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The amorphous TiO2 derived from hydroxylation has become an effective approach for the enhancement of photocatalytic activity of TiO2 since a kind of special black TiO2 was prepared by engineering disordered layers on TiO2 nanocrystals via hydrogenation. In this contribution, we prepared totally amorphous TiO2 with various degrees of blackness by introducing hydroxyls via ultrasonic irradiation, through which can we remarkably enhance the photocatalytic activity of TiO2 with improved light harvesting and narrowed band gap.

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A hydrothermal precursor was first obtained by isopropyl titanate reacting with tetramethylammonium hydroxide (TMAOH), which acts as a source of nitrogen and carbon. A facile post-thermal treatment was employed to enhance the crystallinity and visible light photocatalytic activity of the as-prepared precursor. The resulting products of post-thermal treatment between 200 °C and 700 °C display different colours from brown to white. Black N-doped TiO2 nanoparticles modified with carbon (denoted as N-TiO2/C) were obtained at 300 °C, while yellow N-doped TiO2 nanoparticles (denoted as N-TiO2) were obtained at 500 °C. X-ray diffraction (XRD), Fourier transform infrared spectroscopy (FTIR), and X-ray photoelectron spectroscopy (XPS) were applied to characterize N-TiO2/C, N-TiO2 and the evolution process during thermal treatment. The results show that for both N-TiO2/C and N-TiO2, nitrogen was doped into the lattice, thus narrowing the band gap and increasing the absorption in the visible light region. Moreover, for N-TiO2/C, the carbon species modified on the surface and between the nanocrystals enhanced the visible light harvesting and increased the adsorption of the dye in the photodegradation measurement. The photocatalytic performance under visible light irradiation is N-TiO2/C > N-TiO2 > undoped TiO2.

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Pseudocapacitance holds great promise for energy density improvement of supercapacitors, but electrode materials show practical capacity far below theoretical values due to limited ion diffusion accessibility and/or low electron transferability. Herein, inducing two kinds of straight ion-movement channels and fast charge storage/delivery for enhanced reaction kinetics is proposed. Very thick electrodes consisting of vertically aligned and ordered arrays of NiCo2S4-nanoflake-covered slender nickel columns (NCs) are achieved via a scalable route. The vertical standing ∼5 nm ultrathin NiCo2S4 flakes build a porous covering with straight ion channels without the “dead volume”, leading to thickness-independent capacity. Benefiting from the architecture acting as a “superhighway” for ultrafast ion/electron transport and providing a large surface area, high electrical conductivity, and abundant availability of electrochemical active sites, the NiCo2S4@NC-array electrode achieves a specific capacity up to 486.9 mAh g–1. The electrode even can work with a high specific capacity of 150 mAh g–1 at a very high current density of 100 A g–1. In particular, due to the advanced structure features, the electrode exhibits excellent flexibility with a unexpected improvement of capacity when being largely bent and excellent cycling stability with an obvious resistance decrease after the cycles. An asymmetric pseudocapacitor applying the NiCo2S4@NC-array as a positive electrode achieves an energy density of 66.5 Wh kg–1 at a power density of 400 W kg–1, superior to the most reported values for asymmetric devices with NiCo2S4 electrodes. This work provides a scalable approach with mold-replication-like simplicity toward achieving thickness-independent electrodes with ultrafast ion/electron transport for energy storage.

Wood is a ubiquitous material, widely used in human society, that features naturally abundant, aligned longitudinal cells (e.g., tracheids in softwood and fibers/vessels in hardwood) with diameters of ≈50–1000 µm. Here, the realization of, fine patterns on a wood surface ranging in size from 40 nm to 50 µm by precision imprinting is described. The precision imprinting is enabled by releasing cellulose fibril aggregates from the bondage of lignin through the delignification process, then imprinting in wet condition and fixing the designed configuration in the dry state. Various precision structures on a wood surface using imprinting technology, including dot arrays, lines, triangular features, and other complex patterns, are successfully demonstrated. Even multiscale structures with nanosized lines on the surface of micrometer hemiballs can be acquired. As a proof of concept, the use of surface‐imprinted wood as a microlens array (MLA), which exhibits superior imaging ability and thermal stability even at a high temperature up to 150 °C compared with traditional polystyrene MLA, is demonstrated. This precision imprinted wood may open new possibilities toward environmentally friendly devices and applications in optics, biology, electronics, etc.

Objective Emerging evidence suggests that brain angiotensin-(1–7) (Ang-(1–7)) deficiency contributes to the pathogenesis of Alzheimer’s disease (AD). Meanwhile, our previous studies revealed that restoration of brain Ang-(1–7) levels provided neuroprotection by inhibition of inflammatory responses during AD progress. However, the potential molecular mechanisms by which Ang-(1–7) modulates neuroinflammation remain unclear. Materials and Methods APP/PS1 mice were injected intraperitoneally with AVE0991 (a nonpeptide analogue of Ang-(1–7)) once a day for 30 consecutive days. Cognitive functions, neuronal and synaptic integrity, and inflammation-related markers were assessed. Since astrocytes played a crucial role in AD-related neuroinflammation whilst long noncoding RNAs (lncRNAs) were reported to participate in modulating inflammatory responses, astrocytes of APP/PS1 mice were isolated for high-throughput lncRNA sequencing to identify the most differentially expressed lncRNA following AVE0991 treatment. Afterward, the downstream pathways of this lncRNA in the anti-inflammatory action of AVE0991 were investigated using primary astrocytes. Results AVE0991 rescued spatial cognitive impairments and alleviated neuronal and synaptic damage in APP/PS1 mice. The levels of Aβ 1-42 in the brain of APP/PS1 mice were not affected by AVE0991. By employing high-throughput lncRNA sequencing, our in vitro study demonstrated for the first time that AVE0991 suppressed astrocytic NLRP3 inflammasome-mediated neuroinflammation via a lncRNA SNHG14-dependent manner. SNHG14 acted as a sponge of miR-223-3p while NLRP3 represented a direct target of miR-223-3p in astrocytes. In addition, miR-223-3p participated in the AVE0991-induced suppression of astrocytic NLRP3 inflammasome. Conclusion Our results suggest that Ang-(1–7) analogue AVE0991 inhibits astrocyte-mediated neuroinflammation via SNHG14/miR-223-3p/NLRP3 pathway and offers neuroprotection in APP/PS1 mice. These findings reveal the underlying mechanisms by which Ang-(1–7) inhibits neuroinflammation under AD condition and uncover the potential of its nonpeptide analogue AVE0991 in AD treatment.