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The Kirkendall effect has been recently used to produce hollow nanostructures by taking advantage of the different diffusion rates of species involved in the chemical transformations of nanoscale objects. Here we demonstrate a nanoscale Kirkendall cavitation process that can transform solid palladium nanocrystals into hollow palladium nanocrystals through insertion and extraction of phosphorus. The key to success in producing monometallic hollow nanocrystals is the effective extraction of phosphorus through an oxidation reaction, which promotes the outward diffusion of phosphorus from the compound nanocrystals of palladium phosphide and consequently the inward diffusion of vacancies and their coalescence into larger voids. We further demonstrate that this Kirkendall cavitation process can be repeated a number of times to gradually inflate the hollow metal nanocrystals, producing nanoshells of increased diameters and decreased thicknesses. The resulting thin palladium nanoshells exhibit enhanced catalytic activity and high durability toward formic acid oxidation.

Objective To investigate the changes of miRNA-145a-5p in liver progenitor cells and mice infected with hepatitis B virus X protein (HBx) at different time points to preliminarily explore the mechanism of HBx causing liver tumor. Methods HBx gene was transfected into 14-19 liver precursor cells by lentivirus vector to construct HBx-EGFP-14-19 cell line, and then the suspension of obtained cells was injected into KM mice through hepatic portal vein to establish an HBx model with a complete immune system. The liver tissues were collected on days 30, 90, 180, and 360. The expression of HBx in HBx-EGFP-14-19 cells and HBx mice was detected by qRT-PCR and Western blotting. After miR-145a-5p mimic and inhibitor was transfected into the HBx-EGFP-14-19 cells and HBx mice having been fed for 180 d, respectively, the RNA expression of miR-145a-5p, c-Myc, Kras, apoptosis-related and cell cycle-related factors was detected by qRT-PCR, and the protein expression of them were detected by Western blotting. The cell proliferation was detected by CCK8 assay. Results The cell model capable of stably expressing HBx and HBx mouse model were established successfully. Overexpression of HBx induced the down-regulation of miR-145a-5p in HBx-EGFP-14-19 cells and HBx mice, while enhanced the expression of c-Myc and Kras. MiR-145a-5p mimic/agomir inhibited cell proliferation and down-regulated the expression of c-Myc, Kras, Bcl-2, CDK4, CyclinE, CyclinD1, and up-regulated the expression of Bad and Bax, while miR-145a-5p inhibitor/antagomir led to the opposite Results from the mimic. Conclusion Overexpression of HBx leads to the occurrence of liver tumor in mice, and its mechanism may be related to its regulation of miR-145a-5p and its target genes c-Myc and Kras and inhibition for cell apoptosis.

Objective To investigate the dynamic changes and the roles of COX-2 and its downstream factors in the carcinogenic process using a mouse model stably expressing hepatitis B virus X (HBx). Methods The expression of HBx in HBx-EGFP-14-19 cells was detected by Western blotting and RT-qPCR. A mouse model with stable expression of HBx was then established by injecting HBx-EGFP-14-19 cells into KM mice via hepatic portal vein. The mice were subsequently sacrificed at 30, 90, 180 and 360 d, respectively, and the liver tissues were collected. Western blotting, RT-qPCR and immunohistochemical assay were used to detect the expression of HBx in the liver; HE staining was adopted to observe the pathological characteristics of liver tissues. In addition, Western blotting and RT-qPCR were also employed to determine the expression changes of COX-2 and its downstream factors, cell cycle- and apoptosis-related factors in the liver tissues, at both mRNA and protein levels. Results The animal model with long-term stable expression of HBx was successfully constructed and eventually developed into liver cancer. The mRNA and protein levels of COX-2 and its downstream factor VEGF were continuously up-regulated even in 90 d after HBx was transferred into mice and the increment was continued until tumorigenesis (P < 0.05). The protein and mRNA levels of liver pro-apoptotic factors Bad and Bax were decreased (P < 0.05), while those of the anti-apoptotic factor Bcl-2 were increased (P < 0.05), and the levels of cell cycle factors Cyclin D1 and CDK4 were increased (P < 0.05). However, the effects of HBx on the above genes were reversed after administration of COX-2 inhibitor celecoxib. Conclusion HBx can cause liver cancer, which may be related to the up-regulation of COX-2 and its downstream factors

Objective To construct a normal immune mouse model carrying hepatitis B virus X (HBx) for long term so as to explore the possible mechanism of HBx causing hepatocellular carcinoma (HCC). Methods Hepatic progenitor cells transfected with HBx were injected into Kunming mice via hepatic portal vein to construct the animal model. The liver tissues were harvested at 30, 90, 180 and 360 d after injection, respectively. The expression of HBx as well as that of Notch1, Notch4 and Hes1 at protein and mRNA levels was detected by Western blotting and RT-qPCR, respectively, and the histopathological changes were observed by HE staining. In addition, a novel γ-secretase inhibitor, DAPT, was intraperitoneally injected at 180 d, and then Western blotting and RT-qPCR were adopted to determine the changes in the expression of apoptosis and cell-cycle-related factors. Results The animal model was successfully constructed, and liver cancer occurred at 360 d. Compared with the control group, the mRNA and protein levels of Notch1, Notch4 and Hes1 were all significantly increased in the HBx group at 30 d (P < 0.05, P < 0.05, P < 0.001), and continued to 360 d (P < 0.05, P < 0.05, P < 0.01); the protein and mRNA levels of Bcl-2, CDK4, CyclinE and CyclinD1 were also up-regulated (protein: P < 0.001, P < 0.01, P < 0.001, P < 0.01; mRNA: P < 0.05, P < 0.001, P < 0.001, P < 0.01), while those of Bax down-regulated in the HBx group (P < 0.001; P < 0.001). However, the inhibitor DAPT significantly reversed the above trends. Conclusion HBx causes anti-apoptosis and abnormal cell cycle changes in mice through persistent activation of the Notch pathway, and then ultimately leads to HCC.

