Vitamin D deficiency triggers intrinsic apoptosis by impairing SPP1-dependent antiapoptotic signaling in chronic hematogenous osteomyelitis.

Chronic hematogenous osteomyelitis (CHOM) is a common bone disease characterized by the development of sequestra after bacterial infection. Emerging evidence has shown that vitamin D (VD) deficiency raises the risk of osteomyelitis, but the underlying mechanisms remain obscure. Here, we establish a CHOM model in VD diet-deficient mice by intravenous inoculation of Staphylococcus aureus. Whole-genome microarray analyses using osteoblast cells isolated from sequestra reveal significant downregulation of SPP1 (secreted phosphoprotein 1). Molecular basis investigations show that VD sufficiency activates the VDR/RXR (VD receptor/retinoid X receptor) heterodimer to recruit NCOA1 (nuclear receptor coactivator 1) and transactivate SPP1 in healthy osteoblast cells. Secreted SPP1 binds to the cell surface molecule CD40 to activate serine/threonine-protein kinase Akt1, which then phosphorylates forkhead box O3a (FOXO3a), blocking FOXO3a-mediated transcription. By contrast, VD deficiency impairs the NCOA1-VDR/RXR-mediated overexpression of SPP1, leading to the inactivation of Akt1 and the accumulation of FOXO3a. FOXO3a then upregulates the expression of the apoptotic genes BAX (Bcl2-associated X-protein), BID (BH3 interacting death domain), and BIM (Bcl2-interacting mediator of cell death), to induce apoptosis. Administration of the NCOA1 inhibitor gossypol to the CHOM mice also promotes the occurrence of sequestra. VD supplementation can reactivate the SPP1-dependent antiapoptotic signaling and improve the outcomes of CHOM. Collectively, our data reveal that VD deficiency promotes bone destruction in CHOM by the removal of SPP1-dependent antiapoptotic signaling.

Morphology characteristics and mode of CaO encapsulation during treatment of electrolytic manganese solid waste.

Electrolytic manganese solid waste (EMSW) is composed of manganese, calcium, and other sulfates. Common practice in China is to treat EMSW with quicklime (CaO); however, the per unit mass treatment efficiency of CaO is low. Studies of the interface between the CaO and EMSW particle and their microstructural characteristics are limited; these interactions may explain the low treatment efficiency. We conducted leaching experiments and measurements of the secondary heat generated by hydration of CaO to assess the extent of excess CaO in EMSW. The microstructure of CaO was also analyzed. It was determined that excess CaO particles in the EMSW were encapsulated, which influenced CaO hydration and morphology. The outer layer of the encapsulated CaO contained high levels of calcium and sulfur, which postulated to be caused by CaSO4 precipitates formed from the reaction of CaO hydration products with soluble sulfate. Three types of CaO encapsulation were identified: fully encapsulated CaO (55 % of the total CaO), partly encapsulated CaO (32 %), and self-encapsulated CaO (13 %). High concentrations of soluble sulfates in EMSW cause CaO encapsulation. These react to form CaSO4, which could negatively influence mass transfer and result in low treatment efficiency of EMSW by CaO.

[Effects of drought on output of Gastrodia elata].

The experiments of water supply showed out drought can decrease water potencial and the output of Gastrodia elata. Those negative effects might be conpensated by hybridi combination, and its output should be increased.