Search

Air sensitivity remains a substantial barrier to the commercialization of sodium (Na)-layered oxides (NLOs). This problem has puzzled the community for decades because of the complexity of interactions between air components and their impact on both bulk and surfaces of NLOs. We show here that water vapor plays a pivotal role in initiating destructive acid and oxidative degradations of NLOs only when coupled with carbon dioxide or oxygen, respectively. Quantification analysis revealed that reducing the defined cation competition coefficient (η), which integrates the effects of ionic potential and sodium content, and increasing the particle size can enhance the resistance to acid attack, whereas using high-potential redox couples can eliminate oxidative degradation. These findings elucidate the underlying air deterioration mechanisms and rationalize the design of air-stable NLOs. [ABSTRACT FROM AUTHOR]

Peroxiredoxins are antioxidant proteins that detoxify peroxynitrite, hydrogen peroxide, and organic hydroperoxides, impacting various physiological processes such as immune responses, apoptosis, cellular homeostasis, and so on. In the present study, we identified and characterized peroxiredoxin 1 from Antheraea pernyi (thereafter designated as ApPrx-1) that encodes a predicted 195 amino acid residue protein with a 21.8 kDa molecular weight. Quantitative real-time PCR analysis revealed that the mRNA level of ApPrx-1 was highest in the hemocyte, fat body, and midgut. Immune-challenged larval fat bodies and hemocytes showed increased ApPrx-1 transcript. Moreover, ApPrx-1 expression was induced in hemocytes and the whole body of A. pernyi following exogenous H 2 O 2 administration. A DNA cleavage assay performed using recombinant ApPrx-1 protein showed that rApPrx-1 protein manifests the ability to protect supercoiled DNA damage from oxidative stress. To test the rApPrx-1 protein antioxidant activity, the ability of the rApPrx-1 protein to remove H 2 O 2 was assessed in vitro using rApPrx-1 protein and DTT, while BSA + DDT served as a control group. The results revealed that ApPrx-1 can efficiently remove H 2 O 2 in vitro. In the loss of function analysis, we found that ApPrx-1 significantly increased the levels of H 2 O 2 in ApPrx-1 -depleted larvae compared to the control group. We also found a significantly lower survival rate in the larvae in which ApPrx-1 was knocked down. Interestingly, the antibacterial activity was significantly higher in the ApPrx-1 depleted larvae, compared to the control. Collectively, evidence strongly suggests that ApPrx-1 may regulate physiological activities and provides a reference for further studies to validate the utility of the key genes involved in reliving oxidative stress conditions and regulating the immune responses of insects. • Prx-1 gene was identified from the Chinese oak silkworm, A. pernyi. • Microbial challenges modulate the expression patterns of ApPrx-1 in immune tissues. • Recombinant ApPrx-1 protein protects supercoiled DNA damage from oxidative stress. • Silencing of ApPrx-1 strongly affected the H 2 O 2 and bacterial clearance in A. pernyi. [ABSTRACT FROM AUTHOR]

The explosion characteristics of ethyl acetate/hydrogen-air (EA/H 2 /air) mixtures have been investigated in this document using a constant volume combustion vessel. The experiments were executed using the initial pressure (1, 2, and 3 bar) and temperature (358 K) over a wide range of equivalence ratios. Hydrogen was mixed with compressed air in the volumetric proportion of 0%, 4%, 8%, and 12% and added to EA. The experimental pressure data were refined to determine the explosion characteristics. The explosion characteristics of EA/H 2 /air using different H 2 fractions were compared. The study indicated that there was a slight difference between the peak explosion pressures of 4%, 8%, and 12% H 2 fraction, however, the explosion with H 2 of 12% had the maximum pressure rise rate and deflagration index when the explosion was evaluated in terms of the pressure rise rate and deflagration index. The explosion time at 8% and 12% hydrogen was relatively shorter than that of 4%. [ABSTRACT FROM AUTHOR]

