The possibility of sports industry business model innovation based on blockchain technology: Evaluation of the innovation efficiency of listed sports companies.

The combination of blockchain and the sports industry is bound to be a trend in terms of innovation and the development of sports industry in the near future. Therefore, after analyzing the problems existing in the current business model of the sports industry, this paper takes 200 innovation indicators of 50 listed companies in the sports industry, among which 15 use blockchain and 35 do not use, as research samples and uses a three-stage DEA model to calculate their innovation efficiency. The results show that sports companies that use blockchain have better performance in terms of innovation efficiency than do those that do not, which illustrates the necessity of blockchain-based business model innovation. Then, by focusing on the internal structure and the case of the "vSport blockchain", this work shows that this business model innovation is feasible. The article first proposes a blockchain-based sports industry business model and then uses a combination of empirical and case studies to prove the necessity and feasibility of sports industry business model innovation.

The RNA-binding protein Musashi2 governs osteoblast-adipocyte lineage commitment by suppressing PPARγ signaling.

Osteoporosis caused by aging is characterized by reduced bone mass and accumulated adipocytes in the bone marrow cavity. How the balance between osteoblastogenesis and adipogenesis from bone marrow mesenchymal stem cells (BMSCs) is lost upon aging is still unclear. Here, we found that the RNA-binding protein Musashi2 (Msi2) regulates BMSC lineage commitment. Msi2 is commonly enriched in stem cells and tumor cells. We found that its expression was downregulated during adipogenic differentiation and upregulated during osteogenic differentiation of BMSCs. Msi2 knockout mice exhibited decreased bone mass with substantial accumulation of marrow adipocytes, similar to aging-induced osteoporosis. Depletion of Msi2 in BMSCs led to increased adipocyte commitment. Transcriptional profiling analysis revealed that Msi2 deficiency led to increased PPARγ signaling. RNA-interacting protein immunoprecipitation assays demonstrated that Msi2 could inhibit the translation of the key adipogenic factor Cebpα, thereby inhibiting PPAR signaling. Furthermore, the expression of Msi2 decreased significantly during the aging process of mice, indicating that decreased Msi2 function during aging contributes to abnormal accumulation of adipocytes in bone marrow and osteoporosis. Thus, our results provide a putative biochemical mechanism for aging-related osteoporosis, suggesting that modulating Msi2 function may benefit the treatment of bone aging.