ABSTRACT
Effective inhibition of metallic corrosion to prevent its consequent loss is one of the serious apprehensions for industries in the modern world. This paper analyses the application of poly(2-ethyl-2-oxazoline) (PEOX) as an effective inhibitor of corrosion, when it is made to be in contact with the surfaces of mild steel (MS). The sustainability of MS against corrosion in 0.1 M Hydrochloric acid solution in the presence of known concentration of PEOX is assessed by potentiodynamic polarization (PDP) measurements, linear polarization studies (LPR), and electrochemical impedance spectroscopy (EIS). It was observed that PEOX behaves as better inhibitor for mild steel corrosion in 0.1 M HCl solution and it show enhanced inhibition efficiency (IE%) 79% at a concentration of 50 ppm. The polarization experiments indicated that addition of PEOX in concentrations varies from 25 ppm to 50 ppm induces a decrease of both cathodic and anodic currents densities. Also, the micrographs recorded by the Scanning Electron Microscopy confirm that molecules of PEOX act as corrosion inhibitors for the surfaces of MS in 0.1 M HCl. The stability of the MS surface in a corrosion-prone environment is traced by measuring the contact angles of water droplets placed on the MS surface, to quantify the extent of deterioration, if any, due to corrosion. The results presented here show that the compound PEOX performs as a mixed-type inhibitor against corrosion at the MS surface in acidic medium. Theoretical studies based on the electronic structure of PEOX in aqueous medium also support its performance as a successful corrosion-inhibitor.
ABSTRACT
The newly identified Src homology and collagen (Shc) family member ShcD was observed to be upregulated in 50% of vertical growth phase and metastatic melanomas. The aim of the present study was to investigate the mechanism by which ShcD mediates cell motility. 293 cell lines were altered to stably express GFP (GF) or GFPShcD (G5). Treatment of the cells with transforming growth factor (TGF)ß2 promoted extracellular signalregulated kinase (ERK) phosphorylation and, to a lesser extent, Smad2 phosphorylation in GFPShcDexpressing cells but not in GFPoverexpressing cells. GFPShcDexpressing cells exhibited upregulated expression of certain epithelialmesenchymal transitionrelated genes, such as snail family transcriptional repressor 1 and SLUG, than GFPexpressing cells. Higher levels of ERK were found in the nuclear fraction of GFPShcDexpressing cells than that of GFPexpressing cells. Overall, GFPShcDexpressing cells demonstrated enhanced migration compared with GFPexpressing cells. A slight increase in cell migration was observed in both cell lines (GF and G5) when the cells were allowed to migrate towards conditioned medium derived from TGFß2treated GFPShcD expressing cells. Collectively, ShcD upregulation was proposed to induce cell migration by affecting the expression of certain epithelialmesenchymal transitionrelated genes. Thus, our findings may improve understanding of the role of ShcD in cell migration.