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With the rapid development of industry, agriculture, and urbanization, various organic pollutants have accumulated in natural water, posing a potential threat to both the ecological environment and human beings, and removing organic pollutants from water is an urgent priority. Piezoelectric techniques, with the advantages of green, simple operation, and high efficiency, are highly sought after in the degradation of environmental organic pollutants. Moreover, combining piezoelectric techniques with advanced oxidation processes (AOPs), photocatalysis, or electrocatalysis can further effectively promote the efficient degradation of target pollutants. Therefore, a perspective is presented on the recent progress of piezoelectric techniques for the degradation of various organic pollutants from aqueous solutions. The classification of various piezoelectric materials, as well as modification strategies for improving piezocatalysis, are first systematically summarized. Furthermore, the latest research on piezocatalysis and its combination with other technologies, such as AOPs, photocatalysis, and electrocatalysis, in the degradation of environmental pollutants is discussed. The potential mechanisms of piezocatalysis are also analyzed in depth. Finally, the urgent challenges and future opportunities for piezoelectric techniques in the degradation of organic pollutants are provided.

Manganese (Mn) overexposure has been associated with the development of neurological damage reminiscent of Parkinson's disease, while the underlying mechanisms have yet to be fully characterized. This study aimed to investigate the mechanisms leading to injury in dopaminergic neurons induced by Mn and identify novel treatment approaches. In the in vivo and in vitro models, ICR mice and dopaminergic neuron-like PC12 cells were exposed to Mn, respectively. We treated them with anti-ferroptotic agents ferrostatin-1 (Fer-1), deferoxamine (DFO), HIF-1α activator dimethyloxalylglycine (DMOG) and inhibitor LW6. We also used p53-siRNA to verify the mechanism underlying Mn-induced neurotoxicity. Fe and Mn concentrations increased in ICR mice brains overexposed to Mn. Additionally, Mn-exposed mice exhibited movement impairment and encephalic pathological changes, with decreased HIF-1α, SLC7A11, and GPX4 proteins and increased p53 protein levels. Fer-1 exhibited protective effects against Mn-induced both behavioral and biochemical changes. Consistently, in vitro, Mn exposure caused ferroptosis-related changes and decreased HIF-1α levels, all ameliorated by Fer-1. Upregulation of HIF-1α by DMOG alleviated the Mn-associated ferroptosis, while LW6 exacerbated Mn-induced neurotoxicity through downregulating HIF-1α. p53 knock-down also rescued Mn-induced ferroptosis without altering HIF-1α protein expression. Mn overexposure resulted in ferroptosis in dopaminergic neurons, mediated through the HIF-1α/p53/SLC7A11 pathway.

To date, significant efforts have been devoted to eliminating hazardous components to purify wastewater through the development of various nanomaterials. Covalent organic frameworks (COFs), an important branch of the porous crystalline family, possess the peculiarity of ultrahigh surface area, adjustable pore size, and facile functionality. Exciting studies from design fabrication to potential applications in water treatment by COF-based membranes (COMs) have emerged. This review summarizes various preparation strategies and synthesis mechanisms for COMs, including layer-by-layer stacking, in situ growth, interfacial polymerization, and electrochemical synthesis, and briefly describes the advanced characterization techniques for COMs. Moreover, the application of COMs in heavy metal removal, dye separation, purification of radionuclides, pollutant detection, sea water desalination, and so on, is described and discussed. Finally, the perspectives on future opportunities for designing COMs in water purification have been proposed.

Three-phase single-switch power factor correction (PFC) circuit has the advantages of simple structure and convenient control, and its current source characteristics is conducive to achieve higher power by parallel interleaving. But theoretical analysis of the circuit was complex and the design theory was not established yet. To solve these problems, a parameters design method based on volt-second balance of the input inductance is proposed. By this method, the key component parameters of a 7.6 kW experimental prototype are designed. At the same time, A constant on-time control method of this circuit based on MATLAB simulation is designed, which can be applied to various converters with constant on-time control. The parameters and control design method of the single-switch PFC circuit are simulated based on the MATLAB. A prototype is built and tested also, the test results verify the correctness of the parameter design theory and constant on-time control simulation method.

