3 research outputs found

    Planetary-wave-induced transport in the stratosphere

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    grantor: University of TorontoThe global mass circulation in the stratosphere is constrained by the downward control principle (Haynes et al. 1991). Stratospheric wave drag, produced by the breaking and dissipation of planetary waves, acts as a pump, drawing tracers from the equator to the pole and resulting in the observed Brewer-Dobson circulation. At present, the theoretical understanding of this process has limitations. It can be shown that for linear, small-amplitude waves, the Lagrangian mean velocities and the transformed Eulerian mean velocities are the same and are a direct result of the wave drag. However, it is not clear that this relationship holds in general; in particular, the stratosphere is clearly a nonlinear system with breaking planetary waves in the surf zone. Thus, while the existence of the wave-induced circulation is not under debate, its quantitative determination remains problematic. The purpose of this work is to include the effects of nonlinear, breaking waves by using a 3d primitive equations model to study the effect of the wave forcing on the traditional diagnostic quantities (the Eliassen-Palm flux divergence and the residual circulation) and to use off-line particle advection to quantify the resulting Lagrangian transport. Attention is deliberately focused on a weak forcing regime, so that sudden warmings do not occur, in order to test the theory in the cleanest possible context. It is shown that while the theory holds for small-amplitude and weakly nonlinear regimes, discrepancies arise in the strongly nonlinear regime. While the EP flux divergence is largely negative in the stratosphere, regions of reversed potential vorticity gradient lead to a positive EP flux divergence. Positive EP flux divergence can be associated with regions of dynamical instability, wherein there is in-situ generation of wave activity. Furthermore, the correspondence between the meridional residual and transport velocities becomes poor in regions where the flow is permitted to develop smaller scales through wave breaking. This is less true for the vertical transport and residual velocities, which seem to show better agreement, even in the surf zone and in regions of large amplitude waves. This is especially the case wherever particle paths are coherent, so that diabatic dispersion is minimized. The results from the primitive equations model are compared with those from the Canadian Middle Atmosphere Model to test the robustness of the results.Ph.D

    Triacetin-based acetate supplementation as a chemotherapeutic adjuvant therapy in glioma.

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    Cancer is associated with epigenetic (i.e., histone hypoacetylation) and metabolic (i.e., aerobic glycolysis) alterations. Levels of N-acetyl-L-aspartate (NAA), the primary storage form of acetate in the brain, and aspartoacylase (ASPA), the enzyme responsible for NAA catalysis to generate acetate, are reduced in glioma; yet, few studies have investigated acetate as a potential therapeutic agent. This preclinical study sought to test the efficacy of the food additive Triacetin (glyceryl triacetate, GTA) as a novel therapy to increase acetate bioavailability in glioma cells. The growth-inhibitory effects of GTA, compared to the histone deacetylase inhibitor Vorinostat (SAHA), were assessed in established human glioma cell lines (HOG and Hs683 oligodendroglioma, U87 and U251 glioblastoma) and primary tumor-derived glioma stem-like cells (GSCs), relative to an oligodendrocyte progenitor line (Oli-Neu), normal astrocytes, and neural stem cells (NSCs) in vitro. GTA was also tested as a chemotherapeutic adjuvant with temozolomide (TMZ) in orthotopically grafted GSCs. GTA-induced cytostatic growth arrest in vitro comparable to Vorinostat, but, unlike Vorinostat, GTA did not alter astrocyte growth and promoted NSC expansion. GTA alone increased survival of mice engrafted with glioblastoma GSCs and potentiated TMZ to extend survival longer than TMZ alone. GTA was most effective on GSCs with a mesenchymal cell phenotype. Given that GTA has been chronically administered safely to infants with Canavan disease, a leukodystrophy due to ASPA mutation, GTA-mediated acetate supplementation may provide a novel, safe chemotherapeutic adjuvant to reduce the growth of glioma tumors, most notably the more rapidly proliferating, glycolytic and hypoacetylated mesenchymal glioma tumors
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