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We successfully synthesized the Bi2WO6 (BWO) with gradient concentration of oxygen vacancies and exhibited the excellent photocatalytic NO oxidation activity. And the oxygen vacancy introduced in photocatalyst is a popular method to enhance the photocatalytic performance. The formation of oxygen vacancy defects in BWO is responsible for the tuning band structure and modifying surface chemical state to improve carriers separation efficiency, enlarge visible light absorption range and facilitate reactant activation, which is unambiguously verified by the UV–vis DRS, XPS, EPR and DFT calculations. Moreover, the role of surface oxygen vacancy defects and reaction mechanism of photocatalytic NO oxidation were discussed in detail by combing the in situ DRIFT and theoretical calculations. This work could be broadly used to the design and synthesize high efficient photocatalysts and pave a way to understand the reaction mechanism of NO oxidization.

Improving the rate capability of transition metal oxides is of great important for the development of high-performance electrodes for supercapacitors. Here, a novel strategy of hydrogenation to enhance the electron transfer rate of manganese dioxide (MnO2) is proposed. Detailed preparative parameters (i.e. hydrogenation temperature and time) are systematically investigated. The hydrogenated MnO2 (H-MnOx) exhibits modified crystal phase/surface structures and increased electrical conductivity. The prepared H-MnOx exhibits high specific capacitance (640 mF cm−2 at current density of 1 mA cm−2), good rate capability (89.6% of capacitance retained from 1 to 10 mA cm−2), and good cycling stability (84.6% retention after 1000 cycles). The high specific capacitance is ascribed to the unique interconnected ultrathin nanosheets structure, which could not only provide porous channels for electrolyte infiltration to offer sufficient electrode/electrolyte interface, but also shorten the ions diffusion distance inside the active material. The good rate capability could be attributed to the good conductivity of the H-MnOx nanosheets, which was confirmed by the DFT calculation. These results highlight the importance of hydrogenation as a facile yet effective strategy to improve the rate capability of transition metal oxides for supercapacitors.

Bronchopulmonary dysplasia (BPD) is a frequent complication characterized by accelerated lung alveolarization in newborns. Long non-coding RNAs (lncRNAs) and microRNAs (miRs) are regarded as essential regulators in various diseases, including BPD. However, the detailed mechanism of the functions of RNA imprinted and accumulated in nucleus (Rian) lncRNA in the progression of BPD have remained elusive. The aim of the present study was to illustrate the interaction between miR-421 and Rian in BPD models and MLE-12 cells. The ability of Rian to protect neonatal lungs from hyperoxia-induced lung damage was examined. A mouse model of BPD and a hyperoxia-stimulated MLE-12 cell damage model were generated and treated with specific plasmid/mimics for the overexpression of Rian/miR-421. The interaction between miR-421 and Rian was predicted and verified using StarBase and a dual-luciferase reporter assay, respectively. The expression levels of miR-421 or Rian in both tissues and the MLE-12 alveolar epithelial cell line were assessed using reverse transcription-quantitative (RT-q)PCR. As parameters of alveolarization, the mean linear intercept (MLI), radial alveolar count (RAC) and the lung weight/body weight (LW/BW) ratio were measured. Furthermore, RT-qPCR was used to measure mRNA levels of pro-inflammatory cytokines (TNF-α, IL-6 and IL-1β) in the lung tissue of mice, and ELISAs were performed to determine the levels of pro-inflammatory cytokines (TNF-α, IL-6 and IL-1β) in the supernatant of MLE-12 cells. Cell growth and apoptosis were evaluated using an MTT assay and flow cytometry, respectively. Furthermore, caspase-3 activity was assessed using a caspase-3 activity detection kit. Prediction with StarBase and the dual-luciferase reporter assay revealed that miR-421 directly targeted Rian. RT-qPCR analysis confirmed that Rian was downregulated and miR-421 was upregulated in lung tissues of the mouse model of BPD and in hyperoxia-induced MLE-12 cells. However, the expression of miR-421 was decreased by Rian-overexpression, an effect that was reversed by miR-421 mimics. In addition, BPD was alleviated by Rian-plasmid, as confirmed by the enhanced RAC and reduced MLI and LW/BW ratio. The present results also indicated that Rian-plasmid inhibited the secretion of pro-inflammatory cytokines (TNF-α, IL-6 and IL-1β) in BPD mouse serum and hyperoxia-induced MLE-12 cells. In addition, Rian-plasmid eliminated the effect of hyperoxia to inhibit cell viability and induce apoptosis in MLE-12 cells. However, all of these effects of Rian were markedly reversed by miR-421 mimics. The present results indicated that Rian may attenuate hyperoxic damage in neonatal lungs and may serve as a novel molecular target for BPD treatment.

