The diffusive transport of gibberellins and abscisic acid through the aleurone layer of germinating barley grain: a mathematical model

A mathematical model of the diffusive transport of abscisic acid (ABA) and gibberellins (GAs) through the aleurone layer of barley (Hordeum vulgare L.) grain is presented. The model consists of two partial differential equations describing the accumulation of phytohormone in the apoplastic and symplasmic compartments of the aleurone layer, both spatially and temporally. The mathematical model contains the morphology of the barley grain and the physicochemical properties of the two phytohormones. A mathematical derivation of the accumulation ratios for the two phytohormones between the symplast and apoplast under equilibrium conditions resulted in different distribution mechanisms for GAs and ABA. A sensitivity analysis of the accumulation ratio for GAs indicated high sensitivity to the apoplastic pH and the membrane potential, whereas the accumulation ratio for ABA proved to be most sensitive to the pH difference between the apoplast and symplast. The diffusive transport time for GAs to the basal site of the aleurone layer as calculated with the mathematical model is within a physiologically plausible timescale according to experimental data from the literature. Abscisic acid cannot be transported by diffusion to the end of the aleurone layer as quickly as GAs, according to model simulations. Therefore, the functional role of ABA in germination is likely to be in the vicinity of the embryo.     

Virus induced adherence of monocytes to endothelial cells

In this study we have demonstrated that infection of human umbilical vein endothelial cells (HUVEC) with Herpes simplex virus type 1 (HSV-1) resulted in an increased adherence of monocytes (MC). This enhanced adherence occurred at 3 h post infection (p.i.) when about 20% of the monolayer is infected and when there is no cytopathic effect observable in the monolayer. The adherence of human MC to virus-infected HUVEC monolayers proved to be effective and reproducible if a multiplicity of infection (MOI) of ten and a ratio of number of MC to number of HUVEC of 5 was used. The increased adherence was also induced by incubating non-infected HUVEC with the 'supernatant medium' of the HSV-1 infected cells, showing that soluble factors induced by viral infection are responsible for the increased adherence. The augmentation of MC adherence to infected endothelium was sensitive to tunicamycin treatment, suggesting that the MC adherence is probably mediated by glycoproteins expressed on the HUVEC membranes by virus infection.     

Virus induced adherence of monocytes to endothelial cells

Abstract In this study we have demonstrated that infection of human umbilical vein endothelial cells (HUVEC) with Herpes simplex virus type 1 (HSV-1) resulted in an increased adherence of monocytes (MC). This enhanced adherence occurred at 3 h post infection (p.i.) when about 20% of the monolayer is infected and when there is no cytopathic effect observable in the monolayer. The adherence of human MC to virus-infected HUVEC monolayers proved to be effective and reproductible if a multiplicity of infection (MOI) of ten and a ratio of number of MC to number of HUVEC of 5 was used. The increased adherence was also induced by incubating non-infected HUVEC with the 'supernatant medium' of the HSV-1 infected cells, showing that soluble factors induced by viral infection are responsible for the increased adherence. The augmentation of MC adherence to infected endothelium was sensitive to tunicamycin treatment, suggesting that the MC adherence is probably mediated by glycoproteins expressed on the HUVEC membranes by virus infection.     

Effects of 1,4-phenylenebis(methylene)selenocyanate on mutagenesis and p53 protein expression in the tongue of lacI rats treated with 4-nitroquinoline-N-oxide

Previously we showed that the organoselenium compound, 1,4-phenylenebis(methylene)selenocyanate (p-XSC)¹ inhibits 4-nitroquinoline-N-oxide (4-NQO)-induced tongue tumorigenesis in Fisher rats. Here we investigate possible mechanisms of this inhibition by monitoring mutagenesis and p53 protein levels in lacI and conventional Fisher rats treated with: (1) a carcinogenic dose of 4-NQO for 10 weeks in drinking water, (2) 4-NQO + p-XSC (15 ppm as selenium), and (3) 4-NQO followed by p-XSC. For mutagenesis studies, rats were euthanized at 7, 12 or 23 weeks after the start of 4-NQO. For studies on p53 levels, rats were euthanized at 11, 15 and 23 weeks. Appropriate controls were also monitored. In the 4-NQO-alone groups, the mutant fraction (MF) in the cII gene in tongue increased at least 50× background level. The MF (in units of mutants/10⁵ plaque forming units) for the 7, 12, and 23 weeks 4-NQO groups were respectively, 184 ± 88, 237 ± 105, and 329 ± 110. Thus, mutagenesis increased with length of exposure and post-treatment time. p-XSC modestly (ca. 15–30%) inhibited mutagenesis under all conditions. The inhibition reached significance at the last time point. When p-XSC was administered after 4-NQO, the MF was also modestly reduced. In 4-NQO-alone animals, levels of p53 in tongue (determined by Western blotting) were 1, 1.5 and 2.4 control levels at 10, 15 and 23 weeks, respectively. In the p-XSC + 4-NQO group, the enhancement in p53 levels by 4-NQO treatment was decreased about 90% at 15 weeks and 45% (P < 0.05) at 23 weeks, and by slightly smaller percentages in corresponding post-treatment groups. p-XSC alone did not alter p53 levels. As p53 levels generally increase in response to DNA damage, these results suggest that p-XSC reduces 4-NQO-induced DNA damage, resulting in reduced 4-NQO-induced mutagenesis and carcinogenesis. However, the fact that p-XSC is also effective when administered after 4-NQO, suggests additional mechanisms of inhibition exist.