ASU Electronic Theses and Dissertations
This collection includes most of the ASU Theses and Dissertations from 2011 to present. ASU Theses and Dissertations are available in downloadable PDF format; however, a small percentage of items are under embargo. Information about the dissertations/theses includes degree information, committee members, an abstract, supporting data or media.
In addition to the electronic theses found in the ASU Digital Repository, ASU Theses and Dissertations can be found in the ASU Library Catalog.
Dissertations and Theses granted by Arizona State University are archived and made available through a joint effort of the ASU Graduate College and the ASU Libraries. For more information or questions about this collection contact or visit the Digital Repository ETD Library Guide or contact the ASU Graduate College at gradformat@asu.edu.
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Description
Proper cell growth and differentiation requires the integration of multiple signaling pathways that are maintained by various post-translational modifications. Many proteins in signal transduction pathways are conserved between humans and model organisms. My dissertation characterizes four previously unknown manners of regulation in the Drosophila Decapentaplegic (Dpp) pathway, a pathway within TGF-beta family. First, I present data that the Dpp signal transducer, Mothers Against Dpp (Mad), is phosphorylated by Zeste-white 3 (Zw3), a kinase involved in the Wingless pathway. This phosphorylation event occurs independently of canonical phosphorylation of Mad by the Dpp receptor. Using ectopic expression of different alleles of Mad, I show that Zw3 phosphorylation of Mad occurs during the cell cycle in pro-neuronal cells and the loss of phosphorylation of Mad by Zw3 results in ectopic neuronal cells. Thus, Mad phosphorylation by Zw3 is necessary for cell cycle control in pro-neuronal cells. Second, I have shown that the regulator dSno, which has previously been shown to be a TGF-beta antagonist and agonist, is also a Wingless pathway antagonist. Loss of function flip-out clones and ectopic expression of dSno both resulted in changes of Wingless signaling. Further analysis revealed that dSno acts at or below the level of Armadillo (Arm) to inhibit target gene expression. Third, I have demonstrated that the protein Bonus, which is known to be involved in chromatin modification, is required in dorsal-ventral patterning. Further experiments discovered that the chromatin modifier is not only a necessary Dpp agonist, but it is also necessary for nuclear localization of Dorsal during Toll signaling. Last, I showed that longitudinal lacking-like (lola-like) is also required in dorsal-ventral patterning. The loss of maternally expressed lola-like prevents dpp transcription. This shows that lola-like is integral in the Dpp pathway. The study of these four proteins integrates different signaling pathways, demonstrating that the process of development is a web of connections rather than a linear pathway.
ContributorsQuijano, Janine C (Author) / Newfeld, Stuart J (Thesis advisor) / Goldstein, Elliott (Committee member) / Chandler, Douglas (Committee member) / Capco, David (Committee member) / Arizona State University (Publisher)
Created2014
Description
Given the current focus on high-stakes accountability in America's public schools, this study examined teacher evaluation specific to physical education. This study revealed current teacher evaluation practices used in physical education, perceptions of school administrators related to the value of the physical education evaluation process, and the perceptions of the physical education teachers related to the value of the evaluation process. The first phase of this study was an interpretive document analysis study conducted on four separate teacher evaluation systems commonly used within the public school system to evaluate physical education teachers. Those four systems were: Marzanos teacher evaluation model, Danielson framework for teaching (FFT), Rewarding Excellence in Instruction and Leadership (REIL), and Teacher Advancement Program (TAP). A separate evaluation instrument specific to physical education created by the National Association of Sport and Physical Education (NASPE) was used as a comparative evaluation tool. Evidence suggests that two of the four teacher evaluation systems had a high percentage of alignment with the NASPE instrument (TAP 87.5%, FFT 82.5%). The Marzano teacher evaluation model had the least amount of alignment with the NASPE instrument (62.5%). The second phase of this study was a phenomenological approach to understanding administrators' and physical education teachers' perceptions to teacher evaluation specific to physical education. The participants in this study were administrators and physical education teachers from an urban school district. An informal survey and formal semi-structured interviews were used to reveal perceptions of teacher evaluation specific to physical education. Evidence from the administrator's informal survey and formal semi-structured interviews revealed four common themes: (1) "I value PE, but I live in reality" (administrators value physical education, but practice in reality); (2) "good teaching is good teaching"; (3) "I know my limitations, and I want
eed help" (relative to teacher evaluation in PE); and (4) where's the training beef? Evidence from the physical education teacher's informal survey and formal semi-structured interviews revealed three common themes: (a) physical education is valued, but not prioritized; (b) teacher evaluation in physical education is "greatly needed, yet not transparent; (c) physical educators are not confident in their evaluator.
