Investigation of deformation behavior and strain-induced precipitations in Al-Zn-Mg-Cu alloys across a wide temperature range.

This study explores the hot deformation behavior of Al-Zn-Mg-Cu alloy through uniaxial hot compression (200 °C-450°C) using the Gleeble-1500. True stress-strain curves were corrected, and three models were established: the Arrhenius model, strain compensated (SC) Arrhenius model, and strain compensated recrystallization temperature (RT) segmentation-based (TS-SC) Arrhenius model. Comparative analysis revealed the limited predictive accuracy of the SC Arrhenius model, with a 25.12% average absolute relative error (AARE), while the TS-SC Arrhenius model exhibited a significantly improved to 9.901% AARE. Material parameter calculations displayed variations across the temperature range. The SC Arrhenius model, utilizing an average slope method for parameter computation, failed to consider temperature-induced disparities, limiting its predictive capability. Hot processing map, utilizing the Murty improved Dynamic Materials Model (DMM), indicated optimal conditions for stable forming of the Al-Zn-Mg-Cu alloy. Microstructural analysis revealed MgZn2 precipitation induced by hot deformation, with crystallographic defects enhancing nucleation rates and precipitate refinement.

Domain function dissection and catalytic properties of Listeria monocytogenes p60 protein with bacteriolytic activity.

The major extracellular protein p60 of Listeria monocytogenes (Lm-p60) is an autolysin that can hydrolyze the peptidoglycan of bacterial cell wall and has been shown to be required for L. monocytogenes virulence. The predicted three-dimensional structure of Lm-p60 showed that Lm-p60 could be split into two independent structural domains at the amino acid residue 270. Conserved motif analysis showed that V30, D207, S395, and H444 are the key amino acid residues of the corresponding motifs. However, not only the actual functions of these two domains but also the catalytic properties of Lm-p60 are unclear. We try to express recombinant Lm-p60 and identify the functions of two domains by residue substitution (V30A, D207A, S395A, and H444A) and peptide truncation. The C-terminal domain was identified as catalytic element and N-terminal domain as substrate recognition and binding element. Either N-terminal domain truncation or C-terminal domain truncation presents corresponding biological activity. The catalytic activity of Lm-p60 with a malfunctioned substrate-binding domain was decreased, while the substrate binding was not affected by a mulfunctioned catalytic domain. With turbidimetric method, we determined the optimal conditions for the bacteriolytic activity of Lm-p60 against Micrococcus lysodeikficus. The assay for the effect of Lm-p60 on the bacteriolytic activity of lysozyme revealed that the combined use of Lm-p60 protein with lysozyme showed a strong synergistic effect on the bacteriolytic activity.

Identification of miR-106b-93 as a negative regulator of brown adipocyte differentiation.

microRNAs (miRNAs) have been reported to play an essential role in the regulation of brown adipocyte adipogenesis. In the present study, we investigated the role of the miR-106b-93 cluster in the differentiation of brown adipocytes. We found that knockdown of miR-106b and miR-93 significantly induced the expression of brown fat-specific genes and promoted the accumulation of lipid-droplet in differentiating brown adipocytes. In addition, ectopic expression of miR-106b and miR-93 suppressed the mRNA level of Ucp1, a selective hallmark of brown adipocytes. Furthermore, the expression levels of miR-106b and miR-93 are higher in brown adipose tissues of high fat diet-induced obese mice compared to control mice. Taken together, our results identify miR-106b and miR-93 as negative regulators of brown adipocyte differentiation and the miR-106b-93 cluster may play an important role in regulating energy homeostasis.