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Transient Simulations of the SLOWPOKE-2 Reactor Using the G4-STORK CodeTan, Andrew 17 December 2015 (has links)
The goal of this thesis is to study the transient behaviour of the SLOWPOKE-2 reactor using Monte-Carlo simulations with the G4-STORK code. G4-STORK is a 3-dimensional Monte-Carlo code derived from the GEANT4 physics simulation toolkit. Methods were developed for the proper treatment of delayed neutrons and a lumped capacitance model was used to track the time-dependent fuel properties (temperature, density) based on the fission power. By validating the methods in G4-STORK with experimental measurements we hope to extend our understanding of reactor transients as well as further develop our methods to model the transients of the next generation reactor designs. A SLOWPOKE-2 reactor such as the one at RMC was chosen for simulation due to its compact size, and well-known transient response of control rod removal and measured temperature feedback. Static simulations in G4-STORK find a neutron flux of order 10^12 cm−2 s−1 which agrees with experiment and a control rod worth of (4.9 ± 2.0) mk compared to the experimentally measured worth of 5.45 mk. Transient simulations from rod pluck-out find similar trends to the experimental findings as our results suggest a negative temperature feedback due to the doppler broadening of the U-238 absorption spectrum which contributes to the overall safety mechanism seen in the SLOWPOKE reactor. It is determined that the methods in G4-STORK provide a reasonable ability to simulate reactor transients and it is recommended that a full-core thermal-hydraulics model be coupled to G4-STORK to achieve a higher level of accuracy. / Thesis / Master of Applied Science (MASc)
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Mechanisms of benzyl alcohol tolerance in Drosophila melanogasterAlhasan, Yazan Mahmoud 19 August 2010 (has links)
Proper neuronal function requires the preservation of appropriate neural excitability. An adaptive increase in neural excitability after exposure to agents that depress neuronal signaling blunts the sedative drug effects upon subsequent drug exposure. This adaptive response to drug exposure leads to changes in drug induced behaviors such as tolerance, withdrawal and addiction. Here I use Drosophila melanogaster to study the cellular and neuronal components which mediate behavioral tolerance to the anesthetic benzyl alcohol. I demonstrate that rapid tolerance to benzyl alcohol is a pharmacodynamic mechanism independent of drug metabolism. Furthermore, tolerance is a cell autonomous response which occurs in the absence of neural signaling. Using genetic and pharmacological manipulations I find the synapse to play an important role in the development of tolerance. In addition, the neural circuits that regulate arousal and sleep also alter benzyl alcohol sensitivity. Beyond previously described transcriptional mechanisms I find a post-translational role of the Ca2+-activated K+-channel, slowpoke in the development of tolerance. Finally, I explore a form of juvenile onset tolerance, which may have origins that differ from rapid tolerance. The implications of this study go beyond tolerance in Drosophila melanogaster to benzyl alcohol and can shed light on human drug tolerance, withdrawal and addiction. / text
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