eed help" (relative to teacher evaluation in PE); and (4) where's the training beef? Evidence from the physical education teacher's informal survey and formal semi-structured interviews revealed three common themes: (a) physical education is valued, but not prioritized; (b) teacher evaluation in physical education is "greatly needed, yet not transparent; (c) physical educators are not confident in their evaluator.
ContributorsNorris, Jason (Author) / Van Der Mars, Hans (Thesis advisor) / Beardsley, Audrey (Thesis advisor) / Kulinna, Pamela (Committee member) / Arizona State University (Publisher)
Created2014
Description
This study aims to unearth monological and monocultural discourses buried under the power of the dominant biomedical model governing the HIV/AIDS debate. The study responds to an apparent consensus, rooted in Western biomedicine and its "standardizations of knowledge," in the production of the current HIV/AIDS discourse, especially in Sub-Saharan Africa. As a result, biomedicine has become the dominant actor (in) writing and rewriting discourse for the masses while marginalizing other forms of medical knowledge. Specifically, in its development, the Western biomedical model has arguably isolated the disease from its human host and the social experiences that facilitate the disease's transmission, placing it in the realm of laboratories and scientific experts and giving full ownership to Western medical discourse. Coupled with Western assumptions about African culture that reproduce a one-sided discourse informing the social construction of HIV/AIDS in Africa, this Western monopoly thus constrained the extent and efficacy of international prevention efforts. In this context, the goal for this study is not to demonize the West and biomedicine in general. Rather, this study seeks an alternative and less monolithic understanding currently absent in scientific discourses of HIV/AIDS that frequently elevates Western biomedicine over indigenous medicine; the Western expert over the local. The study takes into account the local voices of Sub-Saharan Africa and how the system has affected them, this study utilizes a Foucauldian approach to analyze discourse as a way to explore how certain ways of knowledge are formed in relation to power. This study also examines how certain knowlege is maintaned and reinforced within specific discourses.
ContributorsAbdalla, Mohamed (Author) / Jacobs, Bertram (Thesis advisor) / Robert, Jason (Committee member) / Klimek, Barbara (Committee member) / Arizona State University (Publisher)
Created2014
Description
Teaching evolution has been shown to be a challenge for faculty, in both K-12 and postsecondary education. Many of these challenges stem from perceived conflicts not only between religion and evolution, but also faculty beliefs about religion, it's compatibility with evolutionary theory, and it's proper role in classroom curriculum. Studies suggest that if educators engage with students' religious beliefs and identity, this may help students have positive attitudes towards evolution. The aim of this study was to reveal attitudes and beliefs professors have about addressing religion and providing religious scientist role models to students when teaching evolution. 15 semi-structured interviews of tenured biology professors were conducted at a large Midwestern universiy regarding their beliefs, experiences, and strategies teaching evolution and particularly, their willingness to address religion in a class section on evolution. Following a qualitative analysis of transcripts, professors did not agree on whether or not it is their job to help students accept evolution (although the majority said it is not), nor did they agree on a definition of "acceptance of evolution". Professors are willing to engage in students' religious beliefs, if this would help their students accept evolution. Finally, professors perceived many challenges to engaging students' religious beliefs in a science classroom such as the appropriateness of the material for a science class, large class sizes, and time constraints. Given the results of this study, the author concludes that instructors must come to a consensus about their goals as biology educators as well as what "acceptance of evolution" means, before they can realistically apply the engagement of student's religious beliefs and identity as an educational strategy.
