Matching Items (392)
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Description
Background: Evidence about the purported hypoglycemic and hypolipidemic effects of nopales (prickly pear cactus pads) is limited. Objective: To evaluate the efficacy of nopales for improving cardiometabolic risk factors and oxidative stress, compared to control, in adults with hypercholesterolemia. Design: In a randomized crossover trial, participants were assigned to a

Background: Evidence about the purported hypoglycemic and hypolipidemic effects of nopales (prickly pear cactus pads) is limited. Objective: To evaluate the efficacy of nopales for improving cardiometabolic risk factors and oxidative stress, compared to control, in adults with hypercholesterolemia. Design: In a randomized crossover trial, participants were assigned to a 2-wk intervention with 2 cups/day of nopales or cucumbers (control), with a 2 to 3-wk washout period. The study included 16 adults (5 male; 46±14 y; BMI = 31.4±5.7 kg/m2) with moderate hypercholesterolemia (low density lipoprotein cholesterol [LDL-c] = 137±21 mg/dL), but otherwise healthy. Main outcomes measured included: dietary intake (energy, macronutrients and micronutrients), cardiometabolic risk markers (total cholesterol, LDL-c, high density lipoprotein cholesterol [HDL-c], triglycerides, cholesterol distribution in LDL and HDL subfractions, glucose, insulin, homeostasis model assessment, and C-reactive protein), and oxidative stress markers (vitamin C, total antioxidant capacity, oxidized LDL, and LDL susceptibility to oxidation). Effects of treatment, time, or interactions were assessed using repeated measures ANOVA. Results: There was no significant treatment-by-time effect for any dietary composition data, lipid profile, cardiometabolic outcomes, or oxidative stress markers. A significant time effect was observed for energy, which was decreased in both treatments (cucumber, -8.3%; nopales, -10.1%; pTime=0.026) mostly due to lower mono and polyunsaturated fatty acids intake (pTime=0.023 and pTime=0.003, respectively). Both treatments significantly increased triglyceride concentrations (cucumber, 14.8%; nopales, 15.2%; pTime=0.020). Despite the lack of significant treatment-by-time effects, great individual response variability was observed for all outcomes. After the cucumber and nopales phases, a decrease in LDL-c was observed in 44% and 63% of the participants respectively. On average LDL-c was decreased by 2.0 mg/dL (-1.4%) after the cucumber phase and 3.9 mg/dL (-2.9%) after the nopales phase (pTime=0.176). Pro-atherogenic changes in HDL subfractions were observed in both interventions over time, by decreasing the proportion of HDL-c in large HDL (cucumber, -5.1%; nopales, -5.9%; pTime=0.021) and increasing the proportion in small HDL (cucumber, 4.1%; nopales, 7.9%; pTime=0.002). Conclusions: These data do not support the purported benefits of nopales at doses of 2 cups/day for 2-wk on markers of lipoprotein profile, cardiometabolic risk, and oxidative stress in hypercholesterolemic adults.
ContributorsPereira Pignotti, Giselle Adriana (Author) / Vega-Lopez, Sonia (Thesis advisor) / Gaesser, Glenn (Committee member) / Keller, Colleen (Committee member) / Shaibi, Gabriel (Committee member) / Sweazea, Karen (Committee member) / Arizona State University (Publisher)
Created2013
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Description
The end of the nineteenth century was an exhilarating and revolutionary era for the flute. This period is the Second Golden Age of the flute, when players and teachers associated with the Paris Conservatory developed what would be considered the birth of the modern flute school. In addition, the founding

