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In the continuous cooling process, the growth of the equiaxed α-phase grains in near-α high-temperature titanium alloys is controlled by the diffusion of alloying elements. Establishing a specific connection between the cooling rate and the diffusion behaviour of alloying elements aids in the precise prediction of the evolution of equiaxed α-phase grain size. This study meticulously controlled the cooling rate during the two-phase region annealing treatment of the Ti65 alloy. Using EPMA technology, the diffusion behaviour of solute elements during cooling was accurately characterized. The study found that slowing the cooling rate promotes the coarsening of the lamellar secondary α-phase grains and the growth of the primary equiaxed α-phase grains. At higher annealing temperatures, the growth of equiaxed α-phase grains can occur at faster cooling rates, while coarse lamellar secondary α-phase grains can be retained at slower cooling rates. The diffusion behaviour of solute elements Al, Ta, Mo, and W between the α-phase and transformed β-phase matrix is significantly influenced by the cooling rate, thus they are considered as the controlling elements for the growth of the equiaxed α-phase grains. Based on the diffusion behaviours of these controlling elements, their single-element diffusion models were categorized and integrated for predicting the grain size of the equiaxed α-phase. The predictions from the revised diffusion model show an excellent agreement with the actual results, with an error margin of about 5%.

By elucidating the progressive relationship from the rolling stress state to the activation of slip systems and then to lattice rotation, this paper clarifies the influence mechanism of strain paths on the evolution of α-phase texture in near-α titanium alloys. The distinct rolling textures obtained further provide a robust foundation for investigating whether the competition between different α-phase textures changes with varying cooling rates during β→α phase transformation. In this study, initial Ti65 alloy sheets underwent rolling using three different strain paths (UDR/CDR/MSCR), resulting in the production of three foils characterized by distinct textures. Compressive stress during rolling promotes the activation of basal and pyramidal-II slipping, leading to the formation of a TD-split basal texture in α-phase. Tensile stress during rolling promotes the activation of prismatic slipping, ultimately resulting in a [10 1‾ 0]//RD (in the case of UDR) or [21‾1‾ 0]//RD (in the case of CDR) texture. Variations in stress states along different strain paths led to differences in the global Schmid factor distribution of α-phase for slip systems, ultimately resulting in diverse texture evolution. Subsequently, foil samples underwent two-phase region heat treatments, followed by furnace cooling and air cooling. After furnace cooling, the strength of the transverse texture increased in each type of foils. Conversely, after air cooling, no specific α-phase texture consistently exhibited an increasing trend in the three foils.

Objective Nowadays, more than 90% of people over 50 years suffer from intervertebral disc degeneration (IDD), but there are exist no ideal drugs. The aim of this study is to identify a new drug for IDD. Methods An approved small molecular drug library including 2040 small molecular compounds was used here. We found that taurocholic acid sodium hydrate (NAT) could induce chondrogenesis and osteogenesis in mesenchymal stem cells (MSCs). Then, an in vivo mouse model of IDD was established and the coccygeal discs transcriptome analysis and surface plasmon resonance analysis (SPR) integrated with liquid chromatography–tandem mass spectrometry assay (LC‐MS) were performed in this study to study the therapy effect and target proteins of NAT for IDD. Micro‐CT was used to evaluate the cancellous bone. The expression of osteogenic (OCN, RNX2), chondrogenic (COL2A1, SOX9), and the target related (ERK1/2, p‐ERK1/2) proteins were detected. The alkaline phosphatase staining was performed to estimate osteogenic differentiation. Blood routine and blood biochemistry indexes were analyzed for the safety of NAT. Results The results showed that NAT could induce chondrogenesis and osteogenesis in MSCs. Further experiments confirmed NAT could ameliorate the secondary osteoporosis and delay the development of IDD in mice. Transcriptome analysis identified 128 common genes and eight Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways for NAT. SPR‐LC–MS assay detected 57 target proteins for NAT, including MAPK3 (mitogen‐activated protein kinase 3), also known as ERK1 (extracellular regulated protein kinase 1). Further verification experiment confirmed that NAT significantly reduced the expression of ERK1/2 phosphorylation. Conclusion NAT would induce chondrogenesis and osteogenesis of MSCs, ameliorate the secondary osteoporosis and delay the progression of IDD in mice by targeting MAPK3.Furthermore, MAPK3, especially the phosphorylation of MAPK3, would be a potential therapeutic target for IDD treatment.