Elevated levels of arsenic may be present in groundwater, and long-term exposure to arsenic increases hepatic fibrosis. T helper 2 (Th2) cells are involved in the fibrotic cascade, and cell metabolism is a regulatory factor participating in CD4+ T cell differentiation and function. However, the mechanism for Th2 cell regulation of arsenite-induced hepatic fibrosis is not fully understood. In present study, for arsenite-fed mice, activated hepatic stellate cells may be involved in the infiltration of CD4+ T cells, accompanied by up-regulation of GATA3, a transcription factor, and IL-13, the major Th2 cytokine. Exposed to arsenite, Jurkat cells had increased aerobic glycolysis to promote the cell cycle and cell proliferation. Further, this process elevated levels of marker molecules, including those of the Th2 paradigm characterized by GATA3, IL-4, and IL-13. LX-2 cells were activated when treated with culture medium from Jurkat cells exposed to arsenite. miR-21 may be a therapeutic target for arsenite-induced hepatic fibrosis. In vitro, miR-21 knock-down caused inhibition of the PTEN/PI3K/AKT pathway induced by arsenite. It also reversed the elevated glycolysis and the accelerated cell cycle and cell proliferation. Indeed, this alteration led to diminished expression of GATA3, IL-4, and IL-13 in T cells differentiated under Th2 conditions, which inhibits activation of LX-2 cells. Consistent with the results in vitro, miR-21 knock-out in mice reversed hepatic fibrosis and attenuated the levels of GATA3 and IL-13 induced by arsenite. These findings indicate that miR-21 regulates the glycolysis of CD4+ T cells through the PTEN/PI3K/AKT pathway to accelerate the cell cycle, thereby facilitating CD4+ T cell polarization toward Th2 and releasing the fibrogenic factor IL-13, which participates in arsenite-associated hepatic fibrosis. Inhibition of Th2 polarization of CD4+T cells or miR-21 could be a therapeutic strategy to combat hepatic fibrosis caused by exposure to arsenic.

The occupational and environmental health safety of rare earths has attracted considerable attention. In China, the rare earth neodymium oxide (Nd2O3) is extensively refined and utilized. However, the mechanisms of Nd2O3-induced lung injury are elusive. In the present study, we found that exposure of mice to Nd2O3 caused an inflammatory reaction and fibrosis in lung tissues, which was in relation to the Nd2O3-induced higher levels of the lncRNA H19 (H19), tumor necrosis factor receptor 1 (TNFRSF1A), p-p65, and p-IKKβ and lower levels of miR-29a-3p. Further, in mouse monocyte macrophage leukemia cells (RAW264.7), Nd2O3 induced an inflammatory reaction, increases of H19 and TNFRSF1A levels, decreases of miR-29a-3p levels, and activation of the nuclear factor (NF)-κB signaling pathway. Further, we established that miR-29a-3p regulates TNFRSF1A expression. Up-regulation of miR-29a-3p and down-regulation of H19 blocked the Nd2O3-induced secretion of TNF-α, MIP-1α, and IL-6; the increases of TNFRSF1A levels; and activation of the NF-κB signaling pathway in RAW264.7 cells. Further, in Nd2O3-treated RAW26.4 cells, H19 inhibited the expression of miR-29a-3p, which targets TNFRSF1A, and activated the NF-κB signaling pathway to enhance the expression of TNF-α, MIP-1α, and IL-6. Moreover, for mice, up-regulation of miR-29a-3p reversed lung tissue inflammation, pulmonary fibrosis, and activation of the NF-κB signaling pathway induced by Nd2O3. In sum, the present investigation shows that H19 via miR-29a-3p is involved in lung inflammation and pulmonary fibrosis induced by Nd2O3, which is a mechanism for the Nd2O3-induced lung inflammatory response and pulmonary fibrosis. This information is useful for development of a biomarker of Nd2O3-induced lung injury.

Adzuki bean (Vigna angularis (Willd.) Ohwi & Ohashi) is an annual cultivated leguminous crop commonly grown in Asia and consumed worldwide. However, there has been limited research regarding adzuki bean genetics, which has prevented the efficient application of genes during breeding. In the present study, we constructed a high-density genetic map based on whole genome re-sequencing technology and validated its utility by mining QTLs related to seed size. Moreover, we analyzed the sequences flanking insertions/deletions (InDels) to develop a set of PCR-based markers useful for characterizing adzuki bean genetics. A total of 2904 markers were mapped to 11 linkage groups (LGs). The total length of the map was 1365.0 cM, with an average distance between markers of 0.47 cM. Among the LGs, the number of markers ranged from 208 (LG7) to 397 (LG1) and the total distance ranged from 97.4 cM (LG9) to 155.6 cM (LG1). Twelve QTLs related to seed size were identified using the constructed map. The two major QTLs in LG2 and LG9 explained 22.1 and 18.8% of the total phenotypic variation, respectively. Ten minor QTLs in LG4, LG5 and LG6 explained 3.0–10.4% of the total phenotypic variation. A total of 9718 primer pairs were designed based on the sequences flanking InDels. Among the 200 selected primer pairs, 75 revealed polymorphisms in 24 adzuki bean germplasms. The genetic map constructed in this study will be useful for screening genes related to other traits. Furthermore, the QTL analysis of seed size and the novel markers described herein may be relevant for future molecular investigations of adzuki bean and will be useful for exploiting the mechanisms underlying legume seed development.