ContributorsBarnes, Maryann Elizabeth (Author) / Brownell, Sara E (Thesis advisor) / Brem, Sarah K. (Thesis advisor) / Lynch, John M. (Committee member) / Ellison, Karin (Committee member) / Arizona State University (Publisher)
Created2014
Description
Facial projection--i.e., the position of the upper face relative to the anterior cranial fossa--is an important component of craniofacial architecture in primates. Study of its variation is therefore important to understanding the bases of primate craniofacial form. Such research is relevant to studies of human evolution because the condition in
Homo sapiens--in which facial projection is highly reduced, with the facial skeleton located primarily inferior (rather than anterior) to the braincase--is derived vis-à-vis other primates species, including others in the genus Homo. Previous research suggested that variation in facial projection is explained by: (1) cranial base angulation; (2) upper
facial length; (3) anterior cranial base length; (4) anterior sphenoid length; and/or (5) anterior middle cranial fossa length. However, previous research was based on taxonomically narrow samples and relatively small sample sizes, and comparative data on facial projection in anthropoid primates, with which these observations could be
contextualized, do not currently exist.
This dissertation fills this gap in knowledge. Specifically, data corresponding to the hypotheses listed above were collected from radiographs from a sample of anthropoid primates (N = 37 species; 756 specimens) . These data were subjected to phylogenetically-controlled multiple regression analyses. In addition, multivariate and univariate models were statistically compared, and the position of Homo sapiens relative to univariate and multivariate regression models was evaluated.
The results suggest that upper facial length, anterior cranial base length, and, to a lesser extent, cranial base angle are the most important predictors of facial projection. Homo sapiens conforms to the patterns found in anthropoid primates, suggesting that these same factors explain the condition in this species. However, a consideration of the
evidence from the fossil record in the context of these findings suggests that upper facial length is the most likely cause of the extremely low degree of facial projection in Homo sapiens. These results downplay the role of the brain in shaping the form of the human cranium. Instead, these results suggest that reduction in facial skeleton size--which may
be due to changes in diet--may be more important than previously suggested.
Homo sapiens--in which facial projection is highly reduced, with the facial skeleton located primarily inferior (rather than anterior) to the braincase--is derived vis-à-vis other primates species, including others in the genus Homo. Previous research suggested that variation in facial projection is explained by: (1) cranial base angulation; (2) upper
facial length; (3) anterior cranial base length; (4) anterior sphenoid length; and/or (5) anterior middle cranial fossa length. However, previous research was based on taxonomically narrow samples and relatively small sample sizes, and comparative data on facial projection in anthropoid primates, with which these observations could be
contextualized, do not currently exist.
This dissertation fills this gap in knowledge. Specifically, data corresponding to the hypotheses listed above were collected from radiographs from a sample of anthropoid primates (N = 37 species; 756 specimens) . These data were subjected to phylogenetically-controlled multiple regression analyses. In addition, multivariate and univariate models were statistically compared, and the position of Homo sapiens relative to univariate and multivariate regression models was evaluated.
The results suggest that upper facial length, anterior cranial base length, and, to a lesser extent, cranial base angle are the most important predictors of facial projection. Homo sapiens conforms to the patterns found in anthropoid primates, suggesting that these same factors explain the condition in this species. However, a consideration of the
evidence from the fossil record in the context of these findings suggests that upper facial length is the most likely cause of the extremely low degree of facial projection in Homo sapiens. These results downplay the role of the brain in shaping the form of the human cranium. Instead, these results suggest that reduction in facial skeleton size--which may
be due to changes in diet--may be more important than previously suggested.
ContributorsRitzman, Terrence (Author) / Schwartz, Gary T (Thesis advisor) / Kimbel, William H. (Committee member) / Kaufman, Jason (Committee member) / Arizona State University (Publisher)
Created2014
Description
There has been important progress in understanding ecological dynamics through the development of the theory of ecological stoichiometry. This fast growing theory provides new constraints and mechanisms that can be formulated into mathematical models. Stoichiometric models incorporate the effects of both food quantity and food quality into a single framework that produce rich dynamics. While the effects of nutrient deficiency on consumer growth are well understood, recent discoveries in ecological stoichiometry suggest that consumer dynamics are not only affected by insufficient food nutrient content (low phosphorus (P): carbon (C) ratio) but also by excess food nutrient content (high P:C). This phenomenon, known as the stoichiometric knife edge, in which animal growth is reduced not only by food with low P content but also by food with high P content, needs to be incorporated into mathematical models. Here we present Lotka-Volterra type models to investigate the growth response of Daphnia to algae of varying P:C ratios. Using a nonsmooth system of two ordinary differential equations (ODEs), we formulate the first model to incorporate the phenomenon of the stoichiometric knife edge. We then extend this stoichiometric model by mechanistically deriving and tracking free P in the environment. This resulting full knife edge model is a nonsmooth system of three ODEs. Bifurcation analysis and numerical simulations of the full model, that explicitly tracks phosphorus, leads to quantitatively different predictions than previous models that neglect to track free nutrients. The full model shows that the grazer population is sensitive to excess nutrient concentrations as a dynamical free nutrient pool induces extreme grazer population density changes. These modeling efforts provide insight on the effects of excess nutrient content on grazer dynamics and deepen our understanding of the effects of stoichiometry on the mechanisms governing population dynamics and the interactions between trophic levels.
