Generation of Charged Nanoparticles During Thermal Evaporation of Silver at Atmospheric Pressure.

The generation of charged silver nanoparticles in the gas phase during thermal evaporation of silver at atmospheric pressure was confirmed by the nano-differential mobility analyzer (DMA). Effects of the evaporation temperature, the nitrogen gas flow rate and the amount of silver to be evaporated on the size distribution of charged nanoparticles (CNPs) were examined. Both positively and negatively-charged nanoparticles were generated under all processing conditions adopted in this study. The deposition behavior of CNPs was affected by the gas flow, which is affected by the temperature gradient in the reactor and by the applied electric bias. The electric bias, which not only enhanced the film growth rate but also produced a much denser film surface, turned out to be an important process parameter under the condition where an appreciable amount of CNPs is generated.

Effects of sFlt-1 and alpha 2-macroglobulin on vascular endothelial growth factor-induced endothelin-1 upregulation in human microvascular endothelial cells.

INTRODUCTION: Soluble fms-like tyrosine kinase-1 (sFlt-1) is a vascular endothelial growth factor (VEGF) binding protein and potent antagonist of VEGF. Alpha 2 macroglobulin (α2M) is another major binding protein for circulating VEGF, which is present in human plasma at higher concentration (2-4 mg/mL) than sFlt-1. This study investigated the effects of sFlt-1 and α2M on VEGF-induced endothelin-1 (ET-1) upregulation in human microvascular endothelial cell-1 (HMEC-1). METHODS: HMEC-1 was cultured and incubated with varying concentrations of sFlt-1 and α2M in combination with VEGF. ET-1 mRNA expression in the cells was measured by real time RT-PCR and ET-1 protein by western blot analysis. RESULTS: ET-1 expression in HMEC-1 incubated with VEGF significantly increased in time- and dose-dependent manners. Next, HMEC-1 was treated with the sFlt-1 (10-1000 ng/mL) or α2M (10-10000 ng/mL) in the presence of VEGF (10 ng/mL). We found that sFlt-1 induced a significant decrease of ET-1 expression upregulated by VEGF, while α2M did not affect the VEGF-induced ET-1 expression. CONCLUSIONS: sFLT-1 suppressed the VEGF-induced the ET-1 expression of HMEC-1. However, α2M did not show a significant effect on the ET-1 expression that was induced by VEGF. The results suggest that a certain proportion of the bound form α2M-VEGF have a biological action involved in the pathophysiology of preeclampsia.