Glioblastoma multiforme (GBM) is a malignant brain tumor with a poor prognosis resulting from tumor resistance to anticancer therapy and a high recurrence rate. Compelling evidence suggests that this is driven by subpopulations of cancer stem cells (CSCs) with tumor-initiating potential. ABC subfamily B member 5 (ABCB5) has been identified as a molecular marker for distinct subsets of chemoresistant tumor-initiating cell populations in diverse human malignancies. In the current study, we examined the potential role of ABCB5 in growth and chemoresistance of GBM. We found that ABCB5 is expressed in primary GBM tumors, in which its expression was significantly correlated with the CSC marker protein CD133 and with overall poor survival. Moreover, ABCB5 was also expressed by CD133-positive CSCs in the established human U-87 MG, LN-18, and LN-229 GBM cell lines. Antibody- or shRNA-mediated functional ABCB5 blockade inhibited proliferation and survival of GBM cells and sensitized them to temozolomide (TMZ)-induced apoptosis in vitro. Likewise, in in vivo human GBM xenograft experiments with immunodeficient mice, mAb treatment inhibited growth of mutant TP53, WTPTEN LN-229 tumors, and sensitized LN-229 tumors to TMZ therapy. Mechanistically, we demonstrate that ABCB5 blockade inhibits TMZinduced G2/M arrest and augments TMZ-mediated cell death. Our results identify ABCB5 as aGBMchemoresistance marker and point to the potential utility of targeting ABCB5 to improve current GBM therapies. [ABSTRACT FROM AUTHOR]

Aims: This study explores the effects of curcumin as a therapeutic agent against oral squamous cell carcinoma (OSCC)., Methods: We acquired the targets of curcumin from three digital databases, including the Comparative Toxicogenomics Database, Search Tool for Interactions of Chemicals, and SwissTargetPrediction. Then, we identified the differentially expressed genes (DEGs) and the weighted gene coexpression network analysis-based key modules using the expression profiles of GSE23558 to acquire the OSCC-related genes. Additionally, the GeneCards and Online Mendelian Inheritance in Man databases were also used to identify the OSCC-related genes. Finally, curcumin-OSCC interaction genes were obtained by overlapping curcumin targets and OSCC-related genes. The enrichment analysis was performed by the ClusterProfiler algorithm and Metascape, respectively. Then, a protein-protein interaction network was created, and the maximal clique centrality algorithm was used to identify the top 10 hub genes. Besides, we examined the expression levels of hub genes in OSCC using The Cancer Genome Atlas database., Results: 927 DEGs were identified, including 308 upregulated ones and 619 downregulated ones. The cluster one-step network construction function of the WGCNA algorithm recognized a soft-thresholding power of 6, and 9083 genes were acquired. 2591 OSCC-related genes were obtained by overlapping the GSE23558-identified genes and the OSCC-related genes from disease target bases. Finally, we identified 70 candidate drug-disease interaction genes by overlapping the disease-related genes with the curcumin target. The enrichment analysis suggested that response to oxidative stress, epithelial cell proliferation, and AGE/RAGE pathway might involve in the effect of curcumin on OSCC. The topologic study identified the ten hub genes, including VEGFA , AKT1 , TNF , HIF1A , EGFR , JUN , STAT3 , MMP9 , EGF , and MAPK3 . A significant difference was observed in VEGFA, AKT1, TNF, HIF1A, EGFR, MMP9, EGF, and MAPK3 expression levels between head and neck squamous cell carcinoma and the normal controls. However, no significant difference was observed in JUN ( P = 0.14) and STAT3 ( P = 0.054)., Conclusion: This study provided an overview and basis for the potential mechanism of curcumin against OSCC. The following experiments should be performed to further understand the effectiveness and safety of curcumin in treating OSCC., Competing Interests: The authors declare that they have no conflicts of interest., (Copyright © 2023 Wu Siyuan et al.)