ContributorsPeace, Angela (Author) / Kuang, Yang (Thesis advisor) / Elser, James J (Committee member) / Baer, Steven (Committee member) / Tang, Wenbo (Committee member) / Kang, Yun (Committee member) / Arizona State University (Publisher)
Created2014
Description
The majority of non-small cell lung cancer (NSCLC) patients (70%) are diagnosed with adenocarcinoma versus other histological subtypes. These patients often present with advanced, metastatic disease and frequently relapse after treatment. The tumor suppressor, Liver Kinase B1, is frequently inactivated in adenocarcinomas and loss of function is associated with a highly aggressive, metastatic tumor (1). Identification of the mechanisms deregulated with LKB1 inactivation could yield targeted therapeutic options for adenocarcinoma patients. Re-purposing the immune system to support tumor growth and aid in metastasis has been shown to be a feature in cancer progression (2). Tumor associated macrophages (TAMs) differentiate from monocytes, which are recruited to the tumor microenvironment via secretion of chemotaxic factors by cancer cells. We find that NSCLC cells deficient in LKB1 display increased secretion of C-C motif ligand 2 (CCL2), a chemokine involved in monocyte recruitment. To elucidate the molecular pathway regulating CCL2 up-regulation, we investigated inhibitors of substrates downstream of LKB1 signaling in A549, H23, H2030 and H838 cell lines. Noticeably, BAY-11-7082 (NF-κB inhibitor) reduced CCL2 secretion by an average 92%. We further demonstrate that a CCR2 antagonist and neutralizing CCL2 antibody substantially reduce monocyte migration to NSCLC (H23) cell line conditioned media. Using an in vivo model of NSCLC, we find that LKB1 deleted tumors demonstrate a discernible increase in CCL2 levels compared to normal lung. Moreover, tumors display an increase in the M2:M1 macrophage ratio and increase in tumor associated neutrophil (TAN) infiltrate compared to normal lung. This M2 shift was significantly reduced in mice treated with anti-CCL2 or a CCR2 antagonist and the TAN infiltrate was significantly reduced with the CCR2 antagonist. These data suggest that deregulation of the CCL2/CCR2 signaling axis could play a role in cancer progression in LKB1 deficient tumors.
ContributorsFriel, Jacqueline (Author) / Inge, Landon (Thesis advisor) / Lake, Douglas (Thesis advisor) / Blattman, Joseph (Committee member) / Arizona State University (Publisher)
Created2015
Description
In this dissertation I employed a culminating cycle of action research following two earlier ones to facilitate the creation of a professional learning community (PLC). My research took place at an elementary school in an urban area of the American southwest. As principal of this school I had initiated the policies and procedures that were often recommended to create PLCs. However, observations of teachers in PLC meetings indicated that conversations focused on logistical planning issues, rather than on the in-depth pedagogical discussions that characterize high functioning PLCs. To address this problem I introduced a form of peer observation into the PLC meeting. This was achieved by showing short video recordings of teachers in their classrooms. I used a mixed methods approach to investigate how this innovation influenced three constructs associated with PLC meetings: professional learning, the sharing of tacit teaching knowledge, and collaboration in the PLC.
Quantitative data consisted of responses to a survey given as a pre-, post-, and retrospective pre-test. Results showed significant gains for all three constructs between the retrospective pre-test and the post-test, but no significant gain between the pre- and post-test. Analysis of qualitative data produced four assertions. First, the process of peer observation during a PLC meeting benefitted the personal learning of teachers. Second, peer observation benefitted teacher teams' abilities to demonstrate the critical behaviors of a true PLC. Third, the process of facilitating peer observation through video recordings evoked negative emotions. Fourth, the degree to which teachers were able to learn from a video was influenced by their perceptions of the video's authenticity and similarity to their own classrooms.
