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

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    The Challenge of Teen Nutrition: An Ecological View of Sociocognitive Influences on Urban, African-American Adolescent Diet Quality
    (2010) Wrobleski, Margaret Mary; Atkinson, Nancy L.; Public and Community Health; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)
    The routine food choices that adolescents make impact their nutritional status, health, and their risk of developing chronic illnesses such as heart disease, cancer, and osteoporosis in the future. Nutrient requirements during adolescence are comparable to those in early infancy, emphasizing the importance of a high quality diet for healthy growth and development. A myriad of personal, social, and environmental factors influence adolescents in shaping their dietary intake and quality of diet. Low-income, African-American adolescents in Baltimore were identified as having sub-optimal nutritional intake compared to national dietary recommendations. This study explored the dynamic and relative contributions that factors within three environmental levels (personal, social, and community) made as predictors of diet quality in a sample of low-income, urban African-American adolescents using an integrated Social Cognitive Theory (SCT) / ecological theoretical framework. It was hypothesized that 1) the personal, social, and community environmental levels of dietary influences would all significantly contribute to diet quality, with community environment making the largest relative contribution; 2) self-efficacy for healthy eating moderated the relationship between parental beliefs about nutrition and diet quality; and 3) self-efficacy for healthy eating moderated the relationship between peer eating behaviors and diet quality. There have been very few studies using an integrated SCT/ecological model to explore the dietary influences on adolescent nutrition, especially on this demographic. The significant influence the SCT construct of observational learning has on adolescents was evidenced in this study by the positive relationship found between diet quality, parental beliefs about nutrition, and peer eating behavior. Younger participants in early adolescence and females were predominately guided by their parents' beliefs about nutrition, while males in this study appeared to identify more with their peers' nutrition-related behaviors. This study revealed that parents and peers play important roles in African-American adolescents' food choices and subsequent diet quality. Nutrition interventions should focus on parent-teen interactions and on improving the dietary habits of parents so they may be more effective role models for youth. Nutrition promotion research targeting young African-American men may consider using group interactive behavioral interventions with peers that build and reinforce peer modeling of positive nutrition behaviors.
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    IS THE CURRENT DEFINITION OF THE METABOLIC SYNDROME A USEFUL TOOL FOR THE DETECTION OF CARDIOVASCULAR DISEASE IN NON-HISPANIC BLACKS?
    (2010) Rodriguez, Omayra Isabel; Song, Jiuzhou; Nutrition; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)
    Blacks in the country suffer from higher prevalences of obesity, diabetes, hypertension and cardiovascular disease compared to whites. Paradoxically, they have the lowest prevalence of the Metabolic Syndrome (MS) compared to whites and Mexican Americans. This is likely due to the fact that blacks tend to have lower triglycerides (TG) and higher high density cholesterol (HDL) levels. We challenged the current lipid criteria established by the Adult Treatment Panel III for the detection of the MS and set out to find more appropriate TG and HDL cutoffs to detect the MS in blacks. Using data from the National Health and Nutrition Examination Survey from 1999-2006, we identified that a more appropriate TG cutoff for blacks to detect the MS is 110 mg/dL but were not able to identify more suitable HDL cutoffs. Our results confirm that race/ethnic-specific criteria should be established for the detection of the MS across racial/ethnic groups.
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    Assessment of Metabolic Syndrome in a sample of Central and South Americans living in the Washington, D.C. area
    (2010) Gill, Regina Marie; Jackson, Robert T.; Nutrition; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)
    The Central/South American population is growing rapidly in the U.S., but little is known about the health status. The purpose of this study was 1) to estimate the prevalence of MS and its individual components, 2) compare risk factors among Hispanic sub-groups, and 3) examine how metabolic syndrome (MS) prevalence estimates have changed from 1993–1994 to 2008–2009 in a sample of Central/South Americans living in the D.C. area. In this cross-sectional, medical record extraction survey, data from 1993–1994 were compared with data from 2008–2009 on 1,042 male and female adults collected by questionnaire. 28% of our subjects had MS. The most prevalent MS components were low HDL (43.2% men; 50.7% women), elevated triglycerides (37%), and high BMI ≥ 25 kg/m2 (75.6%). Among Central/South Americans, Salvadorans had the highest prevalence of MS (30.7%). MS prevalence was significantly greater for the 2008–2009 subjects (27.9%) compared with 1993–1994 subjects (19.7%) (p ≤ 0.05).
