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Visible light-active rhodium and antimony-co-doped SrTiO3 nanocubes (Rh/Sb:SrTiO3 NCs) were synthesized at low temperatures from Rh/Sb:TiO2 nanorods by the molten salt flux method. The effects of different calcination temperatures (700, 800, and 900 °C) and addition of transition metal oxides (NiOx, CoOx, and CuOx) on the photocatalytic properties of the Rh/Sb:SrTiO3 NCs were studied. The phase composition and morphology of the Rh/Sb:SrTiO3 NC photocatalysts (after calcination) were characterized using standard analytical techniques. The synergistic effect of the metal oxides and Rh/Sb:SrTiO3 NCs boosted the photocatalytic degradation of orange II dye and bisphenol A as well as the inactivation of bacteria. 2 wt% CoOx-loaded Rh/Sb:SrTiO3 photocatalyst showed higher photocatalytic performance for the degradation of orange II (96.3%) and bisphenol A (87%) in aqueous solution than Ni (2 wt%) and Cu (2 wt%)-loaded Rh/Sb:SrTiO3 NC composites. In addition, inactivation of Escherichia coli (96%) and Staphylococcus aureus (97.1%) was achieved over CoOx (2 wt%)-loaded Rh/Sb:SrTiO3 for 2 h under visible light irradiation (λ ≥ 420 nm). Further, scavenging experiments confirmed that superoxide anion radicals (·O2−) and holes (h+) are the major active species and OH· is a minor species responsible for the photocatalytic degradation of the studied organic pollutants. The synthetic strategy presented here offers a novel approach to the design of highly active visible light active photocatalysts for the removal of organic pollutants and inactivation of bacteria in wastewater. [ABSTRACT FROM AUTHOR]

A nanoscale artificial extracellular matrix (nanoshell) formed by layer‐by‐layer adsorption can enhance and modulate the function of stem cells by transferring biochemical stimulus to the cell directly. Here, the nanoshell composed of fibronectin (FN) and chondroitin sulfate (CS) is demonstrated to promote chondrogenic differentiation of mesenchymal stem cells (MSCs). The multilayer structure of nanoshell is formed by repeating self‐assembly of FN and CS, and its thickness can be controlled through the number of layers. The expression of chondrogenic markers in MSCs coated with the FN/CS nanoshell was increased as the number of bilayers in the nanoshell increased until four, but when it exceeds five bilayers, the effect began to decrease. Finally, the MSCs coated with optimized four bilayers of FN/CS nanoshell have high chondrogenic differentiation efficiency and showed the potential to increase formation of cartilage tissue when it is transplanted into mouse kidney. So, the precise regulation of stem cell fate at single cell level can be possible through the cellular surface modification by self‐assembled polymeric film. [ABSTRACT FROM AUTHOR]

Aim of the Study: We aimed to evaluate the anti-allergic effect of luteolin treatment in mice with allergic asthma and rhinitis., Material and Methods: Thirty-two BALB/c mice (n = 8 for each group) were used. Mice in group A (nonallergic group) were exposed to saline, while those in Group B (allergic group) were exposed to ovalbumin (OVA) intraperitoneal (i.p.) injection and intranasal (i.n.) challenge. Null treatment group (Group C) received sterile saline (150 μl) i.p. injection, 30 minutes before each i.n. challenge. Finally, the treatment group (Group D) received luteolin (0.1 mg/kg) by i.p. injection, 30 minutes before each i.n. challenge. We evaluated the number of inflammatory cells including eosinophils, neutrophils and lymphocytes in bronchoalveolar lavage (BAL) fluid, the titers of IL-4, IL-5 and IL-13 in lung homogenate, and we also evaluated histopathologic findings, including infiltration of inflammatory cells into the pulmonary parenchyma and nasal mucosa., Results: After the OVA challenge, the number of eosinophils, neutrophils and lymphocytes in BAL fluid was significantly increased in group B, compared to group A (p < 0.001). Mice in group C had no significant difference (p > 0.05). On the other hand, group D showed a significant decrease in all inflammatory cells compared to group B (p < 0.05). Also, group D showed a significant decrease in IL-4, IL-5 and IL-13 in their lung homogenate compared to groups B and C (p < 0.05). Group D also showed a significant decrease in inflammatory cell infiltration after luteolin treatment (p < 0.05)., Conclusion: Luteolin had an anti-allergic effect in a murine model of allergic asthma and rhinitis., Competing Interests: The authors declare no conflict of interest.

Vascular endothelial growth factor (VEGF) activates the VEGF-VEGF receptor (VEGFR) signaling pathway in angiogenesis. Some cancer cell lines show decreased expression of the two VEGFRs, Flt-1 and KDR, even though VEGF is uniformly expressed in cancer cell lines. Promoter methylation is a well-known cause of epigenetic gene silencing in cancer cells. Although VEGF, Flt-1 and KDR have typical CpG islands in their promoter regions, the epigenetic transcriptional alterations of these genes have not yet been described. The present study evaluated the epigenetic gene silencing of VEGF and VEGFR genes in cancer tissues. We also analyzed whether the epigenetic alterations of VEGFR genes influence VEGFR expression concurrently with VEGF activation in cancer tissues. All cancer tissues we tested showed no methylation of VEGF, and variable promoter hypermethylation of Flt-1 and KDR. The promoter hypermethylation of Flt-1 and KDR was correlated with decreasing expression of the respective genes. In contrast, an increase in VEGF expression was positively correlated with Flt-1 and KDR expression in primary cancer tissues. The opposing influences of promoter methylation of VEGFR and increased VEGF expression concurrently influence Flt-1 and KDR expression in stomach cancer, colon cancer and hepatocellular carcinoma. The findings we observed showed that the epigenetic alteration developing in VEGFR genes might be an important factor to concurrently modulate expressions of the genes in addition to VEGF stimulation in cancer tissues. The epigenetic silencing of VEGFR genes should be considered in the activation of VEGF-VEGFR signaling pathway in the cancer cells.