In the discussion, complementarity of the quantitative and qualitative data was described and results were explained in terms of previous research and established theory. Additionally, practical lessons that were learned, limitations, and research implications were described. In a concluding section, I discussed my personal learning regarding leadership, innovation, and action research; the purpose of the doctorate in education; and strengthening connections between research and practitioners.
Quantitative data consisted of responses to a survey given as a pre-, post-, and retrospective pre-test. Results showed significant gains for all three constructs between the retrospective pre-test and the post-test, but no significant gain between the pre- and post-test. Analysis of qualitative data produced four assertions. First, the process of peer observation during a PLC meeting benefitted the personal learning of teachers. Second, peer observation benefitted teacher teams' abilities to demonstrate the critical behaviors of a true PLC. Third, the process of facilitating peer observation through video recordings evoked negative emotions. Fourth, the degree to which teachers were able to learn from a video was influenced by their perceptions of the video's authenticity and similarity to their own classrooms.
In the discussion, complementarity of the quantitative and qualitative data was described and results were explained in terms of previous research and established theory. Additionally, practical lessons that were learned, limitations, and research implications were described. In a concluding section, I discussed my personal learning regarding leadership, innovation, and action research; the purpose of the doctorate in education; and strengthening connections between research and practitioners.
ContributorsMacKinney, Bennett (Author) / Buss, Ray R (Thesis advisor) / Zucker, Stanley (Committee member) / Haghighat, Ibi (Committee member) / Arizona State University (Publisher)
Created2015
Description
The phycologist, M. R. Droop, studied vitamin B12 limitation in the flagellate Monochrysis lutheri and concluded that its specific growth rate depended on the concentration of the vitamin within the cell; i.e. the cell quota of the vitamin B12. The Droop model provides a mathematical expression to link growth rate to the intracellular concentration of a limiting nutrient. Although the Droop model has been an important modeling tool in ecology, it has only recently been applied to study cancer biology. Cancer cells live in an ecological setting, interacting and competing with normal and other cancerous cells for nutrients and space, and evolving and adapting to their environment. Here, the Droop equation is used to model three cancers.
First, prostate cancer is modeled, where androgen is considered the limiting nutrient since most tumors depend on androgen for proliferation and survival. The model's accuracy for predicting the biomarker for patients on intermittent androgen deprivation therapy is tested by comparing the simulation results to clinical data as well as to an existing simpler model. The results suggest that a simpler model may be more beneficial for a predictive use, although further research is needed in this field prior to implementing mathematical models as a predictive method in a clinical setting.
Next, two chronic myeloid leukemia models are compared that consider Imatinib treatment, a drug that inhibits the constitutively active tyrosine kinase BCR-ABL. Both models describe the competition of leukemic and normal cells, however the first model also describes intracellular dynamics by considering BCR-ABL as the limiting nutrient. Using clinical data, the differences in estimated parameters between the models and the capacity for each model to predict drug resistance are analyzed.
Last, a simple model is presented that considers ovarian tumor growth and tumor induced angiogenesis, subject to on and off anti-angiogenesis treatment. In this environment, the cell quota represents the intracellular concentration of necessary nutrients provided through blood supply. Mathematical analysis of the model is presented and model simulation results are compared to pre-clinical data. This simple model is able to fit both on- and off-treatment data using the same biologically relevant parameters.
First, prostate cancer is modeled, where androgen is considered the limiting nutrient since most tumors depend on androgen for proliferation and survival. The model's accuracy for predicting the biomarker for patients on intermittent androgen deprivation therapy is tested by comparing the simulation results to clinical data as well as to an existing simpler model. The results suggest that a simpler model may be more beneficial for a predictive use, although further research is needed in this field prior to implementing mathematical models as a predictive method in a clinical setting.
Next, two chronic myeloid leukemia models are compared that consider Imatinib treatment, a drug that inhibits the constitutively active tyrosine kinase BCR-ABL. Both models describe the competition of leukemic and normal cells, however the first model also describes intracellular dynamics by considering BCR-ABL as the limiting nutrient. Using clinical data, the differences in estimated parameters between the models and the capacity for each model to predict drug resistance are analyzed.
