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Description
Objectives
This cross-sectional study sought to assess the eating and physical activity behaviors among in-state and out-of-state college freshmen attending Arizona State University and to determine if social connectedness mediated the relationship between residency status and eating and physical activity behaviors.
Methods
College freshmen from two dormitories were recruited for participation from Arizona State University’s Tempe campus. A 128-item survey assessing demographics, college life, eating and physical activity behaviors, and social connectedness was administered. In addition, participants completed up to three days of dietary recall. Multivariate linear regression models, adjusting for age, gender, race, ethnicity, highest parental education, dormitory, Pell grant status, number of dietary recalls, and availability of a weekend day of dietary recall were used to assess the relationships between residency status, social connectedness, and eating and physical activity behaviors.
Results
No associations were observed between residency status and calories, grams and percentage of calories from fat, and added sugar. There was a statistically significant association between residency status and moderate-to-vigorous physical activity (MVPA). In-state students reported 21 minutes less per day of MVPA than out-of-state students did (β=-20.85; 95% CI=-30.68, -11.02; p<0.001). There was no relationship between residency status and social connectedness. Social connectedness and eating and physical activity behaviors were not associated. Social connectedness did not mediate the relationship between residency status and eating and physical activity behaviors.
Conclusions
In-state and out-of-state students differed in their MVPA; however, this relationship was not mediated by social connectedness. Further studies are needed to confirm the relationship between MVPA and residency status. In addition, more studies are needed to assess the relationship between social connectedness and MVPA.
This cross-sectional study sought to assess the eating and physical activity behaviors among in-state and out-of-state college freshmen attending Arizona State University and to determine if social connectedness mediated the relationship between residency status and eating and physical activity behaviors.
Methods
College freshmen from two dormitories were recruited for participation from Arizona State University’s Tempe campus. A 128-item survey assessing demographics, college life, eating and physical activity behaviors, and social connectedness was administered. In addition, participants completed up to three days of dietary recall. Multivariate linear regression models, adjusting for age, gender, race, ethnicity, highest parental education, dormitory, Pell grant status, number of dietary recalls, and availability of a weekend day of dietary recall were used to assess the relationships between residency status, social connectedness, and eating and physical activity behaviors.
Results
No associations were observed between residency status and calories, grams and percentage of calories from fat, and added sugar. There was a statistically significant association between residency status and moderate-to-vigorous physical activity (MVPA). In-state students reported 21 minutes less per day of MVPA than out-of-state students did (β=-20.85; 95% CI=-30.68, -11.02; p<0.001). There was no relationship between residency status and social connectedness. Social connectedness and eating and physical activity behaviors were not associated. Social connectedness did not mediate the relationship between residency status and eating and physical activity behaviors.
Conclusions
In-state and out-of-state students differed in their MVPA; however, this relationship was not mediated by social connectedness. Further studies are needed to confirm the relationship between MVPA and residency status. In addition, more studies are needed to assess the relationship between social connectedness and MVPA.