Microplastics is a type of widespread contaminant found in numerous aquatic ecosystems. Conventional methods of microplastic identification and quantitation require tedious sample pretreatment procedures and complex instrument, therefore, it is highly in demand to develop portable sensitive methods for rapid field application of detection. Herein, a sensitive detection method based on surface enhanced Raman spectroscopy (SERS) for trace microplastics in non-pretreated water samples was reported, which used a sponge supported Au nanoparticle (NPs) layer as the SERS substrate and locally concentrating microplastics. The sponge pores decorated with Au nanoparticles could effectively capture and concentrate microplastics in the pores from aquaes sample. Interestingly, the adjustable size of the sponge could allow the distance between the “hot spots” on the substrate surface to be controlled, hence controlling the SERS signal intensity. The Raman signal for microplastics in water was greatly enhanced on the proposed substrate, whereas no Raman signal enhancement was observed on the un-supported Au NPs. It has been demonstrated that trace microplastics could be readily detected when higher sample volume was used. Furthermore, the practical applicability of the developed method has been demonstrated by the successful detection of microplastics in snow water, seawater, river water, and rainwater. This sensitive platform provided a possible opportunity for in-field microplastic detection without pretreatment coupled with a portable Raman instrument.

With the wide application of neodymium oxide nanoparticles (NPs-Nd2O3) in various fields, their health hazards have aroused public concern in recent years. However, data regarding the cytotoxicity of NPs-Nd2O3 is limited. In this study, we investigated the function and mechanism of long-chain non-coding RNAs (lncRNAs) in NPs-Nd2O3-induced airway inflammation. Treatment with NPs-Nd2O3 induced an inflammatory response in human bronchial epithelial cells (16HBE) by upregulating the expression of interleukin-6 (IL-6) and interleukin-8 (IL-8). The levels of LDH and intracellular ROS in the cells treated by various doses of NPs-Nd2O3 also increased significantly. After treatment with 10 μg/ml NPs-Nd2O3, RNA microarray and real-time quantitative polymerase chain reaction (qRT-PCR) showed a significant upregulation of lncRNA loc105377478. Functional experiments suggested lncRNA loc105377478 enhanced the expression of IL-6, IL-8 and ROS in NPs-Nd2O3-treated 16HBE cells, and it was further demonstrated that lncRNA loc105377478 promoted the activation of NF-κB by negatively regulating ADIPOR1 expression. Moreover, the expression of IL-6 and IL-8 in NPs-Nd2O3-treated 16HBE cells was regulated by lncRNA loc105377478, which was mediated by the NF-κB signaling pathway. In conclusion, lncRNA loc105377478 promotes NF-κB activation by negatively regulating ADIPOR1 expression, thereby upregulating the expression of IL-6 and IL-8 in 16HBE cells treated with NPs-Nd2O3.

Acrylonitrile (AN) is widely used in the manufacturing of fibers, plastics and pharmaceuticals. Free radical-mediated lipid peroxidation is implicated in the toxicity of AN. The present study was designed to examine the ability of curcumin, a natural polyphenolic compound, to attenuate acute AN-induced lipid peroxidation in the brain and liver of rats. Male Sprague-Dawley rats were orally administered curcumin at doses of 0 (olive oil control), 50 or 100 mg/kg bodyweight daily for 7 consecutive days. Two hours after the last dose of curcumin, rats received an intraperitoneal injection of 50 mg AN/kg bodyweight. Acute exposure to AN significantly increased the generation of lipid peroxidation products, reflected by high levels of malondialdehyde (MDA) both in the brain and liver. These increases were accompanied by a significant decrease in reduced glutathione (GSH) content and a significant reduction in catalase (CAT) activity in the same tissues. No consistent changes in superoxide dismutase (SOD) activity were observed between the control and AN-treatment groups in both tissues. Pretreatment with curcumin reversed the AN-induced effects, reducing the levels of MDA and enhancing CAT activity and increasing reduced GSH content both in the brain and liver. Furthermore, curcumin effectively prevented AN-induced decrease in cytochrome c oxidase activity in both liver and brain. These results establish that curcumin pretreatment has a beneficial role in mitigating AN-induced oxidative stress both in the brains and livers of exposed rats and these effects are mediated independently of cytochrome P450 2E1 inhibition. Accordingly, curcumin should be considered as a potential safe and effective approach in attenuating the adverse effects produced by AN-related toxicants., (2009 Elsevier Ireland Ltd. All rights reserved.)