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Nonmetallic particles of crushed waste printed circuit boards usually contain 8.0–12.3 wt% of brominated flame retardants, which are harmful to humans and environment. Some articles proposed the method of pyrolysis to treat nonmetallic particles, but the pyrolysis products were still hazardous wastes. In this study, a novel process of vacuum-gasification-condensation was proposed to directionally concentrate bromine from the nonmetallic particles. Organic components of nonmetallic particles were completely gasified at the temperature of 700 °C and then cooled at 200 °C and 50 °C. Oils, floc, gases and residue were obtained and the bromine were concentrated in different products. Residue contained 0.19 wt % bromine and was no longer hazardous waste. Meanwhile, another breakthrough was that bromine migrated directionally to floc (36.15% of total bromine) and gases (46.37% of total bromine), which would be beneficial for the reduction of hazardous wastes. Additionally, we forecasted the future work about the treatment of the nonmetallic particles. To maximize the reuse of the nonmetallic particle, the key is to keep the bonds of other macromolecular organics stable and break C–Br bond only. This paper contributed a novel technology to collect bromine from the brominated wastes. Image 1 [ABSTRACT FROM AUTHOR]

Lipotoxicity leads to insulin secretion deficiency, which is among the important causes for the onset of type 2 diabetes mellitus. Thus, the restoration of β-cell mass and preservation of its endocrine function are long-sought goals in diabetes research. Previous studies have suggested that the membrane protein caveolin-1 (Cav-1) is implicated in β-cell apoptosis and insulin secretion, however, the underlying mechanisms still remains unclear. Our objective is to explore whether Cav-1 depletion protects pancreatic β cells from lipotoxicity and what are the underlying mechanisms. In this study, we found that Cav-1 silencing significantly promoted β-cell proliferation, inhibited palmitate (PA)-induced pancreatic β-cell apoptosis and enhanced insulin production and secretion. These effects were associated with enhanced activities of Akt and ERK1/2, which in turn downregulated the expression of cell cycle inhibitors (FOXO1, GSK3β, P21, P27 and P53) and upregulated the expression of Cyclin D2 and Cyclin D3. Subsequent inhibition of PI3K/Akt and ERK/MAPK pathways abolished Cav-1 depletion induced β-cell mass protection. Furthermore, under PA induced endoplasmic reticulum (ER) stress, Cav-1 silencing significantly reduced eIF2α phosphorylation and the expression of ER stress-responsive markers BiP and CHOP, which are among the known sensitizers of lipotoxicity. Our findings suggest Cav-1 as potential target molecule in T2DM treatment via the preservation of lipotoxicity-induced β-cell mass reduction and the attenuation of insulin secretion dysfunction. [ABSTRACT FROM AUTHOR]