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    HYPERLEPTINEMIA, METABOLIC SYNDROME, AND MORTALITY IN OLDER ADULTS
    (2010) Mishra, Suruchi; Sahyoun, Nadine R; Mehta, Mira; Nutrition; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)
    Background: Abdominal adiposity and fat mass increase with aging, and as does insulin resistance which is frequently associated with hyperleptinemia and leptin resistance. Serum leptin may predict risk of metabolic syndrome and mortality among older adults. Objectives: The objectives of the present study were to evaluate the relationship of serum leptin with risk of metabolic syndrome and mortality and to examine these associations in relation to the measures of body adiposity and proinflammatory cytokines. The influence of leptin receptor (I/D) gene polymorphism on diabetes as a contributing cause of mortality was also examined. Gender specific serum leptin cut off values as a biomarker for the risk of metabolic syndrome were determined. Design: The Health, Aging and Body Composition (HABC) study is a prospective cohort of 3,075 older adults aged 70 to 79 years. Body composition, demographic information, biochemical variables including, markers of systemic inflammation, and genetic variation were assessed in detail. Results: Women in quintile 2, 3, 4 and 5 of serum leptin were at significantly lower risk for metabolic syndrome as compared to those in quintile 1 after controlling for confounders. Serum leptin was independently associated with risk of metabolic syndrome after sequentially adjusting for demographic variables (p<0.0001), fat depots (p=.0024), and proinflammatory cytokines (p=.0098) in women. Among men, the association between serum leptin and risk of metabolic syndrome was explained by body adiposity. Women in quartile 2 and 3 of serum leptin were at lower risk than women in quintile 1 for all-cause mortality and mortality from cardiovascular disease independent of body fat and proinflammatory cytokines. Additionally, elevated level of serum leptin was associated with increased risk for diabetes as a contributing cause of mortality for both genders after sequentially adjusting for potential confounders, body fat and proinflammatory cytokines. Significant interaction was found between leptin receptor genotype and total percent fat (p=0.008) in association with diabetes as a contributing cause of mortality among women. The cut off serum leptin level that suggests the possible risk of metabolic syndrome was determined to be 6.45 ng/ml with 60% sensitivity and 63% specificity among men and 18.25 ng/ml with 55% sensitivity and 62% specificity among women. Conclusion: Elevated levels of serum leptin may be associated with increased risk of metabolic syndrome and risk of diabetes as a contributing cause of mortality among older women. However, intermediary levels of serum leptin may lower the risk of all-cause mortality and mortality from CVD, suggesting a paradoxical association of serum leptin with cardiovascular risk factors and mortality from CVD among older women
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    HOW SELENIUM MODIFIES CROSS-TALK BETWEEN THE PIKK FAMILY AND INSIGHTS ON THE REGULATION OF DNA-PKcs
    (2009) Rocourt, Caroline; Cheng, Wen-Hsing; Nutrition; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)
    We recently found that ATM is required for a selenium-induced senescence response in non-cancerous cells. We hypothesize the selenium-induced DNA damage response modifies ATM and DNA-PKcs cross-talk. Phospho-specific antibodies against ATM and DNA-PKcs were used to follow the phosphorylation events after selenium treatment in normal human cells and two human cancer cell lines. Results from immunofluorescence analysis showed that selenium treatment induces hyperphosphorylation of DNA-PKcs at T2647 and S2056 in non-cancerous MRC-5 cells but not in U-2 OS cancer cells. Further studies in MRC-5 cells treated with an ATM kinase inhibitor, KU 55933, showed attenuation of the selenium-induced DNA-PKcs phosphorylation at both foci, whereas pre-treatment with a DNA-PKcs kinase inhibitor, NU 7026, does not prevent ATM phosphorylation at S1981, an event leading to ATM pathway activation. These results give evidence that DNA-PKcs and ATM have a cooperative role in the DNA damage response pathway.