ContributorsNelson, Stephanie A. (Stephanie Anne), 1958- (Author) / Bruening, Meg (Thesis advisor) / Ohri-Vachaspati, Punam (Committee member) / Whisner, Corrie (Committee member) / Arizona State University (Publisher)
Created2016
Description
Background: Hispanic women are at high risk for Type 2 Diabetes (T2D), in part due to their high prevalence of obesity, which may influence the development of insulin resistance and disease onset. Unhealthy eating contributes to T2D risk. Dietary patterns are the combination of total foods and beverages among individual’s over time, but there is limited information regarding its role on T2D risk factors among Hispanic women. Objective: To identify a posteriori dietary patterns and their associations with diabetes risk factors (age, BMI, abdominal obesity, elevated fasting blood glucose, and hemoglobin A1c) among overweight/obese Hispanic women. Design: Cross-sectional dietary data were collected among 191 women with or at risk for T2D using the Southwestern Food Frequency Questionnaire capturing the prior three months of intake. Dietary patterns were derived using exploratory factor analysis. Regression scores were used to explore associations between dietary patterns and diabetes risk factors. Results: The patterns derived were: 1) “sugar and fat-laden”, with high loads of sweets, drinks, pastries, and fats; 2) “plant foods and fish”, with high loads of vegetables, fruits, fish, and beans; 3) “soups and starchy dishes”, with high loads of soups, starchy foods, and mixed dishes; 4) “meats and snacks”, with high loads of red meat, salty snacks, and condiments; 5) “beans and grains”, with high loads of beans and seeds, whole-wheat and refined grain foods, fish, and alcohol; and 6) “eggs and dairy”, with high loads of eggs, dairy, and fats. The “sugar and fat-laden” and “meats and snacks” patterns were negatively associated with age (r= -0.230, p= 0.001 and r= -0.298, p<0.001, respectively). Scores for “plant foods and fish” were associated with fasting blood glucose (r= 0.152, p= 0.037). There were no other statistically significant relationships between the dietary patterns and risk factors for T2D. Conclusions: A variety of patterns with healthy and unhealthy traits among Hispanic women were observed. Being younger may play an important role in adhering to a dietary pattern rich in sugary and high-fat foods and highlights the importance of assessing dietary patterns among young women to early identify dietary traits detrimental for their health.
ContributorsArias-Gastelum, Mayra (Author) / Vega-Lopez, Sonia (Thesis advisor) / Der Ananian, Cheryl (Committee member) / Whisner, Corrie (Committee member) / Bruening, Meg (Committee member) / Hooker, Steven (Committee member) / Arizona State University (Publisher)
Created2018
Description
According to a 2016 census, eight million adults conform to a vegetarian diet within the United States, and about 50% of these adults follow a vegan diet. The census determined that plant-based diets are quickly growing in popularity particularly in young adults between the ages of 18 to 34 years. Many Americans are aware of the health benefits of a plant-based diet, however, the dietary risks associated with these diets are not well emphasized. Health concerns such as vitamin deficiencies and altered metabolism are heightened in vegetarian populations.
One Particular nutrient that is commonly lacking in the vegetarian diet is vitamin B12. Vitamin B12 is found mainly in animal-derived food sources such as meat, poultry, fish, dairy, and eggs. Although some vegetarians, called lacto-ovo vegetarians, consume dairy and eggs, vegans do not consume any animal products at all. Vitamin B12 deficiency can have devastating consequences on the human body due to its role as a methylation cofactor. Metabolism, DNA replication, and cancer formation all involve methylation processes.
This cross-sectional, differential study aimed to further understand the relationship between vegetarianism, vitamin B12 status, and methylation capacity in healthy adults. A group of 34 healthy adults (18 vegetarians and 16 omnivores) was recruited to analyze serum B12, homocysteine, methylmalonic acid, serum total folate, and transcobalamin II status. It was hypothesized that (1) vegetarians would have a lower vitamin B12 status, and thus, a lower methylation capacity than omnivores and that (2) low vitamin B12 status would be correlated with low methylation capacity.
The data show that vegetarians did not have significantly lower vitamin B12 methylation capacity status than omnivores. Nor was vitamin B12 status correlated with methylation capacity. However, the data revealed that diet quality had a positive influence on folate status. There was also a statistical trend (p=0.08) for homocysteine reduction in participants consuming high-quality diets. The data herein suggest that methylation capacity may be impacted by the quality of diet rather than the type of diet.
One Particular nutrient that is commonly lacking in the vegetarian diet is vitamin B12. Vitamin B12 is found mainly in animal-derived food sources such as meat, poultry, fish, dairy, and eggs. Although some vegetarians, called lacto-ovo vegetarians, consume dairy and eggs, vegans do not consume any animal products at all. Vitamin B12 deficiency can have devastating consequences on the human body due to its role as a methylation cofactor. Metabolism, DNA replication, and cancer formation all involve methylation processes.
