• 한국안전학회지
• /
• 제37권2호
• /
• pp.1-9
• /
• 2022

Most factories deal with toxic or flammable chemicals in their industrial processes. These hazardous substances pose a risk of leakage due to accidents, such as fire and explosion. In the event of chemical release, massive casualties and property damage can result; hence, quantitative risk prediction and assessment are necessary. Several methods are available for evaluating chemical dispersion in the atmosphere, and most analyses are considered neutral in dispersion models and under far-field wind condition. The foregoing assumption renders a model valid only after a considerable time has elapsed from the moment chemicals are released or dispersed from a source. Hence, an initial dispersion model is required to assess risk quantitatively and predict the extent of damage because the most dangerous locations are those near a leak source. In this study, the dispersion model for initial consequence analysis was developed with three-dimensional unsteady advective diffusion equation. In this expression, instantaneous leakage is assumed as a puff, and wind velocity is considered as a coordinate transform in the solution. To minimize the buoyant force, ethane is used as leaked fuel, and two different diffusion coefficients are introduced. The calculated concentration field with a molecular diffusion coefficient shows a moving circular iso-line in the horizontal plane. The maximum concentration decreases as time progresses and distance increases. In the case of using a coefficient for turbulent diffusion, the dispersion along the wind velocity direction is enhanced, and an elliptic iso-contour line is found. The result yielded by a widely used commercial program, ALOHA, was compared with the end point of the lower explosion limit. In the future, we plan to build a more accurate and general initial risk assessment model by considering the turbulence diffusion and buoyancy effect on dispersion.

• The Korean Journal of Physiology and Pharmacology
• /
• 제19권1호
• /
• pp.51-57
• /
• 2015

The etiology of periodontal disease is multifactorial. Exogenous stimuli such as bacterial pathogens can interact with toll-like receptors to activate intracellular calcium signaling in gingival epithelium and other tissues. The triggering of calcium signaling induces the secretion of pro-inflammatory cytokines such as interleukin-8 as part of the inflammatory response; however, the exact mechanism of calcium signaling induced by bacterial toxins when gingival epithelial cells are exposed to pathogens is unclear. Here, we investigate calcium signaling induced by bacteria and expression of inflammatory cytokines in human gingival epithelial cells. We found that peptidoglycan, a constituent of grampositive bacteria and an agonist of toll-like receptor 2, increases intracellular calcium in a concentration-dependent manner. Peptidoglycan-induced calcium signaling was abolished by treatment with blockers of phospholipase C (U73122), inositol 1,4,5-trisphosphate receptors, indicating the release of calcium from intracellular calcium stores. Peptidoglycan-mediated interleukin-8 expression was blocked by U73122 and 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid tetrakis (acetoxymethyl ester). Moreover, interleukin-8 expression was induced by thapsigargin, a selective inhibitor of the sarco/endoplasmic reticulum calcium ATPase, when thapsigargin was treated alone or co-treated with peptidoglycan. These results suggest that the gram-positive bacterial toxin peptidoglycan induces calcium signaling via the phospholipase C/inositol 1,4,5-trisphosphate pathway, and that increased interleukin-8 expression is mediated by intracellular calcium levels in human gingival epithelial cells.