Degradation of methyl orange and Alizarin Red S from waste water using poly(azomethine)/ZnO nanocomposite as a photocatalyst

2020 ◽  
Author(s):  
S. J. Pradeeba ◽  
K. Sampath
2020 ◽  
Vol 16 ◽  
Author(s):  
Nimisha Jadon ◽  
Gulzar Ahmad Bhat ◽  
Manoharmayum Vishwanath Sharma ◽  
Harendra Kumar Sharma

Background: The study focuses on the synthesis of chitosan/ Fe2O3 nanocomposite, its characterization and application in methyl orange dye degradation. Methods: The synthesized chitosan/ Fe2O3 nanocomposite was characterized with Powder X-Ray Diffraction, Fourier Transformation Infrared Spectroscopy (FTIR), Transmission Electron Microscopy (TEM) and UV-Vis Spectroscopy. Results: The characterization showed that the Fe2O3nanoparticles were embedded in the polymer matrix of chitosan. The size of the Fe2O3nanoparticles were less than 10nm and the crystallite size was 1.22 nm.The synthesized chitosan/ Fe2O3nanocomposite was tested for methyl orange degradation using different parameters such as effect of contact time, effect of dose, effect of concentration and effect of pH for the degradation of methyl orange dye in aqueous solution.The Fruendlich, Langmuir and Temkin isotherm studies were also conducted for adsoption of methyl orange on Chitosan/ Fe2O3nanocomposite. Conclusion: The study indicated that the synthesized chitosan/Fe2O3 nanocomposite had the potential of degrading methyl orange dye up to 75.04% under the set condition in this experiment which indicate that Chitosan/ Fe2O3 nanocomposite is a viable option that can be used for the degradation of methyl orange dye.


2019 ◽  
Vol 95 ◽  
pp. 105933
Author(s):  
Guohui Wang ◽  
Ruiqi Huang ◽  
Annan Zhou ◽  
Qinghong Xu

Author(s):  
Yun Zhou ◽  
Li-Long Wei ◽  
Rui-Ping Zhang ◽  
Cheng-Wu Han ◽  
Yongtong Cao

AbstractLipid metabolism is closely related to the improvement of vascular calcification (VC) in chronic kidney disease (CKD). Globular adiponectin (gAd) has been reported to be involved in the development of VC in CKD, but the detailed regulatory role remains unclear. The present study is aimed to investigate the biological function and the underlying regulation mechanism of gAd in the process of VC during CKD. Vascular smooth muscle cells (VSMCs) calcification was determined by Alizarin Red S staining. Protein signaling related with VC was tested by western blotting. The expression and intracellular localization of runt-related transcription factor 2 (Runx2) was detected by immunofluorescence and uraemic rat with VC was established by a two-step nephrectomy. Combined with the results of Alizarin Red S staining, we discovered that β-glycerophosphate (β-Gp)-induced the osteoblastic differentiation of VSMCs was significantly reversed by gAd treatment. Along with the VSMCs calcification and the increase of Runx2 in β-Gp-exposed VSMCs, the activities of protein kinase B (AKT) and Wnt/β-catenin pathway were enhanced, but that were counteracted by the exposure of gAd in rat and human VSMCs. After administration with agonists of the Wnt (SKL2001) and AKT (SC79), there appeared more osteoblastic differentiation and higher expression of Runx2 in gAd-treated VSMCs, but showing lower impact in the presence of SC79 than that in the presence of SKL2001. In the in vivo experiments, intravenous injection of gAd also significantly inhibited VC and Runx2 level in uraemic rat in a dose-dependent manner, possibly through regulating Wnt/β-catenin pathway. This study demonstrates that gAd ameliorates osteoblastic differentiation of VSMCs possibly by blocking PI3K/AKT and Wnt/β-catenin signaling transduction. The findings provide an important foundation for gAd in treating VC in kidney diseases.


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