This cross-sectional, differential study aimed to further understand the relationship between vegetarianism, vitamin B12 status, and methylation capacity in healthy adults. A group of 34 healthy adults (18 vegetarians and 16 omnivores) was recruited to analyze serum B12, homocysteine, methylmalonic acid, serum total folate, and transcobalamin II status. It was hypothesized that (1) vegetarians would have a lower vitamin B12 status, and thus, a lower methylation capacity than omnivores and that (2) low vitamin B12 status would be correlated with low methylation capacity.
The data show that vegetarians did not have significantly lower vitamin B12 methylation capacity status than omnivores. Nor was vitamin B12 status correlated with methylation capacity. However, the data revealed that diet quality had a positive influence on folate status. There was also a statistical trend (p=0.08) for homocysteine reduction in participants consuming high-quality diets. The data herein suggest that methylation capacity may be impacted by the quality of diet rather than the type of diet.
ContributorsUgarte, Noel (Author) / Johnston, Carol S (Thesis advisor) / Whisner, Corrie (Committee member) / Sweazea, Karen (Committee member) / Arizona State University (Publisher)
Created2019
Description
The prevalence of obesity and obesity-related disorders have increased world-wide. In the last decade, the intestinal microbiome has become a major indicator of metabolic and gastrointestinal health. Previous research has shown that high-fat diet (HFD) consumption can alter the microbial composition of the gut by increasing the abundance of gram-positive bacteria associated with the onset of obesity and type 2 diabetes. Although, the most common form of obesity and metabolic syndrome intervention is exercise and diet, these recommendations may not improve severe cases of obesity. Thus, an important relevance of my project was to investigate whether the intake of an organometallic complex (OMC) would prevent the onset of metabolic and gastrointestinal complications associated with high-fat diet intake. I hypothesized that the consumption of a HFD for 6 weeks would promote the development of metabolic and gastrointestinal disease risk factors. Next, it was hypothesized that OMC treatment would decrease metabolic risk factors by improving insulin sensitivity and decreasing weight gain. Finally, I hypothesized that HFD-intake would increase the abundance of gram-positive bacteria associated with gastrointestinal disease. My preliminary data investigated the effects of a 6-week HFD on the development of hepatic steatosis, intestinal permeability and inflammation in male Sprague Dawley rats. I found that a 6-week HFD increases hepatic triglyceride concentrations, plasma endotoxins and promotes the production of pro-inflammatory cytokines in the cecum wall. I then investigated whether OMC treatment could prevent metabolic risk factors in male Sprague-Dawley rats fed a HFD for 10 weeks and found that OMC can mitigate risk factors such hyperglycemia, liver disease, impaired endothelial function, and inflammation. Lastly, I investigated the effects of a 10-week HFD on the gastrointestinal system and found an increase in liver triglycerides and free glycerol and alterations of the distal gut microbiome. My results support the hypothesis that a HFD can promote metabolic risk factors, alter the gut microbiome and increase systemic inflammation and that OMC treatment may help mitigate some of these effects. Together, these studies are among the first to demonstrate the effects of a soil-derived compound on metabolic complications. Additionally, these conclusions also provide an essential basis for future gastrointestinal and microbiome studies of OMC treatment.
ContributorsCrawford, Meli'sa Shaunte (Author) / Sweazea, Karen L (Thesis advisor) / Deviche, Pierre (Thesis advisor) / Al-Nakkash, Layla (Committee member) / Whisner, Corrie (Committee member) / Hyatt, Jon-Philippe (Committee member) / Arizona State University (Publisher)
Created2019
Description
Many developing countries do not have health care systems that can afford technological biomedical devices or supplies to make such devices operational. To fill this void, nonprofit organizations, like Project C.U.R.E., recondition retired biomedical instrumentation so they can send medical supplies to help these developing countries. One of the issues with this is that sometimes the devices are unusable because components or expendable supplies are not available (Bhadelia). This issue has also been shown in the Impact Evaluations that Project C.U.R.E. receives from the clinics that explain the reasons why certain devices are no longer in use. That need underlies the idea on which this honors thesis has come into being. The purpose of this honors project was to create packing lists for biomedical instruments that Project C.U.R.E. recycles. This packing list would decrease the likelihood of important items being forgotten when sending devices. If an extra fuse, battery, light bulb, cuff or transducer is the difference between a functional or a nonfunctional medical device, such a list would be of benefit to Project C.U.R.E and these developing countries. In order to make this packing list, manuals for each device were used to determine what supplies were required, what was necessary for cleaning, and what supplies were desirable but functionally optional. This list was then added into a database that could be easily navigated and could help when packing up boxes for a shipment. The database also makes adding and editing the packing list simple and easy so that as Project C.U.R.E. gets more donated devices the packing list can grow.
