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The radially varying kinetics of electrons and excited atoms in the cylindrical axially homogeneous positive column of a dc glow discharge in a gas mixture of helium and 2% xenon was studied. The experimental investigations comprise the radially resolved measurements of the isotropic part of the electron velocity distribution function (EVDF) using a single-probe technique and of the densities of atoms in the lower excited states by using a laser diode absorption method. The theoretical investigations are based on the solution of the space-dependent kinetic equation for the EVDF and the balance equations of excited gas atoms. Besides a strict solution, various simplified treatments of the electron kinetics as the conventional homogeneous approach and the nonlocal approach have been applied. The electron kinetic behavior in the helium–xenon column plasma changes remarkably with increasing helium gas pressure from a distinctly nonlocal behavior at a low pressure of 100 Pa to a nearly local behavior at a medium pressure of 600 Pa.

A hybrid method for measuring the electron distribution function in the low temperature plasma is described. The time resolution of the measurement is of the order of several µsec.

The degree of dissociation of oxygen has been measured in the positive column plasma of a glow discharge by two different methods (the ozone method and the Wrede-Harteck method). The results of both methods are in a good agreement. The pressure was varied from 66 to 266 Pa, the discharge current from 4 to 100 mA, and the discharge tube was of 2.0 cm inside diameter. As expected, the degree of dissociation increases with increasing discharge current and decreases with increasing pressure. Calculations of the degree of dissociation show that the main loss process of the oxygen atoms is caused by the recombination on the wall of the discharge tube for pressures up to several 100 Pa. We found that the value of the recombination coefficient for the glass wall of the discharge tube (?˜4.6·10-4) is about a factor 2 larger than that for a tube outside of the discharge (?˜2.2·10-4). Ozone processes, including metastable oxygen molecules, have increasing influence on the balance of the oxygen atoms as the pressure increases.

It is well accepted that the induction of endothelial cell (EC) adhesion molecules is a critical component in acute inflammatory responses as well as allogeneic interactions in vascularized allografts and, possibly, atherogenesis. The "inflammatory triad" of interleukin 1 (IL-1), tumor necrosis factor, and lipopolysaccharide are potent stimulators of the EC activation/adhesion molecules intercellular adhesion molecule 1 (ICAM-1), endothelial-leukocyte adhesion molecule 1 (ELAM-1), and vascular cell adhesion molecule 1 (VCAM-1). To address whether there exist differing thresholds to cytokine-mediated EC activation, we utilized a panel of genetically distinct human umbilical vein EC lines, assessing their modulated EC surface expression and transcriptional responses to cytokines, with regard to the cell adhesion molecules (CAMs) ELAM-1, ICAM-1, and VCAM-1. With submaximal concentrations of cytokine, EC ELAM-1 surface expression varied from negligible to marked. This phenotypic response was maintained over numerous passages in culture and was observed in ex vivo organ culture analyses with cytokine-treated umbilical vein sections. Relative patterns of ELAM-1, ICAM-1, and VCAM-1 induction were similar in response to multiple stimuli (IL-1, tumor necrosis factor, and lipopolysaccharide, but not phorbol 12-myristate 13-acetate). Nuclear run-off experiments demonstrated that the "high responder" phenotype is a consequence of enhanced transcriptional activation of the CAM genes in response to IL-1 (1 unit/ml), whereas transcriptional responses in "low responders" are minimal. Despite the known involvement of NF-kappa B in endothelial CAM transcription, gel shift assays failed to demonstrate a correlation between the levels of IL-1-mediated nuclear NF-kappa B expression and CAM induction in high and low responding lines. We postulate that varying EC activation thresholds to cytokines observed here, in vitro, may be a critical determinant in the susceptibility to vasculopathic states.