Fluoride removal from coal mining water using novel polymeric aluminum modified activated carbon prepared through mechanochemical process.

Defluoridation of coal mining water is of great significance for sustainable development of coal industry in western China. A novel one-step mechanochemical method was developed to prepare polymeric aluminum modified powder activated carbon (PAC) for effective fluoride removal from coal mining water. Aluminum was stably loaded on the PAC through facile solid-phase reaction between polymeric aluminum (polyaluminum chloride (PACl) or polyaluminum ferric chloride (PAFC)) and PAC (1:15 W/W). Fluoride adsorption on PACl and PAFC modified PAC (C-PACl and C-PAFC) all reached equilibrium within 5 min, at rate of 2.56 g mg-1 sec-1 and 1.31 g mg-1 sec-1 respectively. Larger increase of binding energy of Al on C-PACl (AlF bond: 76.64 eV and AlFOH bond: 77.70 eV) relative to that of Al on C-PAFC (AlF bond: 76.52 eV) explained higher fluoride uptake capacity of C-PACl. Less chloride was released from C-PACl than that from C-PAFC due to its higher proportion of covalent chlorine and lower proportion of ionic chlorine. The elements mapping and atomic composition proved the stability of Al loaded on the PAC as well as the enrichment of fluoride on both C-PACl and C-PAFC. The Bader charge, formation energy and bond length obtained from DFT computational results explained the fluoride adsorption mechanism further. The carbon emission was 7.73 kg CO2-eq/kg adsorbent prepared through mechanochemical process, which was as low as 1:82.3 to 1:8.07 × 104 compared with the ones prepared by conventional hydrothermal methods.

Overexpression of miR-204-5p Alleviates Osteogenic Differentiation and Calcification of Human Aortic Vascular Smooth Muscle Cells by Targeting Calcium/Calmodulin-dependent Protein Kinase 1.

ABSTRACT: Vascular calcification (VC), a major complication in chronic kidney disease (CKD), is predominantly driven by osteoblastic differentiation. Recent studies have highlighted the crucial role of microRNAs in CKD's pathogenesis. Here, our research focused on the effects of miR-204-5p and its molecular mechanisms within VC. We initially found a notable decrease in miR-204-5p levels in human aortic vascular smooth muscle cells stimulated with inorganic phosphate, using this as a VC model in vitro. Following the overexpression of miR-204-5p, a decrease in VC was observed, as indicated by alizarin red S staining and measurements of calcium content. This decrease was accompanied by lower levels of the osteogenic marker, runt-related transcription factor 2, and higher levels of α-smooth muscle actin, a marker of contractility. Further investigation showed that calcium/calmodulin-dependent protein kinase 1 (CAMK1), which is a predicted target of miR-204-5p, promotes VC. Conversely, overexpressing miR-204-5p reduced VC by suppressing CAMK1 activity. Overexpressing miR-204-5p also effectively mitigated aortic calcification in an in vivo rat model. In summary, our research indicated that targeting the miR-204-5p/CAMK1 pathway could be a viable strategy for mitigating VC in CKD patients.

MiR-92a-3p Knockdown Attenuates Transforming Growth Factor-ß1-induced Tubulointerstitial Fibrosis by Targeting LIN28A-mediated EMT Pathway.

ABSTRACT: The role of microRNAs in regulating tubulointerstitial fibrosis, a key feature of progressive chronic kidney disease, is of significant importance. LIN28A has been reported to attenuate renal fibrosis in obstructive nephropathy. Here, our objective was to investigate the precise biological function of the miR-92a-3p/LIN28A axis in tubulointerstitial fibrosis. The human renal proximal tubular epithelial (HK-2) cell line was exposed to transforming growth factor (TGF)-ß1, establishing an in vitro model mimicking tubulointerstitial fibrosis. Luciferase reporter assay was utilized to investigate the relationship between miR-92a-3p and LIN28A. Cell transfection techniques were employed to modify the expression of miR-92a-3p and LIN28A. An in vivo model of tubulointerstitial fibrosis was created by inducing unilateral ureteral obstruction (UUO) in C57BL/6N mice. Our initial observations showed that TGF-ß1 treatment of HK-2 cells and the UUO mice model led to an increase in miR-92a-3p expression and a decrease in LIN28A expression. We confirmed that miR-92a-3p directly targeted LIN28A in HK-2 cells. In TGF-ß1-stimulated HK-2 cells, knocking down miR-92a-3p notably reduced the levels of alpha smooth muscle actin and vimentin and concurrently enhanced the expression of E-cadherin. These changes were counteracted upon transfection with si-LIN28A. Thus, directing interventions toward miR-92a-3p holds the potential to emerge as a viable therapeutic approach for addressing tubulointerstitial fibrosis.