ContributorsGraft, Kelsey Anne (Author) / Coursen, Jerry (Thesis director) / Walters, Danielle (Committee member) / Harrington Bioengineering Program (Contributor) / Barrett, The Honors College (Contributor)
Created2018-05
Description
The Hippo signaling pathway is responsible for regulating organ size through cell proliferation, stemness, and apoptosis. Through targeting proteins Yes-associated kinase 1(YAP) and transcriptional co-activator with a PDZ-binding domain(TAZ), YAP/TAZ are unable to enter the nucleus and bind with coactivators to express target genes. To understand YAP/TAZ dynamics and its role in tumorigenesis, tissue regeneration, and tissue degeneration, a regulatory network was modeled by ordinary differential equations. Using MATLAB, the deterministic behavior of the network was observed to determine YAP/TAZ activity in different states. Performing the bifurcation analysis of the system through Oscill8, three states were identified: tumorigenic/regenerative, degenerative, and homeostatic states. Further analysis through parameter modification allowed a better understanding of which proteins can be targeted for cancer and degenerative disease.
ContributorsBarra Avila, Diego Rodrigo (Author) / Tian, Xiaojun (Thesis director) / Wang, Xiao (Committee member) / Harrington Bioengineering Program (Contributor, Contributor) / Barrett, The Honors College (Contributor)
Created2020-05
Description
Based on James Marcia's theory, identity development in youth is the degree to which one has explored and committed to a vocation [1], [2]. During the path to an engineering identity, students will experience a crisis, when one's values and choices are examined and reevaluated, and a commitment, when the outcome of the crisis leads the student to commit to becoming an engineer. During the crisis phase, students are offered a multitude of experiences to shape their values and choices to influence commitment to becoming an engineering student. Student's identities in engineering are fostered through mentoring from industry, alumni, and peer coaching [3], [4]; experiences that emphasize awareness of the importance of professional interactions [5]; and experiences that show creativity, collaboration, and communication as crucial components to engineering. Further strategies to increase students' persistence include support in their transition to becoming an engineering student, education about professional engineers and the workplace [6], and engagement in engineering activities beyond the classroom. Though these strategies are applied to all students, there are challenges students face in confronting their current identity and beliefs before they can understand their value to society and achieve personal satisfaction. To understand student's progression in developing their engineering identity, first year engineering students were surveyed at the beginning and end of their first semester. Students were asked to rate their level of agreement with 22 statements about their engineering experience. Data included 840 cases. Items with factor loading less than 0.6 suggesting no sufficient explanation were removed in successive factor analysis to identify the four factors. Factor analysis indicated that 60.69% of the total variance was explained by the successive factors. Survey questions were categorized into three factors: engineering identity as defined by sense of belonging and self-efficacy, doubts about becoming an engineer, and exploring engineering. Statements in exploring engineering indicated student awareness, interest and enjoyment within engineering. Students were asked to think about whether they spent time learning what engineers do and participating in engineering activities. Statements about doubts about engineering to engineering indicated whether students had formed opinions about their engineering experience and had understanding about their environment. Engineering identity required thought in belonging and self-efficacy. Belonging statements called for thought about one's opinion in the importance of being an engineer, the meaning of engineering, an attachment to engineering, and self-identification as an engineer. Statements about self-efficacy required students to contemplate their personal judgement of whether they would be able to succeed and their ability to become an engineer. Effort in engineering indicated student willingness to invest time and effort and their choices and effort in their engineering discipline.
