[Adsorption Capacity and Mechanism of Biochar Derived from Typical Agricultural Wastes for Cadmium in Aqueous Solutions].

Twelve biochar types were derived from animal manure (cow manure, chicken manure, and pig manure) and crop straw (wheat straw, rice straw, and corn straw) at different temperatures (300℃/700℃ and 300℃/500℃) for Cd2+ in a solution system in the present study. A scanning electron microscope, Fourier infrared spectrometer, X-ray diffraction, and CHN analyzer were applied to analyze the physical and chemical properties, surface structure, and elemental composition of the biochar. The adsorption capacity and related mechanism of biochar for Cd2+ in an aqueous solution was studied. The results showed that the maximum adsorption capacity of cow manure, chicken manure, and pig manure biochar for Cd2+ increased from 83.40, 19.65, and 96.74 mg·g-1 to 106.54, 268.89, and 164.53 mg·g-1, respectively, with the increase in pyrolysis temperature. With the increase in pyrolysis temperature, the pore structure of biochar became more abundant, oxygen-containing functional groups increased, and the aromatic structure appeared. Quantitative analyses revealed that ion exchange accounted for 12%-52%, chemical precipitation accounted for 27%-79%, complexation accounted for 1%-8%, and cation-π accounted for 1%-28% of the total adsorption capacity of Cd2+. With the increase in pyrolysis temperature, the proportion of cation-π interaction increased from 1%-13% to 8%-30%, but the proportion of chemical precipitation and ion exchange were still very high (70%-93%). Therefore, ion exchange and chemical precipitation could be the main mechanisms of agricultural waste biochar adsorption for Cd2+.

CCR5 facilitates endothelial progenitor cell recruitment and promotes the stabilization of atherosclerotic plaques in ApoE-/- mice.

INTRODUCTION: Unstable atherosclerotic plaques are prone to rupture, which leads to atherothrombosis. Endothelial progenitor cells (EPCs) are bone marrow-derived precursor cells that may repair vascular injury in atherosclerosis. Chemokine (C-C motif) receptor 5 (CCR5) promotes mobilization of EPCs. In this study, we investigated the therapeutic potential of CCR5-overexpressing EPCs on plaque stabilization in an apolipoprotein E (ApoE)-/- mouse model. METHODS: The expression of CCR5 and its cognate ligand chemokine (C-C motif) ligand 5 (CCL5) was examined in atherosclerotic aortas of humans and mice by immunohistochemistry. Splenectomized ApoE-/- C57BL/6 J mice fed a high-fat diet for 24 weeks were intravenously injected with EPCs transfected with CCR5 overexpression lentivirus. The recruitment of EPCs over the atherosclerotic plaques was evaluated by immunofluorescence. The content of lipid, smooth muscle cells, monocytes/macrophages, and endothelial cells in atherosclerotic plaques was assayed by specific immunostaining. The serum levels of atherosclerosis-related inflammatory factors in ApoE-/- mice were measured by mouse atherosclerosis antibody array I. RESULTS: CCR5 and CCL5 are highly expressed in atherosclerotic plaques in both humans and mice. The ApoE-/- mice with CCR5-overexpressing EPC treatment demonstrated a more stable plaque formation with enhanced recruitment of EPC, reduced lipid, and macrophage content in the atherosclerotic plaques. CCR5-overexpressing EPC treatment also increased the content of endothelial cells and nitric oxide production in the plaques. In addition, the serum levels of interleukin-3 (IL-3), IL-5, IL-6, IL-13, CD40, and tumor necrosis factor-alpha and the plaque contents of IL-6 and matrix metalloproteinase-9 were reduced in mice with CCR5-overexpressing EPC treatment. CONCLUSIONS: These findings suggest that CCR5 is a novel therapeutic target in EPC treatment for stabilization of atherosclerotic plaques.