CuSCN/Si heterojunction near-infrared photodetector based on micro/nano light-trapping structure.

In this paper, high-performance CuSCN/Si heterojunction near-infrared photodetectors were successfully prepared using nanoscale light-trapping optical structures. Various light-trapping structures of ortho-pyramids, inverted pyramids and silicon nanowires were prepared on silicon substrates. Then, CuSCN films were spin-coated on silicon substrates with high crystalline properties for the assembly of CuSCN/Si photodetectors. Their reflectance spectra and interfacial passivation properties were characterized, demonstrating their superiority of light-trapping structures in high light response. Under the irradiation of 980 nm near-infrared light, a maximum responsivity of 2.88 A W-1at -4 V bias and a specific detectivity of 5.427 × 1010Jones were obtained in the CuSCN/Si heterojunction photodetectors prepared on planner silicon due to 3.6 eV band gap of CuSCN. The substrates of the light-trapping structure were then applied to the CuSCN/Si heterojunction photodetectors. A maximum responsivity of 10.16 A W-1and a maximum specific detectivity of 1.001 × 1011Jones were achieved under the 980 nm near-infrared light irradiation and -4 V bias, demonstrating the advanced performance of CuSCN/Si heterojunction photodetectors with micro-nano light-trapping substrates in the field of near-infrared photodetection compared to other silicon-based photodetectors.

Correlation between copper speciation and transport pathway in Caco-2 cells.

BACKGROUND: Previous studies have demonstrated that, in contrast to the properties of food-derived copper, water-derived copper exerts neurotoxic effects and exhibits different speciation during digestion. The cellular uptake efficiencies of different speciation of copper are distinct. However, it is unclear whether these different speciation share the same transport pathway in intestinal epithelial cells. In the present study, the intracellular accumulation of copper derived from copper ion and copper complex solutions was investigated in Caco-2 cells. RESULTS: The cellular accumulation of copper derived from copper ions was higher than that of copper derived from the copper complex. Treatment with carboplatin and Ag+ , which are copper transporter receptor 1 (Ctr1, LC31A1) inhibitors, did not inhibit copper accumulation in Caco-2 cells, but inhibited copper accumulation in HepG2 cells. Zinc ion significantly decreased the intracellular copper content from 114 ± 7 µg g-1 protein to 88 ± 4 µg g-1 protein in the copper ion-treated Caco-2 cells, but not in the copper complex-treated Caco-2 cells (84.6 ± 14 µg g-1 protein versus 87.7 ± 20 µg g-1 protein, P > 0.05). Additionally, copper accumulation in Caco-2 and HepG2 cells significantly differed depending on different solvents (Hanks' balanced salt solution and NaNO3 , P < 0.05). CONCLUSION: These results indicate that the intracellular accumulation of copper derived from copper ion and copper complex is mediated by distinct copper transport pathways. Copper speciation may be an important factor that affects copper absorption and toxicity. © 2022 Society of Chemical Industry.

LncRNA SNHG16 promotes non-small cell lung cancer development through regulating EphA2 expression by sponging miR-520a-3p.