ContributorsNguyen, Amanda (Author) / Ganesh, Tirupalavanam (Thesis director) / Robinson, Carrie (Committee member) / Harrington Bioengineering Program (Contributor) / Barrett, The Honors College (Contributor)
Created2018-05
Description
Alzheimer’s Disease (AD) affects over 5 million individuals in the U.S. and has a direct cost estimated in excess of $200 billion per year. Broadly speaking, there are two forms of AD—early-onset, familial AD (FAD) and late-onset-sporadic AD (SAD). Animal models of AD, which rely on the overexpression of FAD-related mutations, have provided important insights into the disease. However, these models do not display important disease-related pathologies and have been limited in their ability to model the complex genetics associated with SAD.
Advances in cellular reprogramming, have enabled the generation of in vitro disease models that can be used to dissect disease mechanisms and evaluate potential therapeutics. To that end, efforts by many groups, including the Brafman laboratory, to generated patient-specific hiPSCs have demonstrated the promise of studying AD in a simplified and accessible system. However, neurons generated from these hiPSCs have shown some, but not all, of the early molecular and cellular hallmarks associated with the disease. Additionally, phenotypes and pathological hallmarks associated with later stages of the human disease have not been observed with current hiPSC-based systems. Further, disease relevant phenotypes in neurons generated from SAD hiPSCs have been highly variable or largely absent. Finally, the reprogramming process erases phenotypes associated with cellular aging and, as a result, iPSC-derived neurons more closely resemble fetal brain rather than adult brain.
It is well-established that in vivo cells reside within a complex 3-D microenvironment that plays a significant role in regulating cell behavior. Signaling and other cellular functions, such as gene expression and differentiation potential, differ in 3-D cultures compared with 2-D substrates. Nonetheless, previous studies using AD hiPSCs have relied on 2-D neuronal culture models that do not reflect the 3-D complexity of native brain tissue, and therefore, are unable to replicate all aspects of AD pathogenesis. Further, the reprogramming process erases cellular aging phenotypes. To address these limitations, this project aimed to develop bioengineering methods for the generation of 3-D organoid-based cultures that mimic in vivo cortical tissue, and to generate an inducible gene repression system to recapitulate cellular aging hallmarks.
Advances in cellular reprogramming, have enabled the generation of in vitro disease models that can be used to dissect disease mechanisms and evaluate potential therapeutics. To that end, efforts by many groups, including the Brafman laboratory, to generated patient-specific hiPSCs have demonstrated the promise of studying AD in a simplified and accessible system. However, neurons generated from these hiPSCs have shown some, but not all, of the early molecular and cellular hallmarks associated with the disease. Additionally, phenotypes and pathological hallmarks associated with later stages of the human disease have not been observed with current hiPSC-based systems. Further, disease relevant phenotypes in neurons generated from SAD hiPSCs have been highly variable or largely absent. Finally, the reprogramming process erases phenotypes associated with cellular aging and, as a result, iPSC-derived neurons more closely resemble fetal brain rather than adult brain.
It is well-established that in vivo cells reside within a complex 3-D microenvironment that plays a significant role in regulating cell behavior. Signaling and other cellular functions, such as gene expression and differentiation potential, differ in 3-D cultures compared with 2-D substrates. Nonetheless, previous studies using AD hiPSCs have relied on 2-D neuronal culture models that do not reflect the 3-D complexity of native brain tissue, and therefore, are unable to replicate all aspects of AD pathogenesis. Further, the reprogramming process erases cellular aging phenotypes. To address these limitations, this project aimed to develop bioengineering methods for the generation of 3-D organoid-based cultures that mimic in vivo cortical tissue, and to generate an inducible gene repression system to recapitulate cellular aging hallmarks.
