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There is growing concern over the future availability of water for electricity generation. Because of a rapidly growing population coupled with an arid climate, the Western United States faces a particularly acute water/energy challenge, as installation of new electricity capacity is expected to be required in the areas with the

There is growing concern over the future availability of water for electricity generation. Because of a rapidly growing population coupled with an arid climate, the Western United States faces a particularly acute water/energy challenge, as installation of new electricity capacity is expected to be required in the areas with the most limited water availability. Electricity trading is anticipated to be an important strategy for avoiding further local water stress, especially during drought and in the areas with the most rapidly growing populations. Transfers of electricity imply transfers of "virtual water" - water required for the production of a product. Yet, as a result of sizable demand growth, there may not be excess capacity in the system to support trade as an adaptive response to long lasting drought. As the grid inevitably expands capacity due to higher demand, or adapts to anticipated climate change, capacity additions should be selected and sited to increase system resilience to drought. This paper explores the tradeoff between virtual water and local water/energy infrastructure development for the purpose of enhancing the Western US power grid's resilience to drought. A simple linear model is developed that estimates the economically optimal configuration of the Western US power grid given water constraints. The model indicates that natural gas combined cycle power plants combined with increased interstate trade in power and virtual water provide the greatest opportunity for cost effective and water efficient grid expansion. Such expansion, as well as drought conditions, may shift and increase virtual water trade patterns, as states with ample water resources and a competitive advantage in developing power sources become net exporters, and states with limited water or higher costs become importers.
ContributorsHerron, Seth (Author) / Ruddell, Benjamin L (Thesis advisor) / Ariaratnam, Samuel (Thesis advisor) / Allenby, Braden (Committee member) / Williams, Eric (Committee member) / Arizona State University (Publisher)
Created2013
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Description
Quantum resilience is a pragmatic theory that allows systems engineers to formally characterize the resilience of systems. As a generalized theory, it not only clarifies resilience in the literature, but also can be applied to all disciplines and domains of discourse. Operationalizing resilience in this manner permits decision-makers to compare

Quantum resilience is a pragmatic theory that allows systems engineers to formally characterize the resilience of systems. As a generalized theory, it not only clarifies resilience in the literature, but also can be applied to all disciplines and domains of discourse. Operationalizing resilience in this manner permits decision-makers to compare and contrast system deployment options for suitability in a variety of environments and allows for consistent treatment of resilience across domains. Systems engineers, whether planning future infrastructures or managing ecosystems, are increasingly asked to deliver resilient systems. Quantum resilience provides a way forward that allows specific resilience requirements to be specified, validated, and verified.

Quantum resilience makes two very important claims. First, resilience cannot be characterized without recognizing both the system and the valued function it provides. Second, resilience is not about disturbances, insults, threats, or perturbations. To avoid crippling infinities, characterization of resilience must be accomplishable without disturbances in mind. In light of this, quantum resilience defines resilience as the extent to which a system delivers its valued functions, and characterizes resilience as a function of system productivity and complexity. System productivity vis-à-vis specified “valued functions” involves (1) the quanta of the valued function delivered, and (2) the number of systems (within the greater system) which deliver it. System complexity is defined structurally and relationally and is a function of a variety of items including (1) system-of-systems hierarchical decomposition, (2) interfaces and connections between systems, and (3) inter-system dependencies.

Among the important features of quantum resilience is that it can be implemented in any system engineering tool that provides sufficient design and specification rigor (i.e., one that supports standards like the Lifecycle and Systems Modeling languages and frameworks like the DoD Architecture Framework). Further, this can be accomplished with minimal software development and has been demonstrated in three model-based system engineering tools, two of which are commercially available, well-respected, and widely used. This pragmatic approach assures transparency and consistency in characterization of resilience in any discipline.
ContributorsRoberts, Thomas Wade (Author) / Allenby, Braden (Thesis advisor) / Chester, Mikhail (Committee member) / Anderies, John M (Committee member) / Arizona State University (Publisher)
Created2015
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Description
Chronic stress results in functional and structural changes to the hippocampus. Decades of research has led to insights into the mechanisms underlying the chronic stress-induced deficits in hippocampal-mediated cognition and reduction of dendritic complexity of hippocampal neurons. Recently, a considerable focus of chronic stress research has investigated the mechanisms behind

