Phosphorene, monolayer or few-layer black phosphorus, exhibits fascinating anisotropic properties and shows interesting semiconducting behavior. The synthesis of phosphorene nanosheets is still a hot topic, including the shaping of its two-dimensional structure into nanoribbons or nanobelts. Here we report electrochemical unzipping of single crystalline black phosphorus into zigzag-phosphorene nanobelts, as well as nanosheets and quantum dots, via an oxygen-driven mechanism. The experimental results agree well with our theoretical calculations. The calculation for the unzipping mechanism study suggests that interstitial oxygen-pairs are the critical intermediate species for generating zigzag-phosphorene nanobelts. Although phosphorene oxidation has been reported, lengthwise cutting is hitherto unreported. Our discovery of phosphorene cut upon oxidation represents a previously unknown mechanism for the formation of various dimensions of phosphorene nanostructures, especially zigzag-phosphorene nanobelts. It opens up a way for studying the quantum effects and electronic properties of zigzag-phosphorene nanobelts.

Antigen CD133 is a glycoprotein present on the surface of cancer stem cells (CSCs), which is a key molecule to regulate the fate of stem cells and a functional marker of stem cells. Herein, a novel fluorescence turn-on nano-aptamer sensor for quantifying CD133 was designed using hybridization between CD133-targeted aptamers and partially complementary paired RNA (ssRNA), which were modified on the surface of quantum dots (QDs) and gold nanoparticles (AuNPs), respectively. Owing to the hybridization of aptamers and ssRNA, the distance between QDs and AuNPs was shortened, which caused fluorescence resonance energy transfer (FRET) between them, and the florescence of QDs was quenched by AuNPs. When CD133 competitively replaced ssRNA and was bound to aptamers, AuNPs-ssRNA could be released, which led to a recovery of fluorescent signals of QDs. The increase in the relative value of fluorescence intensity was investigated to linearly correlate with the CD133 concentration in the range of 0-1.539 μM, and the detection limit was 6.99 nM. In confocal images of A549 cells, the CD133 aptamer sensor was further proved applicable in lung cancer cell samples with specificity, precision, and accuracy. Compared with complicated methods, this study provided a fresh approach to develop a highly sensitive and selective detection sensor for CSC markers.

Leukocyte cell-derived chemotaxin 2 (LECT2) is linked to various immune diseases. Previously, we reported that serum LECT2 levels correlate with disease severity in atopic dermatitis (AD) patients. To investigate the role of LECT2 in AD and elucidate its potential mechanisms, we used LECT2 to treat an AD mouse model induced by 1-Chloro-2,4-dinitrobenzene (DNCB) in LECT2 knockout (KO) and wild-type (WT) mice, and an AD cell model using TNF-α/IFN-γ-induced HaCaT cells. Inflammatory factors and barrier proteins were analyzed by histology, immunohistochemistry, RT-qPCR, ELISA, and Western Blot. Activation of the NF-κB signaling pathway was evaluated by Western Blot and immunofluorescence. In the AD mouse model, LECT2 treatment increased epidermal and dermal thickness, mast cell infiltration, and downregulated barrier proteins. Inflammatory factors were increased in skin lesions and serum. In the AD cell model, LECT2 decreased barrier protein levels and increased inflammatory factor levels, enhancing NF-κB P65 nuclear translocation. These results indicate that LECT2 exacerbates AD-like responses by dysregulating the NF-κB signaling pathway, highlighting its potential as a therapeutic target for AD management.