Theses and Dissertations from UMD
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New submissions to the thesis/dissertation collections are added automatically as they are received from the Graduate School. Currently, the Graduate School deposits all theses and dissertations from a given semester after the official graduation date. This means that there may be up to a 4 month delay in the appearance of a give thesis/dissertation in DRUM
More information is available at Theses and Dissertations at University of Maryland Libraries.
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Item INVESTIGATING COMPOSTING AS A METHOD FOR REDUCING ESTROGENICTY IN POULTRY LITTER AND BIOSOLIDS(2015) Hammett, Kirsten; Yonkos, Lance; Environmental Science and Technology; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)Biosolids and poultry litter contain the natural estrogens 17β-estradiol and estrone, which can be transported to receiving waters via runoff when these materials are used as fertilizers. Estrogens are of concern because of their ability to act as endocrine disruptors and feminize fish. In this study, In-Vessel Aerated and Turned composting was investigated for its efficacy at mitigating estrogen concerns in BS and PL. Pre- and post- composted, BS and PL samples were investigated for total estrogenicity and estrogen species concentrations. In addition, conversion of estrone to 17β-estradiol was investigated by measuring the creation of deuterated 17β-estradiol from a deuterium-labeled estrone stock within aqueous PL mixtures. Data from these studies indicates that there may be efficacy in composting BS and PL prior to land application and suggest that estrone is capable of converting to the more potent 17β-estradiol species as a result of entering microbially active environments.Item EFFICACY OF ESTROGEN TREATMENT IN A MURINE MODEL OF ALZHEIMER'S DISEASE(2012) Schlappal, Anna Elise; Ottinger, Mary Ann; Neuroscience and Cognitive Science; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)Clinically, Alzheimer's Disease (AD) presents with cognitive dysfunction, cell death, and amyloid-beta (AB) plaque and neurofibrillary tangle (NFT) formation. Moreover, age and gender are primary risk factors; women are at much higher risk for developing AD compared to men. Estrogens may be neuroprotective; however, clinical use in hormone replacement therapy (HRT) is controversial due to potential adverse effects. Experiments were conducted using the APPswe/PS1dE9 (DTG) and APPswe/PS1M146V/TauP301L (3xTgAD) transgenic mouse models to assess the efficacy of an estrogen pro-drug, estradiol-quinol (E2Q). Treatment groups consisted of vehicle, estradiol (E2), or E2Q in intact and ovariectomized (OVX) DTG females, intact DTG males, and intact 3xTgAD females and males. The objectives of this study were to 1) characterize AD progression in a double transgenic (DTG) murine model and compare the efficacy of treatment with estradiol (E2) or E2Q in ovariectomized (OVX) and intact females, 2) compare the effects of E2Q in males, 3) determine if E2Q affects neurodegenerative disease progression in the triple transgenic (3xTgAD) murine model in both males and females, and 4) assess the effects of the neurodegenerative disease progression on mitochondrial function and determine if E2Q affects these endpoints. E2Q did not stimulate uterine tissue and proved to be an effective intervention; treated DTG mice had better cognitive behavior, decreased amyloid precursor protein (APP), and amyloid beta (AB) protein levels. Taken together, these data suggest that E2Q has potential as a therapeutic for AD patients.Item Estrogen and Progesterone enhance Neisseria gonorrhoeae Transmigration across a Polarized Monolayer via a Mechanism that Hijacks EGFR(2012) Edwards, Vonetta Lisa; Song, Wenxia; Cell Biology & Molecular Genetics; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)Gonorrhea, a common sexually transmitted infection, is caused by the gram-negative bacterium Neisseria gonorrhoeae. In the female reproductive tract, gonococci (GC) initiate infection at the apical surface of columnar endocervical epithelial cells. These cells provide a physical barrier against mucosal pathogens by forming continuous apical junctional complexes between neighboring cells. This study examines the interaction of GC with polarized epithelial cells. We show that viable, but not gentamicin killed, GC preferentially localize at the apical side of the cell-cell junction in polarized endometrial and colonic epithelial cells, HEC-1-B and T84, respectively. In GC infected epithelial cells, continuous apical junctional complexes are disrupted, and the junction-associated protein β-catenin is redistributed from the apical junction to the cytoplasm and to GC adherent sites. However, GC inoculation does not change the overall cellular level of junctional proteins. This redistribution of junctional proteins is associated with a decrease in the apical junction's barrier function against the lateral movement between the apical and basolateral membranes, but not against the permeability through the paracellular space. Disruption of the apical junction by removing calcium increases GC transmigration across the epithelial monolayer. GC inoculation induces the phosphorylation of both epidermal growth factor receptor (EGFR) and β-catenin, while inhibition of EGFR kinase significantly reduces both GC-induced β-catenin redistribution and GC transmigration. These results suggest a relationship between junction protein redistribution from the plasma membrane with the resultant weakening of the junctional complex, and an increase in the ability of GC to transmigrate. The presence of the female sex hormones estrogen and progesterone, lead to an increased degree of disruption of the junctional complex and enhance GC transmigration across the monolayer. Therefore, GC are capable of weakening the apical junction and the polarity of epithelial cells via activating EGFR, which facilitates GC transmigration across the epithelium.