Determination of Critical Conditions of Spontaneous Combustion of Coal in Longwall Gob Areas / Wyznaczanie Warunków Krytycznych Samozapalania Węgla W Zrobach Ścian

Decades of experience in the fight against endogenous fire hazard in coal mines indicate a major influence of certain conditions in a given area of the mine on the possibility of fire occurrence, such as: susceptibility of coals to spontaneous combustion, oxygen content in the air incoming to the self-heating coal, conditions of heat exchange between the self-heating coal mass and the environment This paper presents a numerical method for determining the critical conditions of spontaneous combustion of coal in longwall gob areas, i.e. conditions under which spontaneous combustion may occur. It has been assumed that crushed coal in the gob has a shape of a flat layer adjacent from the roof and floor side to the rocks. Our considerations have been limited to coals containing small amount of moisture. A simple model of oxidation kinetics on the coal surface expressed by the Arrhenius equation has been adopted. His model assumes that oxidation rate is independent of the amount of oxygen absorbed by coal. The rate of reaction depends only on temperature, with the parameters of the equation changing after the coal Has reached the critical temperature. The article presents also a mathematical model of spontaneous heating of the coal layer in the gob area. It describes the heat balance in the coal as well as the oxygen and heat balance in the flowing gases. The model consists of a system of differential equations which are solved using numerical techniques. The developed computer program enables to perform the relevant calculations. In this paper, on the example of coal from a seam 405, we present the method for determining the following critical parameters of the layer of crushed coal: thickness of the layer, oxygen content in a stream of gases flowing through the layer and thermal conductivity of surrounding rocks.Wieloletnie doświadczenie w zakresie zwalczania zagrożenia pożarem endogenicznym w kopalniach wskazują na zasadniczy wpływ na możliwość zaistnienia pożaru niektórych warunków panujących w danym miejscu kopalni, takich jak: skłonność węgla do samozapalania zawartość tlenu w powietrzu dopływającym do zagrzewającego się węgla. W pracy przedstawiono numeryczną metodę wyznaczania warunków krytycznych samozapalania węgla w zrobach ścian, czyli takich po spełnieniu których może dojść do samozapalenia. Przyjęto, że znajdujący się w zrobach rozkruszony węgiel ma kształt płaskiej warstwy, sąsiadującej od stropu i spągu ze skałami. Rozważania ograniczono do węgli charakteryzujących się niską zawartością wilgoci. Przyjęto prosty model kinetyki utleniania na powierzchni węgla wyrażony równaniem Arrheniusa. Model ten zakłada niezależność szybkości utleniania od ilości tlenu pochłoniętego przez węgiel. Szybkość reakcji zależy jedynie od temperatury , przy czym występujące w równaniu parametry zmieniają się po osiągnięciu przez węgiel temperatury krytycznej. W artykule przedstawiono matematyczny model samozagrzewania warstwy węgla w zrobach opisujący bilans ciepła w węglu oraz bilans tlenu i bilans ciepła w przepływających gazach. Tworzące model układy równań różniczkowych cząstkowych rozwiązywane są metodami numerycznymi. Opracowany program komputerowy umożliwia wykonywanie stosownych obliczeń. W pracy, na przykładzie węgla z pokładu 405 , przedstawiono sposób wyznaczania warunków krytycznych warstwy rozkruszonego węgla: grubości warstwy, zawartości tlenu w przepływających przez warstwę gazach oraz przewodności cieplnej otaczających skał

Cyclosporine A kinetics in brain cell cultures and its potential of crossing the blood-brain barrier.

There is an increasing need to develop improved systems for predicting the safety of xenobiotics. However, to move beyond hazard identification the available concentration of the test compounds needs to be incorporated. In this study cyclosporine A (CsA) was used as a model compound to assess the kinetic profiles in two rodent brain cell cultures after single and repeated exposures. CsA induced-cyclophilin B (Cyp-B) secretion was also determined as CsA-specific pharmacodynamic endpoint. Since CsA is a potent p-glycoprotein substrate, the ability of this compound to cross the blood-brain barrier (BBB) was also investigated using an in vitro bovine model with repeated exposures up to 14 days. Finally, CsA uptake mechanisms were studied using a parallel artificial membrane assay (PAMPA) in combination with a Caco-2 model. Kinetic results indicate a low intracellular CsA uptake, with no marked bioaccumulation or biotransformation. In addition, only low CsA amounts crossed the BBB. PAMPA and Caco-2 experiments revealed that CsA is mostly trapped to lipophilic compartments and exits the cell apically via active transport. Thus, although CsA is unlikely to enter the brain at cytotoxic concentrations, it may cause alterations in electrical activity and is likely to increase the CNS concentration of other compounds by occupying the BBBs extrusion capacity. Such an integrated testing system, incorporating BBB, brain culture models and kinetics could be applied for assessing neurotoxicity potential of compounds

Kinetics and dynamics of cyclosporine A in three hepatic cell culture systems

International audienceIn vitro experiments have a high potential to improve current chemical safety assessment and reduce the number of animals used. However, most studies conduct hazard assessment alone, largely ignoring exposure and kinetic parameters. Therefore, in this study the kinetics of cyclosporine A (CsA) and the dynamics of CsA-induced cyclophilin B (Cyp-B) secretion were investigated in three widely used hepatic in vitro models: primary rat hepatocytes (PRH), primary human hepatocytes (PHH) and HepaRG cells. Cells were exposed daily to CsA for up to 14 days. CsA in cells and culture media was quantified by LC-MS/MS and used for pharmacokinetic modeling. Cyp-B was quantified by western blot analysis in cells and media. All cell systems took up CsA rapidly from the medium after initial exposure and all showed a time- and concentration-dependent Cyp-B cellular depletion and extracellular secretion. Only in PRH an accumulation of CsA over 14 days repeated exposure was observed. Donor-specific effects in CsA clearance were observed in the PHH model and both PHH and HepaRG cells significantly metabolized CsA, with no bioaccumulation being observed after repeated exposure. The developed kinetic models are described in detail and show that all models under-predict the in vivo hepatic clearance of CsA, but to different extents with 27-, 24- and 2-fold for PRH, PHH and HepaRG cells, respectively. This study highlights the need for more attention to kinetics in in vitro studie