The end of the nineteenth century was an exhilarating and revolutionary era for the flute. This period is the Second Golden Age of the flute, when players and teachers associated with the Paris Conservatory developed what would be considered the birth of the modern flute school. In addition, the founding in 1871 of the Société Nationale de Musique by Camille Saint-Saëns (1835-1921) and Romain Bussine (1830-1899) made possible the promotion of contemporary French composers. The founding of the Société des Instruments à Vent by Paul Taffanel (1844-1908) in 1879 also invigorated a new era of chamber music for wind instruments. Within this groundbreaking environment, Mélanie Hélène Bonis (pen name Mel Bonis) entered the Paris Conservatory in 1876, under the tutelage of César Franck (1822-1890). Many flutists are dismayed by the scarcity of repertoire for the instrument in the Romantic and post-Romantic traditions; they make up for this absence by borrowing the violin sonatas of Gabriel Fauré (1845-1924) and Franck. The flute and piano works of Mel Bonis help to fill this void with music composed originally for flute. Bonis was a prolific composer with over 300 works to her credit, but her works for flute and piano have not been researched or professionally recorded in the United States before the present study. Although virtually unknown today in the American flute community, Bonis's music received much acclaim from her contemporaries and deserves a prominent place in the flutist's repertoire. After a brief biographical introduction, this document examines Mel Bonis's musical style and describes in detail her six works for flute and piano while also offering performance suggestions.
ContributorsDaum, Jenna Elyse (Author) / Buck, Elizabeth (Thesis advisor) / Holbrook, Amy (Committee member) / Micklich, Albie (Committee member) / Schuring, Martin (Committee member) / Norton, Kay (Committee member) / Arizona State University (Publisher)
Created2013
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Description
Mitochondria produce most of the ATP needed for the cell as an energy source. It is well known that cellular respiration results in oxidative damage to the cell due to the production of reactive oxygen species (ROS). Mitochondrial dysfunction is believed to contribute to a number of degenerative diseases; because

Mitochondria produce most of the ATP needed for the cell as an energy source. It is well known that cellular respiration results in oxidative damage to the cell due to the production of reactive oxygen species (ROS). Mitochondrial dysfunction is believed to contribute to a number of degenerative diseases; because of this the mitochondrial respiratory chain is considered as potential drug target. A few series of idebenone analogues with quinone, pyridinol and pyrimidinol redox cores have been synthesized and evaluated as antioxidants able to protect cellular integrity and, more specifically, mitochondrial function. The compounds exhibited a range of activities. The activities observed were used for the design of analogues with enhanced properties as antioxidants. Compounds were identified which provide better protection against oxidative stress than idebenone, and it is thought that they do so catalytically.
ContributorsArce Amezquita, Pablo M (Author) / Hecht, Sidney M. (Thesis advisor) / Moore, Ana (Committee member) / Rose, Seth (Committee member) / Arizona State University (Publisher)
Created2012
ContributorsMatthews, Eyona (Performer) / Yoo, Katie Jihye (Performer) / Roubison, Ryan (Performer) / ASU Library. Music Library (Publisher)
Created2018-03-25
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Description
Reactive oxygen species (ROS) are a series of molecules, ions, and radicals derived from oxygen that possess remarkable reactivity. They act as signaling molecules when their concentration in cells is within a normal range. When the levels of ROS increase, reaching a concentration in which the antioxidants cannot readily quench

