plus serine/threonine-rich domain of TM (rTMD23) in LPS-induced inflammation remains unknown. In the current study, we found that rTMD23 markedly suppressed the activation of intracellular signaling pathways and the production of inflammatory cytokines induced by LPS. The anti-inflammatory activity of rTMD23 was independent of activated protein C. We also found that rTMD23 interacted with the soluble and membrane forms of CD14 and inhibited the CD14-mediated inflammatory response. Knockdown of CD14 in macrophages suppressed the production of inflammatory cytokines induced by LPS, and rTMD23 inhibited LPS-induced IL-6 production in CD14-knockdown macrophages. rTMD23 suppressed the binding of LPS to macrophages by blocking the association between monocytic membrane-bound TM and CD14. The administration of rTMD23 in mice, both pretreatment and posttreatment, significantly increased the survival rate and reduced the inflammatory response to LPS. Notably, the serine/threonine-rich domain is essential for the anti-inflammatory activity of rTMD23. To summarize, we show that rTMD23 suppresses the LPS-induced inflammatory response in mice by targeting CD14 and that the serine/threonine-rich domain is crucial for the inhibitory effect of rTMD23 on LPS-induced inflammation.