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Carbonyl sulfide (COS), whose molecular structure is similar to CO2 and CS2, could be used as a better alternative carbonyl reagent due to its high chemical activity. However, the unfriendly by‐product H2S would be generated when COS is used as a carbonyl reagent in the carbonylation reaction. In this report, the odorless and stable disulfide was used to replace the traditional foul smelling and unstable o‐aminobenzenethiol to react with COS for preparing benzothiazolone derivatives in excellent yield, in which coupling reaction of H2S generation and S–S bond cleavage was firstly designed. Notably, the C=O of COS was converted into benzothiazolone derivatives by carbonylation reaction and the sulfur of COS was transformed into sulfur and sulfide after cleaving the S–S bond by a domino reaction of disulfide and COS under mild conditions. This efficient synthetic methodology provided a promising process for the utilization of COS.

Background Osteoarthritis (OA) is the most prevalent age-related disease in the world. Chondrocytes undergo an age-dependent decline in their proliferation and synthetic capacity, which is the main cause of OA development. However, the intrinsic mechanism of chondrocyte senescence is still unclear. This study aimed to investigate the role of a novel long non-coding RNA (lncRNA), AC006064.4–201 in the regulation of chondrocyte senescence and OA progression and to elucidate the underlying molecular mechanisms. Methods The function of AC006064.4–201 in chondrocytes was assessed using western blotting, quantitative real-time polymerase chain reaction (qRT-PCR), immunofluorescence (IF) and β-galactosidase staining. The interaction between AC006064.4–201 and polypyrimidine tract-binding protein 1 (PTBP1), as well as cyclin-dependent kinase inhibitor 1B (CDKN1B), was evaluated using RPD-MS, fluorescence in situ hybridization (FISH), RNA immunoprecipitation (RIP) and RNA pull-down assays. Mice models were used to investigate the role of AC006064.4–201 in post-traumatic and age-related OA in vivo. Results Our research revealed that AC006064.4–201 was downregulated in senescent and degenerated human cartilage, which could alleviate senescence and regulate metabolism in chondrocytes. Mechanically, AC006064.4–201 directly interacts with PTBP1 and blocks the binding between PTBP1 and CDKN1B mRNA, thereby destabilizing CDKN1B mRNA and decreasing the translation of CDKN1B. The in vivo experiments were consistent with the results of the in vitro experiments. Conclusions The AC006064.4–201/PTBP1/CDKN1B axis plays an important role in OA development and provides new molecular markers for the early diagnosis and treatment of OA in the future. Graphical Abstract Schematic diagram of AC006064.4–201 mechanism. A schematic diagram of the mechanism underlying the effect of AC006064.4–201

Electrical field activated sintering technology combined with micro-forming (Micro-FAST), as a new rapid powder sintering/forming method, is used to fabricate FeCo alloy parts. The successfully prepared FeCo parts have a high saturation of 214.11 emu/g and a low coercivity of 16 Oe, and these values are 20% and 10% higher than that of commercially available FeCoV alloy parts on the saturation and coercivity respectively. During the sintering process, the high current application shortened the densification time and enhanced the uniformity of the microstructure significantly. The grain sizes of FeCo alloys were in a range of 5–6 µm, and good isotropy was also shown. The low angle grain boundary (LAGB) accounted for more than 30% and the low angle misorientation accounted for more than 30% of the sample parts. Furthermore, the formation of the nano B2 phase was promoted during the Micro-FAST, and the size of the B2 phase was about 5 nm. The coherent interface between α and B2 was conducive for reducing the coercivity. As a consequence, the outstanding microstructure formed by Micro-FAST makes the FeCo alloys have high saturation and low coercivity.