Sonochemical Synthesis of Spherical Silica Nanoparticles and Polymeric Nanocomposites

2015 ◽  
Vol 27 (1) ◽  
pp. 39-53 ◽  
Author(s):  
Maryam Masjedi-Arani ◽  
Davood Ghanbari ◽  
Masoud Salavati-Niasari ◽  
Samira Bagheri
2018 ◽  
Vol 44 (7) ◽  
pp. 8720-8724 ◽  
Author(s):  
S. Sankar ◽  
Narinder Kaur ◽  
Sejoon Lee ◽  
Deuk Young Kim

2020 ◽  
Vol 54 (29) ◽  
pp. 4611-4620 ◽  
Author(s):  
Akm Samsur Rahman ◽  
Chirag Shah ◽  
Nikhil Gupta

The current research is focused on developing a geopolymer binder using rice husk ash–derived silica nanoparticles. Four types of rice husks were collected directly from various rice fields of Bangladesh in order to evaluate the pozzolanic activity and compatibility of the derived rice husk ashes with precursors of sodium-based geopolymers. Silicon carbide whiskers were introduced into sodium-based geopolymers in order to evaluate the response of silicon carbide whiskers to the interfacial bonding and strength of sodium-based geopolymers along with rice husk ashes. Compression, flexural and short beam shear tests were performed to investigate the synergistic effect of rice husk ashes–derived silica and commercially available silicon carbide whiskers. Results show that rice husk ashes–derived spherical silica nanoparticles reduced nano-porosity of the geopolymers by ∼20% and doubled the compressive strength. The simultaneous additions of rice husk ashes and silicon carbide whiskers resulted in flexural strength improvement by ∼27% and ∼97%, respectively. The increase in compressive strength due to the inclusion of silica nanoparticles is related to the reduction in porosity. The increase in flexural strength due to simultaneous inclusion of silica and silicon carbide whiskers suggest that silica particles are compatible with the metakaolin-based geopolymers, which is effective in consolidation. Finally, microscopy suggest that silicon carbide whiskers are effective in increasing bridged network and crack resistance.


2005 ◽  
Vol 77 (1) ◽  
pp. 354-354 ◽  
Author(s):  
Huang-Hao Yang ◽  
Shu-Qiong Zhang ◽  
Xiao-Lan Chen ◽  
Zhi-Xia Zhuang ◽  
Jin-Gou Xu ◽  
...  

2004 ◽  
pp. 240-244
Author(s):  
C. Poncet-Legr ◽  
L. Petit ◽  
S. Reculusa ◽  
C. Mingotaud ◽  
E. Duguet ◽  
...  

2019 ◽  
Vol 54 (23) ◽  
pp. 14296-14308
Author(s):  
A. L. Muñoz-Rosas ◽  
A. Rodríguez-Gómez ◽  
J. C. Alonso-Huitrón ◽  
N. Qureshi

2008 ◽  
Vol 16 (7) ◽  
pp. 4698 ◽  
Author(s):  
Thomas A. Germer ◽  
Christian Wolters ◽  
Don Brayton

2018 ◽  
Vol 296 (2) ◽  
pp. 379-384 ◽  
Author(s):  
Qian Guo ◽  
Guoqiang Yang ◽  
Danchun Huang ◽  
Wenbin Cao ◽  
Lin Ge ◽  
...  

2019 ◽  
Vol 47 (3) ◽  
pp. 1264-1278 ◽  
Author(s):  
Chong Guo ◽  
Ding-Yun You ◽  
Huan Li ◽  
Xiao-Yu Tuo ◽  
Zi-Jie Liu

Objective This study aimed to examine the role of spherical silica nanoparticles (SiNPs) on human bronchial epithelial (BEAS-2B) cells through inflammation. Methods Human mononuclear (THP-1) cells and BEAS-2B cells were co-cultured in transwell chambers and treated with 800 mmol/L benzo[ a]pyrene-7, 8-dihydrodiol-9, 10-epoxide (BPDE) and 12.5 µg/mL SiNPs for 24 hours. For controls, cells were treated with BPDE alone. Subcutaneous tumorigenicity and epithelial-mesenchymal transition (EMT) of BEAS-2B cells were measured. The cells were blocked with a stromal cell-derived factor-1α (SDF-1α)-specific antibody. EMT was analyzed in cells treated with 800 mmol/L BPDE and 12.5 µg/mL SiNPs relative to matched control cells and xenografts in vivo. Serum SDF-1α levels were measured in 23 patients with lung adenocarcinoma in Xuanwei, in 25 with lung adenocarcinoma outside Xuanwei, and in 22 with benign pulmonary lesions in Xuanwei. Results SiNPs significantly promoted tumorigenesis and EMT, induced the release of SDF-1α, and activated AKT (ser473) in BEAS-2B cells. EMT and phosphorylated AKT (ser473) and glycogen synthase kinase-3β levels were decreased when blocked by SDF-1α antibody in BEAS-2B cells. SDF-1α was mainly secreted by THP-1 cells. Conclusion SiNPs combined with BPDE promote EMT of BEAS-2B cells via the AKT pathway by inducing release of SDF-1α from THP-1 cells.


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