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Abstract: Several Fe3Al-based iron aluminides with the addition of alloying elements carbon, niobium and titanium were produced by vacuum induction melting (VIM) and hot spinning forging. Analytic techniques including transmission electron microscopy (TEM), scanning electron microscopy (SEM) and X-ray diffraction (XRD) were used in studying the microstructure and fracture manner of these alloys. The results show that due to the addition of alloying elements, the superlattice dislocations tend towards multiple slipping, leaving behind on their slip plane ribbons of square-shaped slip-induced antiphase boundaries. The elongation of Fe3Al in tension at room temperature increased to about 10% by the addition of suitable alloying elements, the usage of thermo-mechanical processing that has the function of refining grains and substructures, and subsequent annealing. [Copyright &y& Elsevier]

Abstract: A very sharp Brass {011}〈211〉 recrystallization texture with astonishingly high intensity has been successfully fabricated through rolling at room temperature by 98% and subsequent two-step annealing 423K for 1200s+973K for 5400s in nitrogen in pure silver sheet that can be used as a substrate for coated Y-123 superconducting tapes without any buffer layers. [Copyright &y& Elsevier]

Abstract Geniposide (GE) is an active component isolated from the fruit of Gardenia jasminoides Ellis that has anti-inflammatory and other pharmacological effects; however, the underlying mechanism of GE action has not been elucidated in rheumatoid arthritis (RA). Previous studies have shown that GE plays a therapeutic role in RA via regulation of the integrin beta 1 (Itgβ1)-mediated Ras-Erk1/2 signalling pathway. However, the specific mechanism of GE action on Itgβ1 has not been clarified. Recent evidence indicates that microRNAs (miRNAs) are involved in the development of RA. In this study, we developed a miRNA-124a-based synoviocyte repair strategy. We demonstrated that miRNA-124a can directly inhibit the expression of the Itgβ1 gene and decrease TNF-α-stimulated cell proliferation in vitro. MH7A cells were obtained from the patient with RA and treated with GE in the presence of TNF-α (10 ng/mL). Additionally, we demonstrated that the expression of miRNA-124a can be regulated by GE. GE upregulated the expression of miRNA-124a and decreased the expression of Itgβ1 at the mRNA and protein levels. The results of the present study are the first to suggest that GE inhibits TNF-α-stimulated cell proliferation and blocks the activation of the Ras-Erk1/2 pathway via the upregulation of miRNA-124a expression. Our study elucidates the role of miRNA-124a as a protected miRNA in RA and may provide a novel strategy for the diagnosis and treatment of RA in the future. Highlights • MiRNAs are crucial players in autoimmune and inflammatory diseases. • The target gene of miR-124 is Itgβ1, and there is a negative control relationship between them in rheumatoid arthritis. • The up-regulation of miR-124a limits the Itgβ1 expression, blocking the activation of the Ras-Erk1/2 signaling pathway. • GE alleviates TNF-α-stimulated MH7A proliferation and blocks activation of the Ras-Erk1/2 signaling pathway via miRNA-124a. [ABSTRACT FROM AUTHOR]