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Metallic corrosion can cause substantial damage at various levels and in almost all types of infrastructure. For metallic corrosion to occur, a certain external environment and the presence of corrodents are the prerequisites. Stray current-induced corrosion, however, is a rather underestimated issue in the field of corrosion and civil engineering. Stray current arising from power sources and then circulating in metal structures may initiate corrosion or even accelerate existing corrosion processes. The most frequent sources of stray current are light rail transits and subways, which are also main traffic tools with continuously accelerating urbanization all over the world. Stray currents from these systems may easily flow into nearby metallic structures, making stray current-induced corrosion the most severe form of damage of buried structures, such as tunnels, pipelines, and various underground reinforced concrete structures. The objective of this paper is to critically review stray current-induced steel corrosion in infrastructure with regard to sources of stray current and the characteristics and mechanism of stray current corrosion in view of electrochemical aspects. The methods and techniques for the evaluation, monitoring, and control of stray current-induced corrosion for steel and reinforced concrete structures are also presented and discussed.

Purpose To study the detailed mechanisms of tumorigenesis and clinical outcomes of centrosomal protein 55 (CEP55) overexpression in renal cell carcinoma. Materials and methods Microarray analysis was performed to explore differentially expressed genes in five pairs of RCC tissues. Data of CEP55 expression and corresponding clinical information for 532 RCC patients of TCGA database were downloaded from cBioPortal. The expression of CEP55 in RCC tissues and cells was determined by real-time quantitative reverse transcription PCR (qRT-PCR), Western blot analysis and immunohistochemistry (IHC). Cells were transfected with siRNAs or lentivirus to regulate the expression of CEP55. The effects of CEP55 on proliferation, migration, invasion and epithelial-to-mesenchymal transition (EMT) of RCC cells were determined by MTS, migration and invasion assay and Western blot analysis. Results CEP55, one of the most upregulated genes in microarray analysis, was overexpressed in RCC tissues and cells. CEP55 expression was significantly correlated with poor outcome including neoplasm disease stage, histologic grade and TNM status, as well as survival status of patients. In vitro experiments showed that downregulation of CEP55 could dramatically inhibit RCC cell proliferation, migration and invasion, while overexpression of CEP55 could promote these biological behaviors. We further demonstrated that CEP55 knockdown suppressed epithelial-mesenchymal transition (EMT), which was mediated via upregulation of E-cadherin and downregulation of N-cadherin and ZEB1, through PI3K/AKT/mTOR pathway. In contrast, overexpression of CEP55 could promote EMT in RCC cells via the activation of PI3K/AKT/mTOR pathway. Importantly, inhibition of PI3K/AKT/mTOR pathway reduced the effects of CEP55 on the migration, invasion and EMT of RCC cells. Conclusion Our study showed that CEP55 could promote EMT through PI3K/AKT/mTOR pathway and might be an effective prognostic marker in RCC.