Last, a simple model is presented that considers ovarian tumor growth and tumor induced angiogenesis, subject to on and off anti-angiogenesis treatment. In this environment, the cell quota represents the intracellular concentration of necessary nutrients provided through blood supply. Mathematical analysis of the model is presented and model simulation results are compared to pre-clinical data. This simple model is able to fit both on- and off-treatment data using the same biologically relevant parameters.
ContributorsEverett, Rebecca Anne (Author) / Kuang, Yang (Thesis advisor) / Nagy, John (Committee member) / Milner, Fabio (Committee member) / Crook, Sharon (Committee member) / Jackiewicz, Zdzislaw (Committee member) / Arizona State University (Publisher)
Created2015
Description
Type 1 diabetes (T1D) is a chronic autoimmune disease characterized by progressive autoimmune destruction of insulin-producing pancreatic β-cells. Genetic, immunological and environmental factors contribute to T1D development. The focus of this dissertation is to track the humoral immune response in T1D by profiling autoantibodies (AAbs) and anti-viral antibodies using an innovative protein array platform called Nucleic Acid Programmable Protein Array (NAPPA).
AAbs provide value in identifying individuals at risk, stratifying patients with different clinical courses, improving our understanding of autoimmune destructions, identifying antigens for cellular immune response and providing candidates for prevention trials in T1D. A two-stage serological AAb screening against 6,000 human proteins was performed. A dual specificity tyrosine-phosphorylation-regulated kinase 2 (DYRK2) was validated with 36% sensitivity at 98% specificity by an orthogonal immunoassay. This is the first systematic screening for novel AAbs against large number of human proteins by protein arrays in T1D. A more comprehensive search for novel AAbs was performed using a knowledge-based approach by ELISA and a screening-based approach against 10,000 human proteins by NAPPA. Six AAbs were identified and validated with sensitivities ranged from 16% to 27% at 95% specificity. These two studies enriched the T1D “autoantigenome” and provided insights into T1D pathophysiology in an unprecedented breadth and width.
The rapid rise of T1D incidence suggests the potential involvement of environmental factors including viral infections. Sero-reactivity to 646 viral antigens was assessed in new-onset T1D patients. Antibody positive rate of EBV was significantly higher in cases than controls that suggested a potential role of EBV in T1D development. A high density-NAPPA platform was demonstrated with high reproducibility and sensitivity in profiling anti-viral antibodies.
This dissertation shows the power of a protein-array based immunoproteomics approach to characterize humoral immunoprofile against human and viral proteomes. The identification of novel T1D-specific AAbs and T1D-associated viruses will help to connect the nodes in T1D etiology and provide better understanding of T1D pathophysiology.
AAbs provide value in identifying individuals at risk, stratifying patients with different clinical courses, improving our understanding of autoimmune destructions, identifying antigens for cellular immune response and providing candidates for prevention trials in T1D. A two-stage serological AAb screening against 6,000 human proteins was performed. A dual specificity tyrosine-phosphorylation-regulated kinase 2 (DYRK2) was validated with 36% sensitivity at 98% specificity by an orthogonal immunoassay. This is the first systematic screening for novel AAbs against large number of human proteins by protein arrays in T1D. A more comprehensive search for novel AAbs was performed using a knowledge-based approach by ELISA and a screening-based approach against 10,000 human proteins by NAPPA. Six AAbs were identified and validated with sensitivities ranged from 16% to 27% at 95% specificity. These two studies enriched the T1D “autoantigenome” and provided insights into T1D pathophysiology in an unprecedented breadth and width.
The rapid rise of T1D incidence suggests the potential involvement of environmental factors including viral infections. Sero-reactivity to 646 viral antigens was assessed in new-onset T1D patients. Antibody positive rate of EBV was significantly higher in cases than controls that suggested a potential role of EBV in T1D development. A high density-NAPPA platform was demonstrated with high reproducibility and sensitivity in profiling anti-viral antibodies.
This dissertation shows the power of a protein-array based immunoproteomics approach to characterize humoral immunoprofile against human and viral proteomes. The identification of novel T1D-specific AAbs and T1D-associated viruses will help to connect the nodes in T1D etiology and provide better understanding of T1D pathophysiology.
ContributorsBian, Xiaofang (Author) / LaBaer, Joshua (Thesis advisor) / Mandarino, Lawrence (Committee member) / Chang, Yung (Committee member) / Arizona State University (Publisher)
Created2015