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Mechanisms by which mild impairment of mitochondrial function increases stress resistance and lifespanLiontis, Thomas January 2020 (has links)
No description available.
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Characterization of Drosophila melanogaster glial cell types using single-cell RNA sequencing dataCouture, Camille January 2020 (has links)
No description available.
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Oculomotor and vestibulo-ocular function post-concussion in children and adolescentsTreleaven, Dakota January 2020 (has links)
No description available.
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Social isolation induced behavioural and microstructural differences in juvenile miceIrwin, Sarah January 2020 (has links)
No description available.
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Convergent epigenetic consequences of mislocalization of ALS-linked RNA-binding proteinsTibshirani, Michael January 2016 (has links)
No description available.
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Tumor necrosis factor-alpha regulates the function of antidepressants and impact of mutant Huntingtin proteinDuseja, Rachna January 2016 (has links)
No description available.
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Resolving the roles for inhibitor of Apoptosis Proteins in cell death and survivalHeard, Kristen January 2016 (has links)
No description available.
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Dynamics of longitudinal biomarker changes in the APP transgenic rat model of ADShin, Monica January 2016 (has links)
No description available.
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Regional brain volume changes following chronic antipsychotic treatment in miceGuma, Elisa January 2016 (has links)
No description available.
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The role of L-carnitine in preventing mitochondrial dysfunction after neonatal hypoxia-ischemiaRau, Thomas Fredrick 24 July 2007 (has links)
Neonatal hypoxia-ischemia (HI) represents an intractable clinical condition that lacks an effective treatment and results in blindness, cerebral palsy, and cognitive deficits. A primary mechanism of cell death induced by neonatal HI is mitochondrial dysfunction leading to metabolic crisis and apoptosis. L-carnitine (LCAR) is an endogenous compound that transports fatty acids across the mitochondrial membrane for metabolism, buffers endogenous acyl-coA pools and improves the health and efficiency of the mitochondria. In light of the mitochondrial dysfunction observed after HI we hypothesized treatment with LCAR would reduce cell death after HI. Using a novel rat hippocampal slice culture model we observed a decrease in cell death in RHSC treated with 5mM LCAR for 2 hours prior to oxygen glucose deprivation (OGD). Under the same conditions we observed an LCAR induced decrease in both necrosis and mitochondrially-mediated apoptosis. To elucidate the mechanism for these data we studied the effect of LCAR on reactive oxygen species (ROS) before and after OGD. We observed a decrease in superoxide and H2O2 in RHSC treated with LCAR and exposed to OGD. In further experiments we observed LCAR treatment increased the expression and activity of superoxide dismutase 1 (SOD1) and catalase prior to OGD and this effect resulted in decreased cell death after OGD. In addition to increased (ROS) scavenging, we observed an LCAR mediated increase in levels of uncoupling protein 2 (UCP-2). In a series of experiments we observed a correlation between UCP-2 expression, the reversible modulation of mitochondrial membrane potential, and a decrease in cell death after OGD. These observations taken together suggest LCAR decreases cell death in RHSC after OGD by increasing ROS scavenging and UCP-2 expression in the mitochondria prior to OGD.
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