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Articles 1 - 6 of 6
Full-Text Articles in Medicine and Health Sciences
Plasma Cysteine/Cystine And Glutathione/Glutathione Disulfide Redox Potentials In Hiv And Copd Patients., Walter H. Watson, Jeffrey D. Ritzenthaler, Paula Peyrani, Timothy L. Wiemken, Stephen P. Furmanek, Andrea Reyes-Vega, Tom J. Burke, Yuxuan Zheng, Julio A. Ramirez, Jesse Roman
Plasma Cysteine/Cystine And Glutathione/Glutathione Disulfide Redox Potentials In Hiv And Copd Patients., Walter H. Watson, Jeffrey D. Ritzenthaler, Paula Peyrani, Timothy L. Wiemken, Stephen P. Furmanek, Andrea Reyes-Vega, Tom J. Burke, Yuxuan Zheng, Julio A. Ramirez, Jesse Roman
Faculty Scholarship
Chronic obstructive pulmonary disease (COPD) is prevalent in patients infected with HIV. The purpose of this study was to test the hypothesis that systemic oxidation correlates with loss of lung function in subjects with COPD, and that HIV infection can contribute to creating such an environment. Subjects were recruited at the University of Louisville in the following groups: HIV-infected (n = 36), COPD (n = 32), HIV and COPD (n = 28), and uninfected controls with normal lung function (n = 34). HIV infection was assessed by viral load and CD4 cell counts. Pulmonary function was determined by spirometry …
Effect Of N-Acetyl-L-Cysteine Prevention Or Intervention On Diet Induced Beta Cell Compensation And Dysfunction, Madison Wallace
Effect Of N-Acetyl-L-Cysteine Prevention Or Intervention On Diet Induced Beta Cell Compensation And Dysfunction, Madison Wallace
Electronic Thesis and Dissertation Repository
Type 2 diabetes mellitus (T2DM) progression increases oxidative stress which contributes to beta cell compensation and eventual dysfunction. To investigate the role of antioxidant N-acetyl-L-cysteine (NAC) on beta cell function and pancreatic stellate cell activation (aSMA+) during early and late stages of compensation, NAC was used for preventative (p) and intervention (i) treatments in C57BL/6N mice fed a 60% kcal high-fat diet (HFD) for 8 or 22 weeks. Significantly improved glucose tolerance was observed at 22 weeks following pNAC treatment in HFD mice. Although 22-week HFD mice displayed hyperinsulinemia, beta cell hypertrophy, decreased beta cell PDX-1 nuclear localization, …
Novel Mechanisms And Biomarkers In Alcohol-Induced Organ Injury., Christine E. Dolin
Novel Mechanisms And Biomarkers In Alcohol-Induced Organ Injury., Christine E. Dolin
Electronic Theses and Dissertations
Background. Ethanol (EtOH) consumption is known to affect multiple organs; this is unsurprising, as the concentration of EtOH in the blood at relevant doses reaches the millimolar range. The overarching goal of this dissertation was to elucidate mechanisms of alcohol-induced organ injury, specifically the effects of alcohol on the hepatic extracellular matrix (ECM) proteome, the alcoholic hepatitis (AH) plasma peptidome, and the effects of alcohol on the renal cortex proteome and transcriptome. Methods. Mice were pair-fed ethanol-containing liquid diet chronically, and then some mice were administered lipopolysaccharide (LPS). Liver sections from these mice were processed in a series of increasingly …
The Effects Of Intermittent Fasting On Chronic Disease In Adults: A Systematic Review, Brendan Teeters
The Effects Of Intermittent Fasting On Chronic Disease In Adults: A Systematic Review, Brendan Teeters
Undergraduate Honors Theses
This systematic review investigated thirteen primary and secondary research studies from the past 20 years to determine the effects of intermittent fasting on chronic disease in adults through evaluation of biological markers pertaining to inflammation, oxidative stress, and the cardiovascular system. The dependent variables examined included heart rate, blood pressure, and cholesterol levels for cardiovascular risk; leptin and TNF-a for inflammatory risk; and F2-Isoprostanes and free radicals for oxidative stress biomarkers. The reviewed studies found that there was a decrease in resting heart rate, systolic and diastolic blood pressure, blood LDL and total cholesterol levels, inflammatory cells, like …
Lipids, Reactive Oxygen Species, And Health, Heather Bowen
Lipids, Reactive Oxygen Species, And Health, Heather Bowen
DNP Research Projects
Cardiovascular disease (CVD) is the leading cause of death in the United States. Coronary artery disease (CAD), where plaque builds up to create atherosclerosis, puts patients at risk for heart attack or stroke. Mitochondrial Reactive Oxygen Species (ROS) have been implicated as a source of oxidative stress that can lead to the development of CAD, and diets high in fat potentiate this occurrence. As certain fats are heated and experience chemical and physical degradation, they cause an increased risk of obesity, diabetes, various forms of cancer, and CVD. This research study, based on CREATION Health ideals, aimed to evaluate the …
A Bird's-Eye View Of The Multiple Biochemical Mechanisms That Propel Pathology Of Alzheimer's Disease: Recent Advances And Mechanistic Perspectives On How To Halt The Disease Progression Targeting Multiple Pathways., Caleb Vegh, Kyle Stokes, Dennis Ma, Darcy Wear, Jerome Cohen, Sidhartha D. Ray, Siyaram Pandey
A Bird's-Eye View Of The Multiple Biochemical Mechanisms That Propel Pathology Of Alzheimer's Disease: Recent Advances And Mechanistic Perspectives On How To Halt The Disease Progression Targeting Multiple Pathways., Caleb Vegh, Kyle Stokes, Dennis Ma, Darcy Wear, Jerome Cohen, Sidhartha D. Ray, Siyaram Pandey
Touro College of Pharmacy (New York) Publications and Research
Neurons consume the highest amount of oxygen, depend on oxidative metabolism for energy, and survive for the lifetime of an individual. Therefore, neurons are vulnerable to death caused by oxidative-stress, accumulation of damaged and dysfunctional proteins and organelles. There is an exponential increase in the number of patients diagnosed with neurodegenerative diseases such as Alzheimer’s (AD) as the number of elderly increases exponentially. Development of AD pathology is a complex phenomenon characterized by neuronal death, accumulation of extracellular amyloid-β plaques and neurofibrillary tangles, and most importantly loss of memory and cognition. These pathologies are most likely caused by mechanisms including …