Mie scattering from submicron-sized CO2 clusters formed in a supersonic expansion of a gas mixture.

A detailed mathematical model is presented for a submicron-sized cluster formation in a binary gas mixture flowing through a three-staged conical nozzle. By measuring the angular distribution of light scattered from the clusters, the size of CO(2) clusters, produced in a supersonic expansion of the mixture gas of CO(2)(30%)/H(2)(70%) or CO(2)(10%)/He(90%), has been evaluated using the Mie scattering method. The mean sizes of CO(2) clusters are estimated to be 0.28 ± 0.03 µm for CO(2)/H(2) and 0.26 ± 0.04 µm for CO(2)/He, respectively. In addition, total gas density profiles in radial direction of the gas jet, measuring the phase shift of the light passing through the target by utilizing an interferometer, are found to be agreed with the numerical modeling within a factor of two. The dryness (= monomer/(monomer + cluster) ratio) in the targets is found to support the numerical modeling. The apparatus developed to evaluate the cluster-gas targets proved that our mathematical model of cluster formation is reliable enough for the binary gas mixture.

Energy increase in multi-MeV ion acceleration in the interaction of a short pulse laser with a cluster-gas target.

An approach for accelerating ions, with the use of a cluster-gas target and an ultrashort pulse laser of 150-mJ energy and 40-fs duration, is presented. Ions with energy 10-20 MeV per nucleon having a small divergence (full angle) of 3.4 degrees are generated in the forward direction, corresponding to approximately tenfold increase in the ion energies compared to previous experiments using solid targets. It is inferred from a particle-in-cell simulation that the high energy ions are generated at the rear side of the target due to the formation of a strong dipole vortex structure in subcritical density plasmas.

Retinoic acid-inducible gene-I is induced in gingival fibroblasts by lipopolysaccharide or poly IC: possible roles in interleukin-1beta, -6 and -8 expression.

Retinoic acid-inducible gene-I (RIG-I) is a member of the DExH family of proteins, and little is known of its biological function in the oral region. We previously reported that interleukin 1beta (IL-1beta) induced RIG-I expression in gingival fibroblasts. In this study, we studied the mechanism of RIG-I expression induced by lipopolysaccharide (LPS) or double-stranded RNA (dsRNA) in gingival fibroblasts. We also addressed the role of RIG-I in the expression of IL-1beta, IL-6 and IL-8 in gingival fibroblasts stimulated with LPS or dsRNA. We stimulated cultured human gingival fibroblasts with LPS or dsRNA, and examined the expression of RIG-I mRNA and protein. The effect of cycloheximide, a protein synthesis inhibitor, on RIG-I induction by these stimuli was examined. The expression of IL-1beta, IL-6 and IL-8 in gingival fibroblasts transfected with RIG-I cDNA stimulated with LPS or dsRNA was examined. LPS or dsRNA induced the expression of mRNA and protein for RIG-I in concentration- and time-dependent manners. We also examined the localization of RIG-I, and found that it was expressed in cytoplasm. Cycloheximide did not suppress the LPS or dsRNA-induced RIG-I expression. Introduction of RIG-I cDNA into gingival fibroblasts resulted in enhanced expression of IL-1beta, IL-6 and IL-8; moreover, overexpression of RIG-I stimulated with LPS or dsRNA synergistically increased expression of IL-1beta, IL-6 and IL-8. RIG-I may have important roles in the innate immune response in the regulation of IL-1beta, IL-6 and IL-8 expression in gingival fibroblasts in response to LPS and dsRNA.

Retinoic acid-inducible gene-I is induced by interleukin-1beta in cultured human gingival fibroblasts.

Retinoic acid-inducible gene-I (RIG-I) is a member of the DExH box family protein, and details of its biological function are not known. We have studied the mechanism of the interleukin-1beta (IL-1beta)-induced RIG-I expression in human gingival fibroblasts in culture. We also addressed the possibility of enhanced expression of COX-2, RANTES and galectin-9 in fibroblasts overexpressed RIG-I. We stimulated cultured human gingival fibroblasts with IL-1beta and examined the expression of RIG-I mRNA and protein by reverse transcriptase-mediated polymerase chain reaction and Western blot analysis. The effect of cycloheximide, a protein synthesis inhibitor, on the IL-1beta-induced expression of RIG-I was examined. The expression of COX-2, RANTES, galectin-9 and monocyte chemoattractant protein-1 in gingival fibroblasts transfected with RIG-I cDNA was also examined. IL-1beta stimulated the expressions of mRNA and protein for RIG-I, in cultured fibroblasts, in a time- and concentration-dependent manner. Cycloheximide did not suppress the IL-1beta-induced RIG-I expression. Introduction of RIG-I cDNA into fibroblasts resulted in enhanced expression of COX-2 mRNA, and slightly enhanced the expression of mRNA for RANTES and galectin-9. In contrast, RIG-I overexpression did not alter the level of mRNA for monocyte chemoattractant protein-1. We conclude that IL-1beta stimulates RIG-I expression in human gingival fibroblasts.

High IL-6 synthesis in cultured fibroblasts isolated from radicular cysts.

OBJECTIVE: Inflammatory cytokines have been reported to be related with inflammation and expansion of jaw cysts. In this study, to examine the relationship between radicular cysts and inflammatory cytokines, it was found that there was notable unique evidence on cytokine synthesis from fibroblasts isolated from radicular cysts. METHODS: The expression of such cytokines, namely, interleukin-1beta, IL-1beta, IL-6, IL-8, IL-10, tumour necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), transforming growth factor-beta1 (TGF-beta1), and granulocyte-macrophage colony-stimulating (GM-CSF) mRNA, in nine radicular cysts was examined and compared with that detected in six specimens of healthy gingival mucosa. Furthermore, separating all fibroblasts from their respective radicular cysts, healthy gingival mucosa, and healthy periodontal ligaments, these fibroblast groups were cultured without stimulators and a supernatant for each was obtained to analyse IL-1beta, IL-6, IL-8, TNF-alpha, and IFN-gamma by ELISA. RESULTS: Differences between radicular cysts and healthy gingival mucosa were not clearly shown by the expression of cytokine mRNA. Analysing inflammatory cytokine synthesis in fibroblast groups from these three kinds of tissues, surprisingly, the levels of IL-6 mRNA and protein were recognised to be higher in fibroblasts of radicular cysts than in those of control tissues by ELISA and a real-time RT-PCR. Significant differences in the cultured supernatants of these fibroblast groups were not recognised in the release of IL-1beta, IL-8, TNF-alpha, and IFN-gamma by ELISA. CONCLUSIONS: From these results, it was suggested that fibroblasts inducing IL-6 production might play important roles in the expansion of radicular cysts. It is considered that fibroblasts around radicular cysts may lead to high IL-6 synthesis over time in chronic inflammation.