BACKGROUND: Recent evidence has found that lncRNA small nucleolar RNA host gene 16 (SNHG16) was associated with cell carcinogenesis in NSCLC. Here, we further investigated the precise functions and mechanisms of SNHG16 in NSCLC progression. METHODS: The expression of SNHG16, microRNA (miR)-520a-3p and EPH Receptor A2 (EphA2) was measured using quantitative real-time polymerase chain reaction and western blot, respectively. Cell proliferation was determined using 3-(4, 5)-dimethylthiahiazo (-z-y1)-3, 5-di-phenytetrazoliumromide (MTT) assay. The migrated and invaded cells were measured by Transwell assay. Flow cytometry was used to detect apoptotic cells. The interaction between miR-520a-3p and SNHG16 or EphA2 was confirmed using a dual-luciferase reporter assay. RESULTS: We found that SNHG16 was upregulated in NSCLC tissues and cell lines, knockdown of SNHG16 inhibited cell proliferation, migration, invasion and induced apoptosis in vitro as well as suppressed tumor growth in vivo. MiR-520a-3p directly bound to SNHG16 and miR-520a-3p, and SNHG16 acted as a ceRNA in regulating EphA2 through competitively binding to miR-520a-3p. Additionally, rescue assay exhibited the anticancer activity mediated by SNHG16 knockdown on NSCLC could be reversed by miR-520a-3p inhibition or EphA2 overexpression. CONCLUSION: SNHG16 promoted NSCLC development by regulating the miR-520a-3p/EphA2 axis, suggesting novel insights for the pathogenesis of NSCLC and new potential therapeutic targets for the treatment of NSCLC. KEY POINTS: Knockdown of SNHG16 inhibited NSCLC cell proliferation, migration, invasion and induced apoptosis in vitro as well as suppressed tumor growth in vivo. SNHG16 directly interacted with miR-520a-3p. EphA2 was a target of miR-520a-3p. SNHG16 could regulate the expression of EphA2 by binding to miR-520a-3p. SNHG16 promoted NSCLC development by regulating the miR-520a-3p/EphA2 axis.

Magnetic solid phase extraction based on magnetite/reduced graphene oxide nanoparticles for determination of trace isocarbophos residues in different matrices.

A simple one-step solvothermal method was applied for the preparation of magnetite/reduced graphene oxide (MRGO), and the synthetic nanocomposites with a magnetic particle size of ∼8nm were used as an adsorbent for magnetic solid phase extraction of isocarbophos (ICP) in different sample matrices prior to gas chromatography (GC) detection. The identity of the nanomaterial was confirmed using Fourier transform infrared spectroscopy, X-ray diffraction, scanning electron microscopy and transmission electron microscopy. It was shown that Fe3O4 nanoparticles with a uniform size were homogeneously anchored on RGO nanosheets. Increased oxidation degrees of graphite oxide, big particle sizes and large loading amounts of Fe3O4 on the surface of RGO led to a decrease of adsorption capacity of MRGO to ICP. The adsorption behavior of this adsorbent was better fitted by the pseudo-second-order kinetic model. Several parameters affecting the extraction efficiency were investigated and optimized, including adsorbent dosage, extraction time, ionic strength and desorption conditions. And then, a rapid and effective method based on MRGO combined with GC was developed for the determination of ICP in aqueous samples. A linear range from 0.05 to 50ngmL(-1) was obtained with a high correlation coefficient (R(2)) of 0.9995, and the limit of detection was found to be 0.0044ngmL(-1). This method was successfully applied to the analysis of ICP in five kinds of samples, including apple, rice, lake water, cowpea and cabbage. The recoveries in different sample matrices were in the range from 81.00% to 108.51% with relative standard deviations less than 9.72%. It can be concluded that the proposed analytical method is highly-efficient, sensitive, precise, accurate and practicable.

[The role of taurine as hydroxyl radical inhibitor and its effect on lipid peroxidation in selenite cataract].

OBJECTIVE: To study the role of taurine as hydroxyl radical and superoxide anion radical inhibitor in vitro and evaluate the effect of intraperitoneal injection of taurine on peroxidation in rat selenite cateractous lenses. METHODS: Electron spin resonance (ESR) was used to detect hydroxyl radical and superoxide anion radical. The concentrations of malondialdehyde (MDA) in normal lenses, selenite-injected lenses and taurine-treated lenses were measured on the 2 nd, 5 th, 9 th and 14 th days after the first injection of selenite. RESULTS: Taurine was an inhibitor of hydroxyl radical and superoxide anion radical. Its effect was very obvious. The concentration of MDA in selenite-injected lenses increased significantly after injection of selenite and became higher with the development of cataract. The concentration of MDA in taurine-treated lenses was lower than that in selenite-injected lenses. CONCLUSION: Taurine is an inhibitor of hydroxyl radical and superoxide radical. It can prevent lipid peroxidation in selenite cataractous lenses.