19 research outputs found

    Coarse Grid Numerical Simulation of Reaction Kinetics Model in the Gas Hydrate Reservoirs

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    ABSTRACT A number of simulation studies of hydrate decomposition in porous media have shown hydrate decomposition zone could be narrow, especially when permeability at initial hydrate saturation is low. Field scale simulation of gas production from hydrate reservoirs with (fine) grid blocks that allow accurate modeling of the decomposition region becomes impractical. This paper proposes a methodology for the use of coarse grid blocks for the simulation of hydrate decomposition without loss of accuracy. This study focuses on the modeling of an energy self sustaining gas production process from hydrate reservoir known as depressurization technique. In this process the pressure reduction diffuses within the hydrate layer resulting in the decomposition of hydrate structures and gas generation. A 1-D mathematical model is introduced which incorporates energy balance, fluid flow and kinetics of hydrate decomposition. Numerical results are shown to demonstrate the lack of accuracy of this solution when coarse grid blocks are used. This study uses Taylor series and determines additional terms and a correction parameter (α), which when are incorporated in the coarse-grid model improves its accuracy. It is shown that a single value of correction parameter (α) is sufficient to improve the accuracy of all variables (pressure, temperature and hydrate saturation), and for all times. A relation is obtained between the correction parameter and the coarse-grid size. The success of methodology in improving the accuracy of modeling with coarse grid cells and matching the results of a solution with a highly refined grid has been demonstrated for two systems with various properties

    Study of Cyclooxygenase-2 Expression in Sprague Dawley Rat Gastric Cancer Induced by H. Pylori

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    Background and Objectives: Gastric cancer is one of the most common gastrointestinal tumors; the incidence and mortality of gastric cancer are on the increase nowadays. Helicobacter pylori(H.Pylori) causes chronic active gastritis and peptic ulcer disease. Cycloocygenase-2 (COX-2) is the central enzyme in the biosynthetic pathway to prostaglandins. Studies from different laboratories suggested that over-expression of COX-2 was detected in colon and other tumors. To obtain direct evidence concerning this relationship, we investigated the immunohistochemical findings of gastric mucosa using an animal model of gastric cancer induced by H. pylori in sprague dawley rat.Methods: The rats were randomly assigned into three groups(n=5). Those of experimental group2 were given MNU. one week after completion of MNU administration, rats in experimental groups 1 were inoculated with H. pylori three times every other day. Rats in control group(group 3) received neither MNU nor H. pylori. Rats of groups 1, 2, and control group were maintained on standard diets throughout the experiment. Rat were weighed and sacrificed under anesthesia with ether at 20 weeks after infection. One half of the excised stomachs, were fixed in neutral-buffered 10% formalin and were cut into approximately six strips, which were processed by standard methods, embedded in paraffin, sectioned at 6 µm, and stained with hematoxylin and eosin (H&E) and immunohistochemistry for Cox-2 protein detection. To confirm H. pylori infection, samples ( 3-mm2) of stomach mucosa transferred to appropriate medium and Colonies were identified by characteristic Gram’s stain morphology, and by urease, catalase, and oxidase activity sample was also placed into the gel of a rapid urease test kit.Results: Data showed a significant decrease of animal body weight in experimental groups compared with control group. Histopathological studies showed severe infiltration of the lamina propria and submucusaal layer by polymorphonuclear and mononuclear cells appeared in the antrum, with an increase in epithelial cell proliferation, and the infiltration of focal oesophageal. Control animals showed no abnormal findings throughout the entire observation period. COX-2 protein was expressed in experimental groups but there were no evidence of cox-2 protein expression in control group.Conclusion: Data showed that the H. pylori caused significant decrease of body weight in experimental group. In addition, histological studies showed evidence of metaplasia in rat stomach. Immunohistochemichas studies showed cox-2 protein expression occurred during early stage of metaplasia induction
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