Defect Engineering of Air-Treated WO₃ and Its Enhanced Visible-Light-Driven Photocatalytic and Electrochemical Performance

In this paper, we reported that oxygen vacancies could be introduced in tungsten oxide hierarchical nanostructures through air treatment at certain temperatures. The production of oxygen vacancies may be due to two mechanisms, i.e., critical phase transition and nanoscale inhomogeneous deformation, depending on the annealing temperature or time and the size of the building block. The oxygen vacancies can be introduced at 300 and 350 °C when critical phase transformation from orthorhombic WO₃·0.33H₂O to hexagonal WO₃ takes place or 350 and 400 °C when nanoscale inhomogeneous deformation occurs in the nanobelts. Moreover, the oxygen vacancy concentration is also influenced by the annealing time. For comparison, the oxygen vacancies are also introduced by hydrogen treatment. It is found that a certain amount of oxygen vacancies introduced by air treatment could trap and transfer electrons, thus decreasing the electron–hole recombination rate and improving the conductivity, while an abundance of oxygen vacancies introduced by hydrogen treatment could facilitate the electron–hole pair recombination and destroy the hexagonal tunnel structure, resulting in lower photocatalytic activity and electrochemical performance. Through air treatment, the constant rate of photocatalytic performance in degrading rhodamine B under visible light irradiation can reach 0.0300 min^–1, and the specific capacitance can improve to 166.7 F/g. It is suggested that both photocatalytic activity and electrochemical performance can be greatly improved by introducing a proper concentration of oxygen vacancies through air treatment

Oligonucleotide sequences of primers used in real-time PCR.

<p>Oligonucleotide sequences of primers used in real-time PCR.</p

Comparison of overall survival between combined inhibition therapy and single inhibition therapy.

<p>Comparison of overall survival between combined inhibition therapy and single inhibition therapy.</p

Comparison of progression-free survival between combined inhibition therapy and single inhibition therapy.

<p>Comparison of progression-free survival between combined inhibition therapy and single inhibition therapy.</p

Identification process for eligible studies.

<p>Identification process for eligible studies.</p

Characteristics of included trials.

<p>Abbreviations: NR, not reported; PD, disease progression; PT, prohibitive toxicity.</p

Summary of toxicities grade 3 or greater.

<p>Summary of toxicities grade 3 or greater.</p

Comparison of objective tumor response rate between combined inhibition therapy and single inhibition therapy.

<p>Comparison of objective tumor response rate between combined inhibition therapy and single inhibition therapy.</p

Bevacizumab attenuates hepatic fibrosis induced by CCl₄ in rats.

<p>CCl₄ was used to construct a hepatic fibrosis model to evaluate the therapeutic effects of bevacizumab(n = 8 for each group). (A) Sirius red and Masson's trichrome staining were used to determine the amount of ECM in the liver tissue of each groups. (B) Semiquantitative analysis of the ECM area was performed to evaluate the relative amount Sirius-red in fibrotic tissue using an image analysis system. (C) The amount of ECM was quantitated by quantitative estimation of hydroxyproline content. (*<i>P<0.05</i>).</p

Effects of CCl₄ on VEGF expression in hepatocytes and effects of conditioned medium collected from hepatocytes on the activation and proliferation of hepatic stellate cells.

<p>(A)BRL cells were exposed to CCl₄ for 12 hours and then the culture medium was replaced with fresh DMEM. After another 24 hours of culture, the conditioned medium was collected. Real-time PCR and ELISA assays were used to assess VEGF expression in hepatocytes after exposure to CCl₄. (B) BRL cells were exposed to CCl₄ for 12 hours and then the culture medium was replaced with fresh DMEM. After another 24 hours of culture, the conditioned medium was collected. The primary HSCs were plated in 6-well plates (1×10⁶ cells/well) and treated by conditioned medium with or without bevacizumab (100 µg/ml) for 72 hours. Then the cells were harvested and real-time PCR was performed to assess the expression of α-SMA and TGF-β1 in HSCs. (C) CCK-8 assay was used to assess the effects of conditioned medium with or without bevacizumab (100 µg/ml) on the proliferation of the HSC-T6 cell line. (D) MTT assay was employed to examine the effects of conditioned medium with or without bevacizumab (100 µg/ml) on the proliferation of the HSC-T6 cell line. (*<i>P<0.05</i>).</p