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    High Sucrose, Fructose, and Glucose Diets and Glucocorticoid Dysregulation in Rats
    (2009) London, Edra; Castonguay, Thomas W; Nutrition; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)
    Approximately two-thirds of U.S. adults are overweight or obese and the prevalence of overweight in children has tripled since 1980. Intake of added sugars has also increased. The etiology of obesity remains unclear and the role of glucocorticoids in obesity is one area of ambiguity. The enzyme 11beta-hydroxysteroid dehydrogenase-1 (11beta-HSD-1) interconverts active and inactive glucocorticoid, thereby regulating intracellular glucocorticoids. Dysregulation of 11beta-HSD-1 in liver and adipose is characteristic of human and animal models of obesity. Hexose-6-phosphate dehydrogenase (H6PDH) is colocalized with 11beta-HSD-1 and determines the set point for 11beta-HSD-1 oxidoreductase activity. In a long-term (10 wk) study, rats given ad libitum access to 16% sucrose solution, chow, and water were fatter than controls, had increased 11beta-HSD-1 mRNA in adipose, suppressed 11beta-HSD-1 mRNA in liver, and increased H6PDH mRNA in both tissues. The primary research questions were as follows: Can high sugar diets induce glucocorticoid dysregulation in the absence of excess adiposity? Does sugar type matter? Energy intake, weight gain, and parameters of lipid and carbohydrate metabolism were measured. Rats were randomly assigned to either ad libitum access to chow and water only (control), or in addition to ad libitum access to either 16% sucrose, fructose, or glucose solution (n=16/gp). After 24h and 1 wk, eight rats per group were randomly selected for sacrifice. Daily caloric intakes among sugar-fed groups did not differ and were higher than the mean intake of the control group. Within 24h, fructose induced increased 11beta-HSD-1 message in mesenteric adipose and liver. Plasma TG and insulin were acutely increased in groups with fructose-containing diets only. All high sugar diets induced suppressed hepatic 11beta-HSD-1 mRNA and protein after 1 wk. Upregulation of H6PDH mRNA observed in response to long-term high sucrose diets may result from increased adiposity and not solely diet. High sugar diets, irrespective of sugar type, initiate glucocorticoid dysregulation in the absence of phenotypic changes associated with obesity. Sucrose, fructose, and glucose have distinct metabolic and endocrine responses. Fructose has the unique ability to induce glucocorticoid dysregulation in liver and adipose in 24h.
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    Appropriate Waist Circumference Cutoff Values for the Diagnosis of Metabolic Syndrome in Mexican American Adults
    (2009) Sarafrazi, Neda; Jackson, Robert T; Nutrition; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)
    Metabolic syndrome increases the risk of cardiovascular disease and diabetes. The International Diabetes Federation (IDF) recently proposed new criteria for the diagnosis of metabolic syndrome, which requires the presence of central obesity as measured by ethnic specific waist circumference (WC) cutoff values. Currently, no specific WC thresholds for diagnosis of central obesity in Hispanics are available. The objectives were to determine the appropriate gender specific WC thresholds for diagnosis of central obesity in Mexican American adults and to estimate the prevalence of metabolic syndrome using IDF definition with and without the modified WC in this population. Data from 3265 Mexican American adults aged 20-80 years who participated in the National Health and Nutrition Examination Survey 1999-2006 were used. The prevalence of metabolic syndrome was compared using IDF criteria with and without the modified waist circumference. Receiver operating characteristic curve analysis suggested that yielding at least 80% sensitivity, the WC value of 90 cm in both genders was more appropriate in predicting the presence of two or more metabolic syndrome risk factors in this population. Based on this cutoff, there was 34% reduction in the prevalence of central obesity in women (82.5% to 54.2%). The age adjusted prevalence of metabolic syndrome decreased from 58.4 to 48.2%. The metabolic syndrome was more common among Mexican American men than women (55.8% in men versus 37.8% in women, P =0.0003). Our findings provided a practical guidance in the assessment and screening of central obesity and metabolic syndrome in Mexican Americans.
