Albumin binding, antioxidant and antibacterial effects of cerium oxide nanoparticles

Herein, the interaction of CeO2 NPs with HSA was explored by fluorescence, CD, UVevis and molecular docking studies. Afterwards, the antioxidant activity of CeO2 NPs against H2O2-induced oxidative stress in BM-MSCs were explored by MTT, ROS and apoptosis assays. Antibacterial assay was also done on two Gram-positive and Gram-negative bacterial strains. Fluorescence study showed that the interaction of CeO2 NPs with HSA occurs through static quenching and hydrophilic interactions are involved in the spontaneous complex formation. The theoretical study also revealed that the distribution of hydrophilic residues of HSA is dominant in the binding site. CD and UVevis techniques also revealed that the ellipticity changes and Tm of HSA, respectively did not alter significantly in the presence of CeO2 NPs. Cellular assays depicted that CeO2 NPs did not induce cytotoxicity against BM-MSC up to 50 mg/ml for 24 h and pretreatment of cells with CeO2 NPs can reduce the cell mortality, ROS production and apoptosis in BM-MSC exposed to oxidative stress. The antibacterial assay revealed that CeO2 NPs have a significant antibacterial effect against all studied bacterial strains. This study may provide useful details about the biomedical applications of CeO2 NPs

Guide to house rebuilding costs

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The origin of microstructure inhomogeneity in Mg-3Al-1Zn processed by severe plastic deformation

A Mg–3Al–1Zn alloy has been severely deformed by accumulative back extrusion to investigate the effects of processing parameters (temperature and deformation pass) on the microstructure homogeneity. The results indicate that the activation of different grain refinement mechanisms in magnesium may result in an inhomogeneous microstructure, i.e. a bimodal grain size distribution. However, a rapid rate of homogeneity development has been occurred through applying further subsequent passes. This has been justified considering the imposed strain reversal during accumulative back extrusion processing.Peer Reviewe

Breast cancer subtype dictates DNA methylation and ALDH1A3-mediated expression of tumor suppressor RARRES1

Breast cancer subtyping, based on the expression of hormone receptors and other genes, can determine patient prognosis and potential options for targeted therapy. Among breast cancer subtypes, tumors of basal-like and claudin-low subtypes are typically associated with worse patient outcomes, are primarily classified as triple-negative breast cancers (TNBC), and cannot be treated with existing hormone-receptor-targeted therapies. Understanding the molecular basis of these subtypes will lead to the development of more effective treatment options for TNBC. In this study, we focus on retinoic acid receptor responder 1 (RARRES1) as a paradigm to determine if breast cancer subtype dictates protein function and gene expression regulation. Patient tumor dataset analysis and gene expression studies of a 26 cell-line panel, representing the five breast cancer subtypes, demonstrate that RARRES1 expression is greatest in basal-like TNBCs. Cell proliferation and tumor growth assays reveal that RARRES1 is a tumor suppressor in TNBC. Furthermore, gene expression studies, Illumina HumanMethylation450 arrays, and chromatin immunoprecipitation demonstrate that expression of RARRES1 is retained in basal-like breast cancers due to hypomethylation of the promoter. Additionally, expression of the cancer stem cell marker, aldehyde dehydrogenase 1A3, which provides the required ligand (retinoic acid) for RARRES1 transcription, is also specific to the basal-like subtype. We functionally demonstrate that the combination of promoter methylation and retinoic acid signaling dictates expression of tumor suppressor RARRES1 in a subtype-specific manner. These findings provide a precedent for a therapeutically-inducible tumor suppressor and suggest novel avenues of therapeutic intervention for patients with basal-like breast cancer