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Effect of waste polyethylene addition on the properties of white portland cement
Miguel A. Valenzuela,Francisco J. Jiménez,Lucía Téllez,이수완,Heberto Balmori-Ramirez 한양대학교 세라믹연구소 2010 Journal of Ceramic Processing Research Vol.11 No.2
The effect of the addition of organic compounds (OC) an ordinary white Portland cement (WPC), on the properties such as compressive strength, fluidity, setting time, porosity and heat of hydration has been studied by adding 0.10-0.80 weight % of OC into the cement. The mixture of organic compounds obtained from a thermo-depolymerization of waste polyethylene (WP)and hydroxylation was composed by alcohols, alkenes and alkanes. The compressive strength was significantly dependent on the amount of OC. The highest value (45.3MPa) was found by adding 0.35 wt.% of the OC. The porosity of the modified WPC did not change in the range 0-0.4 wt.% OC, however from 0.5-0.8 wt.% OC caused a linear increase of the porosity.
Guartazaca-Guerrero Sebastián,Rodríguez-Morales Jahir,Rizo-Téllez Salma A.,Solleiro-Villavicencio Helena,Hernández-Valencia Aldo F.,Carrillo-Ruiz José Damián,Escobedo Galileo,Méndez-García Lucía A. 한국뇌신경과학회 2021 Experimental Neurobiology Vol.30 No.3
The coronavirus family has tropism for the Central Nervous System (CNS), however, there is no solid evidence demonstrating that the neurological effects of COVID-19 result from direct viral infection or systemic inflammation. The goals of this study were to examine the cytokine profile and the presence of SARS-CoV-2 messenger ribonucleic acid (mRNA) in cerebrospinal fluids (CSF) from two patients with cerebrovascular disease and COVID-19. Although the SARS-CoV-2 mRNA was not detected in CSF of both patients, we found abnormally high levels of numerous proinflammatory cytokines and chemokines, especially IL-8 and MCP-1. Since these chemokines mediate activation and recruitment of neutrophils, monocytes, and macrophages, it is feasible that cerebrovascular disease related-neuroinflammation found in both patients results from an exacerbated inflammatory response instead of SARS-CoV-2 direct invasion to CNS. These results suggest that neuroinflammation plays a key role in cerebrovascular disease and COVID-19.