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PDF | p> Investing in the stock market is closely related to the risk of price movements. Investors used technical analysis to minimize the risk involved. But that was before fundamental analysis was developed. Not so long ago, the first fundamental institution for the development and promotion of technical analysis was created in the UK. In the late 1980s, after the adoption of a legislative act regulating the trading of financial instruments, the market for financial instruments became available to a wide range of investors. Many of them realized for the first time that the financial market is not just a market for financial instruments.
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Yes, TA’s are not (that I’m aware of) accessible in the free version of PDF-Explorer.
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Accumulating evidence shows a link between higher levels of glucocorticoid hormones, cognitive deficits in humans and impaired cognition in animal models of disease. However, precise mechanisms through which glucocorticoids cause cognitive impairment have not been identified. The hypothesis proposed here is that glucocorticoid excess causes mitochondrial dysfunction in the brain and this leads to neuronal cell death. We will establish that cognitive impairment and neuronal cell death in an Alzheimer’s disease mouse model are mediated by mitochondrial dysfunction caused by glucocorticoid excess. Two levels of mitochondrial dysfunction will be evaluated: mitochondrial membrane damage and mitochondrial oxidative stress. In specific aim 1, we will demonstrate that glucocorticoid excess leads to a decreased ATP/ADP ratio. Based on our preliminary data, we hypothesize that this is due to a decrease in the activity of the F1 ATP synthase, a component of the mitochondrial membrane. We will utilize a combination of approaches, including whole brain imaging of [18F]fluoro-2-deoxyglucose ([18F]FDG) uptake, to determine whether [18F]FDG uptake is decreased in the brain. Changes in [18F]FDG uptake will be correlated with measures of oxidative stress, mitochondrial function and markers of cell death. In specific aim 2, we will determine whether inhibition of mitochondrial function blocks glucocorticoid-induced cell death and improves cognitive function. We will evaluate the effect of mitochondrial inhibitors on glucocorticoid-induced cell death and mitochondrial dysfunction. In specific aim 3, we will determine whether treatment of mice with mitochondrial inhibitors improves cognitive impairment. We will evaluate the effect of mitochondrial inhibition on memory in a contextual fear conditioning test. We will also evaluate the
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