Enhancement of nitrogen and phosphorus removal, sludge reduction and microbial community structure in an anaerobic/anoxic/oxic process coupled with composite ferrate solution disintegration.

Waste activated sludge (WAS) was disintegrated by composite ferrate solution (CFS) in this work, and the effect of CFS disintegrated sludge supernatant (CDSS), as a supplementary carbon source, on enhancement of nitrogen and phosphorus removal and sludge reduction in an AAO-CFSSDR (Anaerobic/Anoxic/Oxic combined with CFS-Sludge disintegration reactor) process was evaluated. The results showed that CDSS was easily utilizable by the denitrification bacteria due to the high content of readily biodegradable substrates. When compared with the AAO process, the operation results of AAO-CFSSDR suggested that the removal efficiencies of TN, NH4+-N and TP increased from 71.15, 79.23 and 85.52% to 85.05, 87.70 and 90.06%, respectively; and the sludge was reduced by 34.79%. The 16SrRNA high-throughput sequencing results showed that the introduction of CDSS weakened the microbial diversity but enhanced the microbial richness; and the abundance of bacteria related to the removal of nitrogen and phosphorus, increased in the AAO-CFSSDR process.

1,25(OH)2D3 deficiency increases TM40D tumor growth in bone and accelerates tumor-induced bone destruction in a breast cancer bone metastasis model.

Breast cancer is one of the most common malignancies and bone is the commonest site of distant metastases. Evidences indicate that adequate supply of vitamin D will decrease the morbidity and mortality of breast cancer. However, the main role of vitamin D deficiency in breast cancer bone metastases remains unclear. In this study, the relationship between vitamin D and breast cancer bone metastases were evaluated. Results showed that 1,25(OH)2D3 can not only inhibit the proliferation, migration and invasion of breast cancer cell TM40D in vitro, but also attenuate the breast cancer cell TM40D-induced bone destruction in vivo, whose underlying mechanism was at least partially through decreasing the number of the osteoclasts. To our knowledge, this is the first to use 1-alpha-hydroxylase [1α(OH)ase] knockout mice which characterized vitamin D deficiency to establish the breast cancer bone metastases model. Based on this model, we also found that vitamin D deficiency will accelerate the osteolytic lesions, and 1,25(OH)2D3 supplement will restrain osteolytic lesions. Therefore, these findings suggest that vitamin D has the potential capacity to be a therapeutic agent for the breast cancer bone metastases.