The solar-driven conversion of CO2 into value-added fuels is regarded as one of the most promising strategies to address the increasing greenhouse effect and energy crisis. However, severe charge recombination and sluggish H2O oxidation kinetics lead to its low efficiency. Herein, a Z-scheme WO3/C3N4 heterojunction was constructed to overcome these issues, with C3N4 nanosheets (NS) and WO3 NS acting as the CO2 reduction centers and H2O oxidation booster, respectively. Driven by the enlarged internal electric field, charge separation and migration in the WO3/C3N4 heterojunction are promoted. Meanwhile, the WO3 NS provide highly oxidative photoinduced holes to accelerate H2O oxidation kinetics. Due to these advantages, the CO and CH4 yields of the optimal sample reached 9.4 μmol g−1 h−1 and 2.6 μmol g−1 h−1, respectively, being approximately 4.5 times and 7.2 times that of the pristine C3N4 NS. Overall, this work contributes to an in-depth understanding of the Z-scheme mechanism and offers a feasible approach to simultaneously modulate the charge separation and surface reaction for enhancing the efficiency of photocatalytic CO2 reduction. [ABSTRACT FROM AUTHOR]

BACKGROUND The total selenium content in the selenium-rich red soils in Fengcheng City of Jiangxi Province was relatively high, but the available selenium content directly absorbed and utilized by plants was low. The bioavailability of selenium in soils is a key factor affecting selenium in crops. OBJECTIVES To find safe and effective ameliorants for improving the availability of selenium in selenium-rich soils. METHODS Biomass carbon and steel slag were used as modifiers, and 8 different experiments were set up. Through indoor soil test and pot experiment, the content of available selenium in the selenium-rich red soils in Fengcheng was determined by atomic fluorescence spectrometry, and the regulation effect of two kinds of ameliorants on available selenium under different treatment levels was investigated. RESULTS The results of the soil tests showed that different amounts of biomass carbon and steel slag can increase the soil pH in the study area by 0.1-3.79 units. The results of elemental speciation analysis indicated that the ameliorant mainly controlled the soil available selenium by affecting the organically bound selenium. The soil organic matter content increased significantly after the application of biochar in the soil, but the organic matter showed a fixed effect on selenium. The available selenium content decreased by 8.4%-15.1%, resulted in the overall lower available selenium content in soils. The significant effect of steel slag on soil pH was beneficial to the activation of selenium in soils, and the soil available selenium content can be increased by 1.4 to 2.0 times. The results of the pot experiment showed that the selenium content of Chinese cabbage increased by more than 30% after treatment with steel slag, while the selenium content of Chinese cabbage decreased by 7.14%-42.8% after treatment with biochar. CONCLUSIONS This study shows that biochar is not suitable for regulating the availability of selenium in the soil of the study area. Steel slag can be used as a control material for soil selenium availability in the study area, which not only realizes solid waste recycling, but also improves the availability of selenium in soil.

Low‐dimensional amorphous metallic nanomaterials provide great possibility for creating high‐performance electrocatalysts owing to their conspicuous reacting merits derived from the flexible coordination structures, but remain extremely challenging in synthesis. Herein, this work reports a facile synthesis of carbon‐loaded amorphous 1.5‐nm‐thick Pt–Ru nanowires (NWs) through a local oxidation induced amorphization process. During annealing premade crystalline Pt–Ru NWs/C in air, a local‐oxidation of the oxyphilic Ru generates abundant random Ru–O bonds and disturbs the order bimetallic lattices. The as‐prepared amorphous Pt53Ru47 (a‐Pt53Ru47) NWs/C exhibits an extremely high activity (13.7 A mg−1 at 25 mV overpotential) and an excellent CO‐tolerance for alkaline hydrogen oxidation reaction (HOR) electrocatalysis, drastically outperforming the crystalline counterpart and commercial benchmarks. Mechanism studies indicate the Pt–Ru bimetallic effects as well as the rich disordered "Pt–Ru–O" and/or "Pt–O–Ru" atomic heterojunctions can weaken the *H binding energy and inversely strengthen the *OH adsorption, thus promoting the alkaline HOR kinetics. More uniquely, the small interatomic spaces derived from the disordered bond nets present a H2/*H‐selected permeability, which spatially obstruct the relatively larger CO molecules to poison the internal catalytic sites during HOR. The CO‐shielded internal catalytic sites and the enriched surface *OH jointly upgrade the CO‐tolerance of the a‐Pt53Ru47 NWs/C catalysts. [ABSTRACT FROM AUTHOR]