Reactive oxygen species (ROS) are a series of molecules, ions, and radicals derived from oxygen that possess remarkable reactivity. They act as signaling molecules when their concentration in cells is within a normal range. When the levels of ROS increase, reaching a concentration in which the antioxidants cannot readily quench them, oxidative stress will affect the cells. These excessive levels of ROS result in direct or indirect ROS-mediated damage of proteins, nucleic acids, and lipids. Excessive oxidative stress, particularly in chronic inflammation, has been linked with mutations and carcinogenesis. One of the main targets of ROS in severe oxidative stress is mitochondrial DNA (mtDNA). The synthesis of analogues of alpha-tocopherol is described as potential compounds with the ability to remediate defective mitochondria. An interesting possibility for eradicating cancer cells is to selectively target them with oxidative species while avoiding any deleterious effects on healthy cells. To accomplish this, analogues of the beta-hydroxyhistidine moiety of the antitumor agent bleomycin (BLM) were synthesized. The first part of this thesis focuses on the synthesis of simplified analogues of alpha-tocopherol. These analogues possess a bicyclic pyridinol as the antioxidant core and an alkyl group as the lipophilic chain to mimic alpha-tocopherol. Additionally, analogues with a completely oxidized pyridinol core were synthesized. Some of these analogues showed promising properties against ROS production and lipid peroxidation. The protection they conferred was shown to be tightly regulated by their concentration. The second part of this thesis focuses on the synthesis of analogues of beta-hydroxyhistidine. BLMs are glycopeptides that possess anticancer activity and have been used to treat testicular carcinomas, Hodgkin's lymphoma, and squamous cell carcinomas. The activity of BLM is based on the degradation of DNA, or possibly RNA, caused by a Fe(II)-BLM complex in the presence of O2. The beta-hydroxyhistidine moiety of BLM contributes to metal coordination via two ligands: the N-3 nitrogen atom of imidazole and possibly the nitrogen atom of the amide. A series of beta-hydroxyhistidine analogues has successfully been synthesized.
ContributorsArmendáriz Guajardo, José Israel (Author) / Hecht, Sidney M. (Thesis advisor) / Moore, Ana (Committee member) / Gould, Ian (Committee member) / Arizona State University (Publisher)
Created2014
ContributorsHoeckley, Stephanie (Performer) / Lee, Juhyun (Performer) / ASU Library. Music Library (Publisher)
Created2018-03-24
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Description
Mitochondria are crucial intracellular organelles which play a pivotal role in providing energy to living organisms in the form of adenosine triphosphate (ATP). The mitochondrial electron transport chain (ETC) coupled with oxidative phosphorylation (OX-PHOS) transforms the chemical energy of amino acids, fatty acids and sugars to ATP. The mitochondrial electron

Mitochondria are crucial intracellular organelles which play a pivotal role in providing energy to living organisms in the form of adenosine triphosphate (ATP). The mitochondrial electron transport chain (ETC) coupled with oxidative phosphorylation (OX-PHOS) transforms the chemical energy of amino acids, fatty acids and sugars to ATP. The mitochondrial electron transport system consumes nearly 90% of the oxygen used by the cell. Reactive oxygen species (ROS) in the form of superoxide anions (O2*-) are generated as byproduct of cellular metabolism due to leakage of electrons from complex I and complex III to oxygen. Under normal conditions, the effects of ROS are offset by a variety of antioxidants (enzymatic and non-enzymatic).

Mitochondrial dysfunction has been proposed in the etiology of various pathologies, including cardiovascular and neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease, ischemia-reperfusion (IR) injury, diabetes and aging. To treat these disorders, it is imperative to target mitochondria, especially the electron transport chain. One of the methodologies currently used for the treatment of mitochondrial and neurodegenerative diseases where endogenous antioxidant defenses are inadequate for protecting against ROS involves the administration of exogenous antioxidants.

As part of our pursuit of effective neuroprotective drugs, a series of pyridinol and pyrimidinol analogues have been rationally designed and synthesized. All the analogues were evaluated for their ability to quench lipid peroxidation and reactive oxygen species (ROS), and preserve mitochondrial membrane potential (Δm) and support ATP synthesis. These studies are summarized in Chapter 2.

Drug discovery and lead identification can be reinforced by assessing the metabolic fate of orally administered drugs using simple microsomal incubation experiments. Accordingly, in vitro microsomal studies were designed and carried out using bovine liver microsomes to screen available pyridinol and pyrimidinol analogues for their metabolic lability. The data obtained was utilized for an initial assessment of potential bioavailability of the compounds screened and is summarized fully in Chapter 3.
ContributorsAlam, Mohammad Parvez (Author) / Hecht, Sidney M. (Thesis advisor) / Gould, Ian R (Committee member) / Moore, Ana (Committee member) / Arizona State University (Publisher)
Created2014
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Description
Birds have plasma glucose levels that are 1.5-2 times greater than mammals of similar body mass in addition to higher free fatty acid concentrations, both of which would typically impair endothelium-dependent vasodilation if observed in mammals. Endothelium-dependent vasodilation can be stimulated in mammals through the use of acetylcholine (ACh), which

