In this paper, an open-air argon plasma plume is generated at atmospheric pressure by a two-electrode jet device with sub-microsecond voltage pulses at a repetitive frequency of 1 kHz. Optical emission spectroscopy measurements showed that spectral irradiance from OH and N2 bands, and Ar lines, characterized the spectrum of the open-air argon plasma plume. The rotational temperature estimation of UV OH band spectra indicated the gas temperature of the plasma plume to be as low as room temperature. A novel diagnostic method, based on two dispersion gratings and an ICCD camera, was designed for investigating the time- and space-resolved propagation behaviour of the excited radicals in the plasma plume. Based on the dispersion feature of gratings, a series of dispersed plasma optical emission volumes, which were formed by irradiance from different excited radiation emitters (excited species) in the plasma plume, were captured in the form of high-speed images by the ICCD camera. From the sequence of dispersed emission images, it is possible to observe the time- and space-resolved behaviour of different excited species in the plasma, and meanwhile, to understand the propagation dynamics of the open-air argon plasma plume. It is found that the OH bands' emission volume exhibited a propagation behaviour distinct from that of N2 and Ar emission volumes. The OH emissions decayed immediately as soon as the plasma travelled out from the nozzle, but were able to last for a longer duration time inside the nozzle than both N2 and Ar emissions. The N2 bands' emission volumes propagated to a far distance and formed the whole length of the argon plasma plume in the surrounding air. The Ar emissions decayed rapidly for the plasma inside and outside the nozzle due to the adverse effect of impurities, in particular the large concentration of diffused air in the open space. These distinct types of dynamic behaviour of the dispersed plasma emission volumes are attributed to the different generation and quenching mechanisms of their corresponding excited species and they shed light on the clear propagation dynamics of the argon plasma plume in open air.

Background: Activated microglia perform many of the immune effector functions typically associated with macrophages. However, the regulators involved in microglial activation are not well defined. Because microglia play a pivotal role in immune surveillance of the CNS, we studied the effect of the neuromediators histamine and substance P on microglia. Methods: The induction of microglial activation by histamine and substance P was examined using primary cultured microglia. Fluorescent images were acquired with a confocal microscope. The levels of TNF-α and IL-6 were measured with a commercial ELISA kit. Intracellular reactive oxygen species (ROS) levels were determined by dichlorodihydrofluorescein oxidation. The mitochondrial membrane potential was assessed with the MitoProbe™ JC-1 assay kit. Results: We found that the neuromediators histamine and substance P were able to stimulate microglial activation and the subsequent production of ROS and proinflammatory factors TNF-α and IL-6. These effects were partially abolished by antagonists of the histamine receptors H1 and H4 and of the substance P receptors NK-1, NK-2 and NK-3. Histamine induced mitochondrial membrane depolarization in microglia. Conclusions: These results indicate that the neuromediators histamine and SP can trigger microglial activation and release of pro-inflammatory factors from microglia, thus contributing to the development of microglia-mediated inflammation in the brain.

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Aims: Epigallocatechin-3-gallate (EGCG), a major catechin found in green tea, displays a variety of pharmacological properties and recently received attention as a prospective dietary intervention in cardiovascular diseases (CVD). This study was conducted to test the hypothesis that EGCG was able to inhibit tumor necrosis factor-a (TNF-a)-induced production of monocyte chemoattractant protein-1 (MCP-1) in human umbilical vein endothelial cells (HUVECs) and investigated the underlying molecular mechanisms. Methods: The inhibitory effect of EGCG on TNF-a-induced expression of MCP-1 was measured using ELISA and RT-qPCR. The effect of EGCG on TNF-a-induced nuclear factor-kappa B (NF-κB) activation was investigated by western blot and luciferase assays. Monocyte adhesion assay was detected by microscope. Results: EGCG significantly suppressed the TNF-a-induced protein and mRNA expression of MCP-1. Investigation of the mechanism suggested that EGCG suppressed the TNF-a-mediated NF-κB activation. In addition, the 67-kD laminin receptor (67LR) was involved in EGCG-mediated suppression of MCP-1 generation. Furthermore, EGCG potently inhibited monocyte adhesion to activated HUVECs. Conclusion: EGCG suppresses TNF-a-induced MCP-1 expression in HUVECs. This effect was mediated by 67LR and was via the inhibition of NF-κB activation. Our results demonstrated that EGCG might be a possible medicine for CVD prevention and treatment.

An atmospheric pressure nonequilibrium Ar micro-plasma generated inside a micro-tube with plasma radius of 3 μm and length of 2.7 cm is reported. The electron density of the plasma plume estimated from the broadening of the Ar emission line reaches as high as 3 × 1016 cm−3. The electron temperature obtained from CR model is 1.5 ev while the gas temperature of the plasma estimated from the N2 rotational spectrum is close to room temperature. The sheath thickness of the plasma could be close to the radius of the plasma. The ignition voltages of the plasma increase one order when the radius of the dielectric tube is decreased from 1 mm to 3 μm.