Purpose -The purpose of this paper is to study the influence of moisture on corrosion behaviour of steel ground rods in mildly desertified soil and the mechanism behind it. Design/methodology/approach -The specimens were used for weight loss corrosion experiments and polarization scans were taken at different moisture levels. Specimen surfaces were characterized using a scanning electron microscope, energy dispersive spectrometer, and using X-ray diffraction.Findings -The results indicated that the moisture content of the soil influenced steel corrosion considerably. The maximum corrosion of 20G and Q235 galvanised steels occurred at 10 per cent and 12.5 per cent soil moisture, respectively. The corrosion products of 20G steel were mostly Fe 2 O 3 and Fe 3 O 4 , whereas that of Q235 galvanised steel was Zn 5 (OH) 8 Cl 2 · H 2 O. Originality/value -The paper provides information regarding the relationship between moisture and corrosion of steel ground rods, which is useful for understanding the mechanism of soil corrosion. The research results can provide theoretical guidelines for preventing the corrosion of steel ground rods buried in mildly desertified soil.

Fibulin-5 is reportedly involved in the pathological process of atherosclerosis (AS) where low expression has been frequently observed in ruptured atherosclerotic plaques. The aim of the present study was to determine the effects of fibulin-5 on the responses of vascular smooth muscle cells (VSMC) to oxidized low-density lipoprotein (ox-LDL). The expression of fibulin-5 was studied in human aortic-VSMCs (HA-VSMCs) treated with ox-LDL. Fibulin-5 was first overexpressed by the transfection of Ov-Fibulin-5 plasmids in HA-VSMCs challenged with ox-LDL to investigate its influence on cell proliferation, migration and invasion using Cell Counting Kit-8, wound healing and Transwell assays. Yin Yang-1 (YY1) was bioinformatically predicted to bind to the promoter sites of fibulin-5, which was subsequently confirmed by dual-luciferase reporter gene assay. Fibulin-5 overexpression was able to suppress cell proliferation, invasion and migration, which was effectively reversed by YY1 silencing by the transfection of siRNA-Fibulin-5 plasmids which could induced fibulin-5 silencing. YY1 binding sites in the promoter region of fibulin-5 were identified and confirmed in vitro by chromatin immunoprecipitation assay and dual-luciferase reporter gene assay. The present results suggested that as a modulator of fibulin-5, YY1 alleviated ox-LDL-induced proliferation, invasion, migration and phenotypic transition from differentiated contractile phenotype to dedifferentiated phenotype in VSMCs. However, the mechanism underlying the YY1-mediated regulation of fibulin-5 expression needs to be confirmed further in vivo . Nevertheless, targeting fibulin-5 and YY1 could be further developed for AS therapy.