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In this work, we studied the formation of the rutile phase of titanium dioxide (TiO2 ) on delaminated MXene (d-Ti3 C2 Tx ) flakes by the reaction of Ti3 C2 Tx with amino acids in water. Three types of amino acids with varied side-chain polarity were used to delaminate Ti3 C2 Tx . d-Ti3 C2 Tx flakes formed stable colloidal solutions due to the negative surface charges of chemisorbed amino acids on the d-Ti3 C2 Tx . Rutile formed on d-Ti3 C2 Tx at room temperature upon the intercalation of aromatic amino acids and subsequent sonication of the solution, while flakes intercalated with aliphatic amino acids did not oxidize. X-Ray diffraction (XRD), transmission electron microscopy (TEM) and Raman spectroscopy revealed the nanosize rutile formation on the surface of Ti3 C2 Tx flakes. The XPS results indicated the surface functionalization of histidine on d-Ti3 C2 Tx flakes. As-synthesized histidine functionalized rutile TiO2 @d-Ti3 C2 Tx hybrid was used for adsorption of Cu2+ ions from aqueous solution with a maximum uptake of 95 mg g-1 . © 2020 Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim.Cell-specific drug delivery remains a major unmet challenge for cancer nanomedicines. Here, light-triggered, cell-specific delivery of liposome-encapsulated doxorubicin to xenograft human cancer cells in live zebrafish embryos is demonstrated. This method relies on light-triggered dePEGylation of liposome surfaces to reveal underlying targeting functionality. To demonstrate general applicability of this method, light-triggered, MDA-MB-231 breast cancer cell specific targeting in vivo (embryonic zebrafish) is shown using both clinically relevant, folate-liposomes, as well as an experimental liposome-cell fusion system. In the case of liposome-cell fusion, the delivery of liposomal doxorubicin direct to the cytosol of target cancer cells results in enhanced cytotoxicity, compared to doxorubicin delivery via either folate-liposomes or free doxorubicin, as well as a significant reduction in xenograft cancer cell burden within the embryonic fish. © 2020 The Authors. Published by WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.Infectious bursal disease virus (IBDV) is the aetiological agent of a highly contagious chicken immunodeficiency disorder known as Gumboro disease, which cause severe economic loses to the poultry worldwide. The emergence of very virulent IBDV strains (vvIBDV) during the late 80s resulted in drastic changes to the epidemiology of IBDV with a dramatic increase in the mortality of the animals affected. Molecular studies determined that the emergence of the vvIBDV was a consequence of a genomic reorganization of IBDV known as reassortant event by which the virus combined two emergent genetic background vvIBDV for segment A and vvIBDV for segment B. In the current study, a retrospective analysis was conducted, and samples collected during acute outbreaks of Gumboro disease in Poland during 1992-2015 were submitted to sequencing and further molecular and phylogenetic analyses. The results obtained not only revealed a high genetic diversity for Polish IBDV strains but a new population of IBDV was identified. These novel reassortant strains with a unique genetic background contain the segment A from very virulent strains and segment B from an unidentified source, phylogenetically segregated and classified as 'transitional lineage'. The results obtained also showed the presence of this new lineage in Finland, evidencing the expansion of this new genomic reorganized viral strain in Europe representing an additional threat to the global situation of IBDV. © 2020 Blackwell Verlag GmbH.The androgen receptor (AR) has been linked to bladder cancer (BCa) progression, but if this involves circular RNAs (circRNAs) remains unclear. Here, we find that AR alters the levels of circRNA-FNTA (circFNTA) to increase BCa cell invasion and chemo-resistance. Mechanistically, AR represses the RNA editing gene ADAR2 via direct binding to its 5' promoter region to increase circFNTA levels, which then sponges the microRNA miR-370-3p to increase the expression of its host gene FNTA. This AR-mediated ADAR2/circFNTA/miR-370-3p/FNTA pathway then activates KRAS signaling to alter BCa cell invasion and chemo-sensitivity to cisplatin. A clinical BCa sample survey shows that circFNTA expression is elevated in BCa tissues, and results from a BCa mouse model indicate that depletion of circFNTA leads to the suppression of BCa metastases and increased cisplatin chemo-sensitivity. Together, based on our results using multiple BCa cell lines and an in vivo mouse model we suggest that targeting this newly identified AR/ADAR2/circFNTA/miR-370-3p/FNTA/KRAS axis may lead to the development of therapies to suppress BCa metastasis and to increase its chemo-sensitivity. © 2020 The Authors.Inappropriate diagnostic imaging (DI) is a burgeoning issue and embraces its overuse and its misapplication. The obverse problem is one of underuse - that is when patients who should undergo imaging fail to do so. This article attempts to define these problems, examines the causes and effects and suggests some potential solutions. © 2020 The Royal Australian and New Zealand College of Radiologists.It has been reported that tripartite motif containing 26 (TRIM26) is involved in the tumorigenesis of some cancers, but its function in non-small cell lung cancer (NSCLC) is still unclear. In this study, we found that TRIM26 was markedly down-regulated in both of NSCLC tumor tissues and cell lines. Additionally, high expression of TRIM26 in NSCLC patients predicted a positive index for patients' overall survival. What is more, overexpression of TRIM26 significantly suppressed NSCLC cell growth. https://www.selleckchem.com/products/dl-thiorphan.html Our further studies indicated that overexpression of TRIM26 inhibited the phosphorylation of PI3K p85 and AKT. And overexpressed TRIM26 regulated cell cycle-related genes' expression, including downregulating CDK4, Cyclin A, Cyclin D1, Cyclin D3, and Cyclin E, and upregulating p27 expression. Finally, we found that TRIM26 up-regulated PTEN expression by stabilizing PTEN protein in NSCLC cells. Collectively, our present study indicated that TRIM26 was decreased in NSCLC and overexpression of TRIM26 inhibited NSCLC cell growth by suppressing PI3K/AKT pathway, which suggested that TRIM26 could be as a potential target for the treatment of NSCLC in the future.