Background. Acute lung injury (ALI) is a fatal syndrome frequently induced by lipopolysaccharide (LPS) released from the bacterial cell wall. LPS could also trigger autophagy of lung bronchial epithelial cell to relieve the inflammation, while the overwhelming LPS would impair the balance of autophagy consequently inducing serious lung injury. Methods. We observed the autophagy variation of 16HBE, human bronchial epithelial cell, under exposure to different concentrations of LPS through western blot, immunofluorescence staining, and electron microscopy. Eight strands of 16HBE were divided into two groups upon 1000 ng/ml LPS stimulation or not, which were sent to be sequenced at whole transcriptome. Subsequently, we analyzed the sequencing data in functional enrichment, pathway analysis, and candidate gene selection and constructed a hsa-miR-663b-related competing endogenous RNA (ceRNA) network. Results. We set a series of concentrations of LPS to stimulate 16HBE and observed the variation of autophagy in related protein expression and autophagosome count. We found that the effective concentration of LPS was 1000 ng/ml at 12 hours of exposure and sequenced the 1000 ng/ml LPS-stimulated 16HBE. As a result, a total of 750 differentially expressed genes (DEGs), 449 differentially expressed lncRNAs (DElncRNAs), 76 differentially expressed circRNAs (DEcircRNAs), and 127 differentially expressed miRNAs (DEmiRNAs) were identified. We constructed the protein-protein interaction (PPI) network to visualize the interaction between DEGs and located 36 genes to comprehend the core discrepancy between LPS-stimulated 16HBE and the negative control group. In combined analysis of differentially expressed RNAs (DERNAs), we analyzed all the targeted relationships of ceRNA in DERNAs and figured hsa-miR-663b as a central mediator in the ceRNA network to play when LPS induced the variation of autophagy in 16HBE. Conclusion. Our research indicated that the hsa-miR-663b-related ceRNA network may contribute to the key regulatory mechanism in LPS-induced changes of autophagy and ALI.

Aims Pyroptosis and inflammation are involved in the development of chronic obstructive pulmonary disease (COPD). However, the cigarette smoke-mediated mechanism of COPD remains unclear. In this study, we aimed to investigate the role of nucleotide-binding domain-like receptor protein-3 (NLRP3) inflammasome-mediated pyroptosis in the death of human bronchial epithelial (HBE) cells after cigarette smoke extract (CSE) exposure. Main methods The protein level of NLRP3 in lung tissue was measured after cigarette smoke exposure in vivo. In vitro, HBE cells were treated with CSE. Subsequently, the activity of caspase-1, lactate dehydrogenase (LDH) release, release of interleukin (IL)-1β and NLRP3 expression levels were measured. The involvement of reactive oxygen species (ROS) was also explored. Key findings After exposure to CSE, increased release of LDH, the transcriptional and translational upregulation of NLRP3, the caspase-1 activity levels, and enhanced IL-1β and IL-18 release were observed in 16HBE cells. In addition, NLRP3 was required to activate the caspase-1. Our results suggested that pre-stimulated of 16HBE with a caspase-1 inhibitor, or using NLRP3 siRNA to silence NLRP3 expression, also caused the decrease of IL-1β release and pyroptosis. Significances. CSE induced inflammation and contributed to pyroptosis through the ROS/NLRP3/caspase-1 pathway in 16HBE cells. The NLRP3 inflammasome participates in CSE-induced HBE cell damage and pyroptosis, which could provide new insights into COPD.

Composting of cattle manure was conducted under four ventilation strategies, i.e., no-aeration (A-00), continuous aeration (B-44), non-aeration for 14 d and then aeration for 42 d (C-04), aeration for 14 d and then no-aeration for 42 d (D-40). Physicochemical parameters and potential ammonia oxidation (PAO) indicated that continuous and intermittent ventilation provide favourable conditions for ammonia-oxidizing bacteria (AOB) and archaea (AOA) to oxidize ammonia. Quantitative PCR (qPCR) analysis showed AOB amoA gene abundance of all treatments on every sampling day ranged from 2.25 × 105 to 2.76 × 109copies/g, was significantly lower than that of archaeal amoA gene from 2.71 × 108 to 9.05 × 1011copies/g. There was also a significantly positive relationship between PAO rates and AOB (r2 ≥ 0.066, p < 0.05) and AOA (r2 ≥ 0.300, p < 0.05) abundance. These data suggested that ammonia oxidation is driven by both AOA and AOB in cattle manure composting.

Composting is a controlled biological process used to stabilize and transform waste into a soil treatment. Aeration rate is one factor that controls the process of composting, as it ensures the growth of adequate aerobic microbe populations. To investigate the effect of aeration rates on the physicochemical indexes of compost and the loss of nitrogen content during composting, aerobic composting processes with different aeration rates (A: 0.2 L/min/kg TS, B: 0.05 L/min/kg TS and C: 0 L/min/kg TS) were studied. Ammonium-nitrogen, nitrate nitrogen, total nitrogen and other factors in compost samples from different periods were measured. The results showed that aeration rate significantly affected O 2 content under different conditions. The aeration rate also significantly affected water content, nitrate nitrogen, and nitrogen loss. NH3 emissions increased as aeration rates increased at high temperatures owing to nitrogen loss. These results showed that aeration rate had a significant effect on total nitrogen and ammonia emissions (p < 0.05). Thus, optimization of the ventilation method could significantly increase seed germination rate.

Transition metal oxides (TMOs) with spinel structures have a promising potential as the electrode materials for supercapacitors application owning to its outstanding theoretical capacity, good redox activity, and eco-friendly feature. In this work, MnCo2O4.5@NiCo2O4 nanowire composites for supercapacitors has been successfully fabricated by using a mild hydrothermal approach without any surfactant. The morphology and physicochemical properties of the prepared products can be well-controlled by adjusting experimental parameters of preparation. The double spinel composite exhibits a high specific capacitance of 325 F g−1 (146 C g−1) and 70.5% capacitance retention after 3,000 cycling tests at 1 A g−1.

Pancreatic cancer (PC) is one of the most aggressive types of human malignancy, which has an overall 5-year survival rate of