RESUMO
The economic impact after the outbreak of porcine reproductive and respiratory syndrome (PRRS) has been proven to be tremendous for pig production worldwide. However, the economic impact of the disease is not well understood in China. In our previous study, we acquired and analyzed the main production data (the number of weaned piglets, health costs, delayed marketing age, etc.) from the management system before and after the PRRS outbreaks occurring in November 2014, March 2015, December 2016, and February 2017. This study aimed to analyze and quantify the economic losses of the four PRRS outbreaks in Chinese herds. A straightforward approach was used to calculate additional costs and decreased revenues based on the PRRS-induced production deficiencies by average cost-of-production indices calculated from annual estimates of costs between 2014 and 2017. The results showed that economic losses varied between ¥668.14 and ¥1004.43 per sow in breeding herds from the outbreaks to regain the basic performance, with an average of ¥822.75 per sow, and the mean costs in the fattening herds (including nursery pigs) were ¥601.62 per sow, ranging from ¥318.64 to ¥937.14. Overall, the economic impact of PRRS on the whole herd was ¥1424.37 per sow. The majority of the losses were due to the reduction in the number of weaned piglets for breeding herds, and the increased feed cost (occupying 44.88%) was the primary source of loss for fattening herds. Our study fills the gap in knowledge of PRRS economics in China, enriches the data for veterinary economics, and re-stresses the necessity for producers and veterinarians to control PRRS effectively.
RESUMO
BACKGROUND: BMP9 induces both osteogenic and adipogenic differentiation of mesenchymal stem cells (MSCs). Nell1 is a secretory glycoprotein with osteoinductive and anti-adipogenic activities. We investigated the role of Nell1 in BMP9-induced osteogenesis and adipogenesis in MSCs. METHODS: Previously characterized MSCs iMEFs were used. Overexpression of BMP9 and NELL1 or silencing of mouse Nell1 was mediated by adenoviral vectors. Early and late osteogenic and adipogenic markers were assessed by staining techniques and qPCR analysis. In vivo activity was assessed in an ectopic bone formation model of athymic mice. RESULTS: We demonstrate that Nell1 expression was up-regulated by BMP9. Exogenous Nell1 potentiated BMP9-induced late stage osteogenic differentiation while inhibiting the early osteogenic marker. Forced Nell1 expression enhanced BMP9-induced osteogenic regulators/markers and inhibited BMP9-upregulated expression of adipogenic regulators/markers in MSCs. In vivo ectopic bone formation assay showed that exogenous Nell1 expression enhanced mineralization and maturity of BMP9-induced bone formation, while inhibiting BMP9-induced adipogenesis. Conversely, silencing Nell1 expression in BMP9-stimulated MSCs led to forming immature chondroid-like matrix. CONCLUSION: Our findings indicate that Nell1 can be up-regulated by BMP9, which in turn accelerates and augments BMP9-induced osteogenesis. Exogenous Nell1 may be exploited to enhance BMP9-induced bone formation while overcoming BMP9-induced adipogenesis in regenerative medicine.
