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Full-Text Articles in Life Sciences
Multi-Tissue Examination Of Exercise Or Metformin On The Consequences Of Doxorubicin Treatment, Amy Dee Mackay
Multi-Tissue Examination Of Exercise Or Metformin On The Consequences Of Doxorubicin Treatment, Amy Dee Mackay
Theses and Dissertations
Doxorubicin (DOX) is an effective chemotherapeutic treatment with lasting deleterious side effects in heart and skeletal muscle. As an increased percentage of patients live many years past their cancer treatments, addressing the long-term side effects of chemotherapy treatment becomes critical. In an attempt to prevent heart and skeletal muscle damage caused by DOX, two co-treatments, exercise (EX) or metformin (MET) were studied for their effectiveness in maintaining muscle function, mitochondrial respiration and iron regulation. DOX is known to bind with iron, contributing to oxidative damage resulting in cardiac and skeletal muscle toxicity. However, the degree to which the toxic side …
Pharmaceutical And Natural (Exercise) Mechanisms To Mitigate The Negative Impact Of Ptsd And Chronic Stress On Synaptic Plasticity And Memory, Roxanne M. Miller
Pharmaceutical And Natural (Exercise) Mechanisms To Mitigate The Negative Impact Of Ptsd And Chronic Stress On Synaptic Plasticity And Memory, Roxanne M. Miller
Theses and Dissertations
Synapses can be altered due to experiences in a process called synaptic plasticity, which causes memory formations. Synapses can be strengthened through methods known as long-term potentiation (LTP) or weakened through long-term depression (LTD). Stresses can cause changes by altering synapses through either LTP or LTD. Rats were used to study the effects of post-traumatic stress disorder (PTSD)-like symptoms and a prophylactic treatment using pharmaceuticals. The first model used was the single prolonged stress (SPS) with two weeks of chronic light, which was not as effective for causing changes in synaptic plasticity. The second model, seven days of social defeat …
Pharmaceutical And Natural (Exercise) Mechanisms To Mitigate The Negative Impact Of Ptsd And Chronic Stress On Synaptic Plasticity And Memory, Roxanne M. Miller
Pharmaceutical And Natural (Exercise) Mechanisms To Mitigate The Negative Impact Of Ptsd And Chronic Stress On Synaptic Plasticity And Memory, Roxanne M. Miller
Theses and Dissertations
Synapses can be altered due to experiences in a process called synaptic plasticity, which causes memory formations. Synapses can be strengthened through methods known as long-term potentiation (LTP) or weakened through long-term depression (LTD). Stresses can cause changes by altering synapses through either LTP or LTD. Rats were used to study the effects of post-traumatic stress disorder (PTSD)-like symptoms and a prophylactic treatment using pharmaceuticals. The first model used was the single prolonged stress (SPS) with two weeks of chronic light, which was not as effective for causing changes in synaptic plasticity. The second model, seven days of social defeat …
Exercising To Stay Mentally Fit, Tyler Hammond, Dr. Jerffrey Edwards
Exercising To Stay Mentally Fit, Tyler Hammond, Dr. Jerffrey Edwards
Journal of Undergraduate Research
Both exercise and stress have an impact on learning and memory. Exercise appears to have positive effects on learning and memory while stress appears to have negative effects on learning and memory. Previous work in our lab has demonstrated that exercise enhances long-term potentiation mediated by electrical stimulus in the hippocampus and that stress decreases long-term potentiation mediated by electrical stimulus in the hippocampus. Long-term potentiation is a measure of the strengthening of the synapses following an electrical stimulus intended to model learning and memory. The hippocampus is the area of the brain commonly deemed responsible for long-term declarative memories.
The Countering Effects Of Exercise On Stress Reduced Long-Term Potentiation In Mouse Hippocampi, Jacob Trotter, Dr. Jerffrey Edwards
The Countering Effects Of Exercise On Stress Reduced Long-Term Potentiation In Mouse Hippocampi, Jacob Trotter, Dr. Jerffrey Edwards
Journal of Undergraduate Research
The hippocampus is an area of the brain that mediates learning and memory by changing the properties of synapses between its neurons. This ability of synapses to change is known as synaptic plasticity. Long-term potentiation (LTP), a long-lasting increase in signal transmission between two neurons, is one of several phenomena underlying synaptic plasticity and is the cellular correlate of memory and learning. Several studies of LTP in mice show that there is a marked impairment of LTP in hippocampal slices taken from rodents exposed to stress. Their data suggests that stress may lead to deficits in learning and memory. In …
The Effects Of Stress And Exercise On Learning And Memory, Teresa Nufer (St. Pierre), Jeffery G. Edwards
The Effects Of Stress And Exercise On Learning And Memory, Teresa Nufer (St. Pierre), Jeffery G. Edwards
Journal of Undergraduate Research
Both stress and exercise have significant physiological effects. Researchers have studied these effects throughout the body, and current evidence suggests that exercise and stress also have profound effects on the brain. While stress decreases brain function, exercise has been show to enhance brain function. Recently, researchers have begun to investigate the effects of stress and exercise on the brain simultaneously, instead of studying the effects individually. Our lab has furthered these studies through the use of electrophysiology and behavioral experiments. Four groups of mice were studied: a control group, a group that experienced a chronic stress protocol, a group that …
Phosphorylation Of Skeletal Muscle Acetyl-Coa Carboxylase By Ampk Enhances Palmitoyl-Coa Inhibition, Dustin S. Rubink
Phosphorylation Of Skeletal Muscle Acetyl-Coa Carboxylase By Ampk Enhances Palmitoyl-Coa Inhibition, Dustin S. Rubink
Theses and Dissertations
Acetyl-CoA carboxylase (ACC) catalyzes the formation of malnoyl-CoA, which in turn controls the rate of fatty acid metabolism. ACC beta or 2 has been shown to be localized on the mitochondria in close proximity to carnintine palmitoyl transferase 1 (CPT-1), the enzyme responsible for the influx of acyl-CoA into the matrix where beta oxidation takes place. CPT-1 is inhibited by malonyl-CoA produced by ACC. It has been well documented that AMP activated kinase (AMPK) when activated phosphorylates and inactivates ACC. ACC is controlled allosterically by citrate, which activates, and by palmitoyl-COA, which inhibits. In this study, we asked the question, …