ContributorsBounds, Lexi Rose (Author) / Brafman, David (Thesis director) / Wang, Xiao (Committee member) / Harrington Bioengineering Program (Contributor) / Barrett, The Honors College (Contributor)
Created2018-05
Description
Osteoporosis is a medical condition that leads to decreased bone mineral density, resulting in increased fracture risk.1 Research regarding the relationship between sleep and bone mass is limited and has primarily been studied in elderly adults. While this population is most affected by osteoporosis, adolescents are the most proactive population in terms of prevention. The purpose of this study was to evaluate the relationship between sleep efficiency and serum osteocalcin in college-aged individuals as a means of osteoporosis prevention. Thirty participants ages 18-25 years (22 females, 8 males) at Arizona State University were involved in this cross-sectional study. Data were collected during one week via self-recorded sleep diaries, quantitative ActiWatch, DEXA imaging, and serum blood draws to measure the bone biomarker osteocalcin. Three participants were excluded from the study as outliers. The median (IQR) for osteocalcin measured by ELISA was 11.6 (9.7, 14.5) ng/mL. The average sleep efficiency measured by actigraphy was 88.3% ± 3.0%. Regression models of sleep efficiency and osteocalcin concentration were not statistically significant. While the addition of covariates helped explain more of the variation in serum osteocalcin concentration, the results remained insignificant. There was a trend between osteocalcin and age, suggesting that as age increases, osteocalcin decreases. This was a limited study, and further investigation regarding the relationship between sleep efficiency and osteocalcin is warranted.
ContributorsMarsh, Courtney Nicole (Author) / Whisner, Corrie (Thesis director) / Mahmood, Tara (Committee member) / School of International Letters and Cultures (Contributor) / School of Nutrition and Health Promotion (Contributor) / Barrett, The Honors College (Contributor)
Created2018-05
Description
The combination of immunohistochemical (IHC) stainings and optical microscopy has allowed for the visualization of specific microscopic structures within tissue; however, limitations in light and antibody penetration mitigate the scale on which these images can be taken (Alshammari et al, 2016; Marx, 2014). Tissue clearing, specifically the removal of lipids to improve sample transparency, solves the former weakness well, but does not improve antibody penetration significantly (Chung et al, 2013; Treweek et al, 2015). Therefore, there is a need to equalize the maximum depth that light can pass through a section with the depth at which there is recognizable fluorescence. This is particularly important when staining blood vessels as traditional size limitations exclusively allows for cross sectional visualization. Passive CLARITY Technique (PACT) has been at the forefront of tissue clearing protocols, utilizing an acrylamide hydrogel solution to maintain structure and sodium dodecyl sulfate to wash out lipids (Tomer et al, 2014). PACT is limited in its ability to clear larger sections and is not conducive to IHC antibody diffusion (Treweek et al, 2015). In order to circumvent these drawbacks, CUBIC was developed as an alternative passive protocol, aimed at being scalable to any tissue size (Richardson, 2015; Susaki et al, 2015). This study compared the effectiveness of both protocols in high and low lipid tissues in the context of blood vessel staining efficacy. Upon initial comparison, it became apparent that there was a statistically significant difference in mean DAPI intensity at all depths, up to 200 micrometers, between CUBIC and PACT \u2014 the former showcasing brighter stainings. Moreover, it was found that PACT does not remove erythrocytes from the tissue meaning that their auto-fluorescence is seen during imaging. Therefore, for blood vessel stainings, only CUBIC was optimized and quantitatively analyzed. In both tissue conditions as well as for two stainings, DAPI and fibronectin (FNCT), optimized CUBIC demonstrated a statistically significant difference from standard CUBIC with regards to mean fluorescent intensity.
ContributorsSidhu, Gurpaul Singh (Author) / VanAuker, Michael (Thesis director) / Kodibagkar, Vikram (Committee member) / Harrington Bioengineering Program (Contributor) / Barrett, The Honors College (Contributor)
Created2018-05