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Musculoskeletal, Neural, and Ocular Physiology Commons™
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Articles 1 - 5 of 5
Full-Text Articles in Musculoskeletal, Neural, and Ocular Physiology
Mitochondria As Causes Of And Therapeutic Targets In Chronic Post-Sepsis Skeletal Muscle Weakness, Meagan Scott Kingren
Mitochondria As Causes Of And Therapeutic Targets In Chronic Post-Sepsis Skeletal Muscle Weakness, Meagan Scott Kingren
Theses and Dissertations--Pharmacology and Nutritional Sciences
Sepsis, or the organ damage that ensues after the body fails to properly contain a local infection, is the leading cause of in-patient hospitalization in the United States. Advances in critical care medicine over the last 20 years have enabled most sepsis patients to survive the life-threatening dysregulated immune response. However, a majority of survivors report chronic weakness and fatigue years after sepsis, and the cause of this weakness remains largely unknown. This dissertation work focused first on elucidating the major causes of post-sepsis muscle weakness (Aim 1). This aim involved a time-course study to determine when muscle weakness was …
High Energy Blue Light Induces Oxidative Stress And Retinal Cell Apoptosis, Jessica Malinsky
High Energy Blue Light Induces Oxidative Stress And Retinal Cell Apoptosis, Jessica Malinsky
Capstone Showcase
Blue light (BL) is a high energy, short wavelength spanning 400 to 500 nm. Found in technological and environmental forms, BL has been shown to induce photochemical damage of the retina by reactive oxygen species (ROS) production. Excess ROS leads to oxidative stress, which disrupts retinal mitochondrial structure and function. As mitochondria amply occupy photoreceptors, they also contribute to oxidative stress due to their selectively significant absorption of BL at 400 to 500 nm. ROS generation that induces oxidative stress subsequently promotes retinal mitochondrial apoptosis. BL filtering and preventative mechanisms have been suggested to improve or repair BL-induced retinal damage, …
Mitochondrial Contributions To Disuse Atrophy: Let’S Talk About Sex, Megan Rosa-Caldwell
Mitochondrial Contributions To Disuse Atrophy: Let’S Talk About Sex, Megan Rosa-Caldwell
Graduate Theses and Dissertations
Skeletal muscle atrophy is a hallmark of many pathologies and is associated with disease prognosis, quality of life, and mortality. Specifically, lack of contractile activity of the muscle can result in disuse-associated atrophy. Disuse-induced atrophy is a common phenomenon in intensive care unit (ICU) patients and significantly impacts patient prognosis and ability to transition of out of intensive care. However, effective therapeutics to mitigate disuse-associated atrophy do not exist, clearly demonstrating the scientific and clinical need to further understand mechanisms contributing to disuse atrophy. In particular, a significant portion of the scientific literature has utilized male models, yet there is …
An Overview Of Leber’S Hereditary Optic Neuropathy, Matthew R. Dalton
An Overview Of Leber’S Hereditary Optic Neuropathy, Matthew R. Dalton
The Kabod
Typically affecting males ranging from 20 to 24 years of age, Leber’s Hereditary Optic Neuropathy (LHON) is a disorder that is characterized by an acute loss of central vision. Although a heritable disease, LHON does not follow the patterns of classical Mendelian genetics. In fact, one of the most striking characteristics of LHON is that the disease is virtually always inherited maternally. Unlike most genetic disorders that result from a mutation in genomic DNA, LHON is caused by a mutation in the genetic information of mitochondria (mtDNA). Currently there is no treatment for LHON. Despite this, pharmaceutical interventions and contemporary …
Tumor-Derived Proteins And Mitochondrial Dysfunction In Lung Cancer-Induced Cachexia, Julie B. Mclean
Tumor-Derived Proteins And Mitochondrial Dysfunction In Lung Cancer-Induced Cachexia, Julie B. Mclean
Theses and Dissertations--Physiology
Lung tumors secrete multiple factors that contribute to cachexia, a severe wasting syndrome that includes loss of muscle mass, weakness, and fatigue. 80% of advanced lung cancer patients experience cachexia, which cannot be reversed by nutritional interventions, diminishes response to and tolerance of cancer treatments, and increases morbidity and mortality. Despite a multitude of clinical trials, there are currently no approved treatments. This deficiency suggests that not all of the factors that contribute to cachexia have been identified.
Cancer is frequently accompanied by an increase in cyclooxygenase-2 (COX-2), a hallmark of inflammation. Clinical trials for COX-2 inhibitors have resulted in …