Chronic stress results in functional and structural changes to the hippocampus. Decades of research has led to insights into the mechanisms underlying the chronic stress-induced deficits in hippocampal-mediated cognition and reduction of dendritic complexity of hippocampal neurons. Recently, a considerable focus of chronic stress research has investigated the mechanisms behind the improvements in hippocampal mediated cognition when chronic stress ends and a post-stress rest period is given. Consequently, the goal of this dissertation is to uncover the mechanisms that allow for spatial ability to improve in the aftermath of chronic stress. In chapter 2, the protein brain derived neurotrophic factor (BDNF) was investigated as a mechanism that allows for spatial ability to show improvements following the end of chronic stress. It was found that decreasing the expression of BDNF in the hippocampus prevented spatial memory improvements following a post-stress rest period. Chapter 3 was performed to determine whether hippocampal CA3 apical dendritic complexity requires BDNF to show improvements following a post-stress rest period, and whether a receptor for BDNF, TrkB, mediates the improvements of spatial ability and dendritic complexity in a temporal manner, i.e. during the rest period only. These experiments showed that decreased hippocampal BDNF expression prevented improvements in dendritic complexity, and administration of a TrkB antagonist during the rest period also prevented the improvements in spatial ability and dendritic complexity. In chapter 4, the role of the GABAergic system on spatial ability following chronic stress and a post-stress rest period was investigated. Following chronic stress, it was found that male rats showed impairments on the acquisition phase of the RAWM and this correlated with limbic glutamic acid decarboxylase, a marker for GABA. In chapter 5, a transgenic mouse that expresses a permanent marker on all GABAergic interneurons was used to assess the effects of chronic stress and a post-stress rest period on hippocampal GABAergic neurons. While no changes were found on the total number of GABAergic interneurons, specific subtypes of GABAergic interneurons were affected by stressor manipulations. Collectively, these studies reveal some mechanisms behind the plasticity seen in the hippocampus in response to a post-stress rest period.
ContributorsOrtiz, J. Bryce (Author) / Conrad, Cheryl D. (Thesis advisor) / Newbern, Jason M. (Committee member) / Orchinik, Miles (Committee member) / Sanabria, Federico (Committee member) / Arizona State University (Publisher)
Created2018
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Description
Infrastructure are increasingly being recognized as too rigid to quickly adapt to a changing climate and a non-stationary future. This rigidness poses risks to and impacts on infrastructure service delivery and public welfare. Adaptivity in infrastructure is critical for managing uncertainties to continue providing services, yet little is known about

Infrastructure are increasingly being recognized as too rigid to quickly adapt to a changing climate and a non-stationary future. This rigidness poses risks to and impacts on infrastructure service delivery and public welfare. Adaptivity in infrastructure is critical for managing uncertainties to continue providing services, yet little is known about how infrastructure can be made more agile and flexible towards improved adaptive capacity. A literature review identified approximately fifty examples of novel infrastructure and technologies which support adaptivity through one or more of ten theoretical competencies of adaptive infrastructure. From these examples emerged several infrastructure forms and possible strategies for adaptivity, including smart technologies, combined centralized/decentralized organizational structures, and renewable electricity generation. With institutional and cultural support, such novel structures and systems have the potential to transform infrastructure provision and management.
ContributorsGilrein, Erica (Author) / Chester, Mikhail (Thesis advisor) / Garcia, Margaret (Committee member) / Allenby, Braden (Committee member) / Arizona State University (Publisher)
Created2018
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Description
Rasopathies are a family of developmental syndromes that exhibit craniofacial abnormalities, cognitive disabilities, developmental delay and increased risk of cancer. However, little is known about the pathogenesis of developmental defects in the nervous system. Frequently, gain-of-function mutations in the Ras/Raf/MEK/ERK cascade (aka ERK/MAPK) are associated with the observed pathogenesis. My

Rasopathies are a family of developmental syndromes that exhibit craniofacial abnormalities, cognitive disabilities, developmental delay and increased risk of cancer. However, little is known about the pathogenesis of developmental defects in the nervous system. Frequently, gain-of-function mutations in the Ras/Raf/MEK/ERK cascade (aka ERK/MAPK) are associated with the observed pathogenesis. My research focuses on defining the relationship between increased ERK/MAPK signaling and its effects on the nervous system, specifically in the context of motor learning. Motor function depends on several neuroanatomically distinct regions, especially the spinal cord, cerebellum, striatum, and cerebral cortex. We tested whether hyperactivation of ERK/MAPK specifically in the cortex was sufficient to drive changes in motor function. We used a series of genetically modified mouse models and cre-lox technology to hyperactivate ERK/MAPK in the cerebral cortex. Nex:Cre/NeuroD6:Cre was employed to express a constitutively active MEK mutation throughout all layers of the cerebral cortex from an early stage of development. RBP4:Cre, caMEK only exhibited hyper activation in cortical glutamatergic neurons responsible for cortical output (neurons in layer V of the cerebral cortex). First, the two mouse strains were tested in an open field paradigm to assess global locomotor abilities and overall fitness for fine motor tasks. Next, a skilled motor reaching task was used to evaluate motor learning capabilities. The results show that Nex:Cre/NeuroD6:Cre, caMEK mutants do not learn the motor reaching task, although they performed normally on the open field task. Preliminary results suggest RBP4:Cre, caMEK mutants exhibit normal locomotor capabilities and a partial lack of learning. The difference in motor learning capabilities might be explained by the extent of altered connectivity in different regions of the corticospinal tract. Once we have identified the neuropathological effects of various layers in the cortex we will be able to determine whether therapeutic interventions are sufficient to reverse these learning defects.
ContributorsRoose, Cassandra Ann (Author) / Newbern, Jason M. (Thesis director) / Olive, Foster (Committee member) / Bjorklund, Reed (Committee member) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2016-12
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Description
The RAS/MAPK (RAS/Mitogen Activated Protein Kinase) pathway is a highly conserved, canonical signaling cascade that is highly involved in cellular growth and proliferation as well as cell migration. As such, it plays an important role in development, specifically in development of the nervous system. Activation of ERK is indispensable for