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    THE FUNCTION OF MRN (MRE11-RAD50-NBS1) COMPLEX DURING WRN (WERNER) FACILITATED ATM (ATAXIA-TELANGIECTASIA MUTATED) ACTIVATION
    (2009) Ma, Junhao; Cheng, Wen-Hsing; Nutrition; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)
    WRN (Werner) protein is a member of the RecQ family showing helicase and exonuclease activity. WRN protein may lose function upon mutation and causes Werner syndrome (WS) which is an autosomal recessive, cancer-prone and premature aging disease. ATM (Ataxia-Telangiectasia mutated) protein initiates a signaling pathway in response to DNA double strand breaks (DSBs). Genomic disorder ataxia-telangiectasia (A-T) is associated with defective ATM. WRN protein is involved in ATM pathway activation when cells are exposed to DSBs associated with replication fork collapse. Because the Mre11-Rad50-Nbs1 (MRN) complex, a sensor of DSBs, is known to interact with WRN and ATM, we investigated whether the MRN complex mediates the WRN-dependent ATM pathway activation. In this study, we employed short-hairpin RNA to generate WRN- and Nbs1-deficient U-2 OS (osteosarcoma) cells. Cells were treated with clastogens which induce collapsed replication forks, thus provided proof for whether WRN facilitates ATM activation via MRN complex. This study serves as a basis for future investigation on the correlation between ATM, MRN complex and WRN, which will ultimately help understand the mechanism of aging and cancer.
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    Depression and Hardiness and their Association with Appetite in Older Adults
    (2009) Engel, Julia; Sahyoun, Nadine; Nutrition; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)
    Poor appetite is common among older adults, and is influenced by factors including chronic disease and depression. The aim of this research is to examine the associations of hardiness (defined as the ability to manage stress), depression, and emotional well-being with appetite in older adults. A survey evaluating hardiness, depression and appetite was administered to 292 adults (60 years and older), at assisted-living facilities or senior centers in the Washington D.C. area. In univariate models, depression, hardiness, and emotional well-being are associated with appetite. In multivariate models, fair/poor emotional well-being increases risk for poor appetite (OR=5.60, 95% CI= 2.60-12.07) and commitment (a dimension of hardiness - which indicates an individual's involvement in life) is associated with appetite (OR=1.35, 95% CI= 1.13-1.61). These variables maintained the strongest associations with appetite in multivariate models. These associations further elucidate the components of mental health which contribute to poor appetite in this population.
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    The effect of trifolirhizin and resveratrol on human prostate cells
    (2008-11-21) Zhang, Junjun; Lei, David K. Y.; Nutrition; Digital Repository at the University of Maryland; University of Maryland (College Park, Md.)
    Trifolirhizin is a potent polycyclic flavonoid with anticarcinogenic effects. The treatment of 25 μM trifolirhizin in human derived prostate cancer LNCaP cells for 6 days decreased cell proliferation by 40%. Higher dosages caused the proliferation inhibition effect to be manifested in as early as 3 days. Another prostate cancer cell line, PC-3, was not affected by trifolirhizin till 125 μM resulting in about 45 % reduction in cell proliferation after 4 to 6 days of incubation. Most importantly, for normal human prostate epithelial (NHPrE) cells, trifolirhizin was effective only at the highest concentration of 200 µM. The proliferation inhibition in trifolirhizin-treated LNCaP and PC-3 cells was associated with cell cycle arrest at the G0/G1 and G2/M phase, respectively. Moreover, the expression of cyclin E was unchanged but that of cyclin D1, p53, p21 and p-Rb was suppressed in 50 μM trifolirhizin-treated LNCaP cells. To evaluate the influence of resveratrol on cellular zinc status, NHPrE cells were treated with 6 levels of resveratrol (0, 0.5, 1, 2.5, 5 and 10 μM) and 4 levels of zinc [0, 4, 16 and 32 μM representing zinc deficient (ZD), zinc normal (ZN), zinc adequate (ZA) and zinc supplemented (ZS), respectively]. Among each zinc treatment, a progressive reduction in cell growth or increase in cellular total zinc was observed with increases of resveratrol from 2.5, 5 and 10 μM or from 5 and 10 μM, respectively. In ZS cells a much higher increase in cellular total zinc was observed as early as 1 μM resveratrol. The resveratrol (10 μM) induced G2/M arrest was found to be responsible for the depressed cell proliferation. An in vitro experiment demonstrated complex formation between resveratrol and zinc ion. Fluorescent spectrofluorimetry and microscope imaging revealed that intracellular free labile zinc decreased in resveratrol-treated ZD and ZN NHPrE cells but increased in high zinc (ZA and ZS) cells. Furthermore, increases in cellular zinc status induced reactive oxygen species (ROS) generation as well as senescence in cells treated with 2.5 or 10 μM resveratrol, especially in ZA and ZS cells. Thus, increase in free labile zinc may induce ROS and senescence.