Birds have plasma glucose levels that are 1.5-2 times greater than mammals of similar body mass in addition to higher free fatty acid concentrations, both of which would typically impair endothelium-dependent vasodilation if observed in mammals. Endothelium-dependent vasodilation can be stimulated in mammals through the use of acetylcholine (ACh), which primarily acts through nitric oxide (NO) and cyclooxygenase (COX)-mediated pathways, with varying reliance on endothelial-derived hyperpolarizing factors (EDHFs). Very few studies have been conducted on small resistance systemic arteries from birds. The hypothesis was that because birds have naturally high glucose and free fatty acid concentrations, ACh-induced vasodilation of isolated arteries from mourning doves (Zenaida macroura) would be independent of endothelial-derived factors and resistant to high glucose-mediated vascular dysfunction. Small resistance mesenteric and cranial tibial (c. tibial) arteries were pre-constricted to 50% of resting inner diameter with phenyleprine then exposed to increasing doses of ACh (10-9 to 10-5 μM) or the NO donor, sodium nitroprusside (SNP; 10-12 to 10-3 μM). For both vessel beds, ACh-induced vasodilation occurred mainly through the activation of potassium channels, whereas vasodilation of mesenteric arteries additionally occurred through COX. Although arteries from both vessel beds fully dilated with exposure to sodium nitroprusside, ACh-mediated vasodilation was independent of NO. To examine the effect of high glucose on endothelium-dependent vasodilation, ACh dose response curves were conducted following exposure of isolated c. tibial arteries to either a control solution (20mM glucose) or high glucose (30mM). ACh-induced vasodilation was significantly impaired (p = 0.013) when exposed to high glucose, but normalized in subsequent vessels with pre-exposure to the superoxide dismutase mimetic tiron (10 mM). Superoxide concentrations were likewise significantly increased (p = 0.0072) following exposure to high glucose. These findings indicate that dove arteries do not appear to have endogenous mechanisms to counteract the deleterious effects of oxidative stress. Additional studies are required to assess whether endogenous mechanisms exist to protect avian vascular reactivity from systemic hyperglycemia.
ContributorsJarrett, Catherine Lee (Author) / Sweazea, Karen L (Thesis advisor) / Johnston, Carol (Committee member) / Gaesser, Glenn (Committee member) / Arizona State University (Publisher)
Created2012
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Description
It has been well established that mitochondria play a critical role in the pathology of Friedreich's Ataxia. This disease is believed to be caused by a deficiency of frataxin, which research suggests is responsible for iron sulfur cluster assembly. This incomplete assembly of iron sulfur clusters is believed to be

It has been well established that mitochondria play a critical role in the pathology of Friedreich's Ataxia. This disease is believed to be caused by a deficiency of frataxin, which research suggests is responsible for iron sulfur cluster assembly. This incomplete assembly of iron sulfur clusters is believed to be linked with dysfunctional complexes in the mitochondrial respiratory chain, increased oxidative stress, and potential cell death. Increased understanding of the pathophysiology of this disease has enabled the development of various therapeutic strategies aimed at restoring mitochondrial respiration. This thesis contains an analysis of the biological activity of several classes of antioxidants against oxidative stress induced by diethyl maleate in Friedreich's Ataxia lymphocytes and CEM leukemia cells. Analogues of vitamin E α-tocopherol have been shown to protect cells under oxidative stress. However, these same analogues show various levels of inhibition towards the electron transport chain complex I. Bicyclic pyridinols containing a ten carbon substituent provided favorable cytoprotection. N-hydroxy-4-pyridone compounds were observed to provide little protection. Similarly, analogues of CoQ10 in the form of pyridinol and pyrimidinol compounds also preserved cell viability at low concentrations.
ContributorsJaruvangsanti, Jennifer (Author) / Hecht, Sidney (Thesis advisor) / Woodbury, Neal (Committee member) / Skibo, Edward (Committee member) / Arizona State University (Publisher)
Created2012
ContributorsMcClain, Katelyn (Performer) / Buringrud, Deanna (Contributor) / Lee, Juhyun (Performer) / ASU Library. Music Library (Publisher)
Created2018-03-31