The RAS/MAPK (RAS/Mitogen Activated Protein Kinase) pathway is a highly conserved, canonical signaling cascade that is highly involved in cellular growth and proliferation as well as cell migration. As such, it plays an important role in development, specifically in development of the nervous system. Activation of ERK is indispensable for the differentiation of Embryonic Stem Cells (ESC) into neuronal precursors (Li z et al, 2006). ERK signaling has also shown to mediate Schwann cell myelination of the peripheral nervous system (PNS) as well as oligodendrocyte proliferation (Newbern et al, 2011). The class of developmental disorders that result in the dysregulation of RAS signaling are known as RASopathies. The molecular and cell-specific consequences of these various pathway mutations remain to be elucidated. While there is evidence for altered DNA transcription in RASopathies, there is little work examining the effects of the RASopathy-linked mutations on protein translation and post-translational modifications in vivo. RASopathies have phenotypic and molecular similarities to other disorders such as Fragile X Syndrome (FXS) and Tuberous Sclerosis (TSC) that show evidence of aberrant protein synthesis and affect related pathways. There are also well-defined downstream RAS pathway elements involved in translation. Additionally, aberrant corticospinal axon outgrowth has been observed in disease models of RASopathies (Xing et al, 2016). For these reasons, this present study examines a subset of proteins involved in translation and translational regulation in the context of RASopathy disease states. Results indicate that in both of the tested RASopathy model systems, there is altered mTOR expression. Additionally the loss of function model showed a decrease in rps6 activation. This data supports a role for the selective dysregulation of translational control elements in RASopathy models. This data also indicates that the primary candidate mechanism for control of altered translation in these modes is through the altered expression of mTOR.
ContributorsHilbert, Alexander Robert (Author) / Newbern, Jason (Thesis director) / Olive, M. Foster (Committee member) / Bjorklund, Reed (Committee member) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2017-05
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Description
Infrastructure managers are continually challenged to reorient their organizations to mitigate disturbances. Disturbances to infrastructure constantly intensify, and the world and its intricate systems are becoming more connected and complex. This complexity often leads to disturbances and cascading failures. Some of these events unfold in extreme ways previously unimagined (i.e.,

Infrastructure managers are continually challenged to reorient their organizations to mitigate disturbances. Disturbances to infrastructure constantly intensify, and the world and its intricate systems are becoming more connected and complex. This complexity often leads to disturbances and cascading failures. Some of these events unfold in extreme ways previously unimagined (i.e., Black Swan events). Infrastructure managers currently seek pathways through this complexity. To this end, reimagined – multifaceted – definitions of resilience must inform future decisions. Moreover, the hazardous environment of the Anthropocene demands flexibility and dynamic reprioritization of infrastructure and resources during disturbances. In this dissertation, the introduction will briefly explain foundational concepts, frameworks, and models that will inform the rest of this work. Chapter 2 investigates the concept of dynamic criticality: the skill to reprioritize amidst disturbances, repeating this process with each new disturbance. There is a dearth of insight requisite skillsets for infrastructure organizations to attain dynamic criticality. Therefore, this dissertation searches other industries and finds goals, structures, sensemaking, and strategic best practices to propose a contextualized framework for infrastructure. Chapters 3 and 4 seek insight into modeling infrastructure interdependencies and cascading failure to elucidate extreme outcomes such as Black Swans. Chapter 3 explores this concept through a theoretical analysis considering the use of realistic but fictional (i.e., synthetic) models to simulate interdependent behavior and cascading failures. This chapter also discusses potential uses of synthetic networks for infrastructure resilience research and barriers to future success. Chapter 4 tests the preceding theoretical analysis with an empirical study. Chapter 4 builds realistic networks with dependency between power and water models and simulates cascading failure. The discussion considers the future application of similar modeling efforts and how these techniques can help infrastructure managers scan the horizon for Black Swans. Finally, Chapter 5 concludes the dissertation with a synthesis of the findings from the previous chapters, discusses the boundaries and limitations, and proposes inspirations for future work.
ContributorsHoff, Ryan Michael (Author) / Chester, Mikhail V (Thesis advisor) / Allenby, Braden (Committee member) / Johnson, Nathan (Committee member) / McPhearson, Timon (Committee member) / Arizona State University (Publisher)
Created2023