Theses and Dissertations
This collection includes both ASU Theses and Dissertations, submitted by graduate students, and the Barrett, Honors College theses submitted by undergraduate students.
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- Creators: School of Life Sciences
Description
The goal of my study is to test the overarching hypothesis that art therapy is effective because it targets emotional dysregulation that often accompanies significant health stressors. By reducing the salience of illness-related stressors, art therapy may improve overall mood and recovery, particularly in patients with cancer. After consulting the primary literature and review papers to develop psychological and neural mechanisms at work in art therapy, I created a hypothetical experimental procedure to test these hypotheses to explain why art therapy is helpful to patients with chronic illness. Studies found that art therapy stimulates activity of multiple brain regions involved in memory retrieval and the arousal of emotions. I hypothesize that patients with chronic illness have a reduced capacity for emotion regulation, or difficulty recognizing, expressing or altering illness-related emotions (Gross & Barrett, 2011). Further I hypothesize that art therapy improves mood and therapeutic outcomes by acting on the emotion-processing regions of the limbic system, and thereby facilitating the healthy expression of emotion, emotional processing, and reappraisal. More mechanistically, I propose art therapy reduces the perception or salience of stressors by reducing amygdala activity leading to decreased activation of the hypothalamic-pituitary-adrenal (HPA) axis. The art therapy literature and my hypothesis about its mechanisms of action became the basis of my proposed study. To assess the effectiveness of art therapy in alleviating symptoms of chronic disease, I am specifically targeting patients with cancer who exhibit a lack of emotional regulation. Saliva is collected 3 times a week on the day of intervention: morning after waking, afternoon, and evening. Stress levels are tested using one-hour art therapy sessions over the course of 3 months. The Perceived Stress Scale (PSS) assesses an individual's perceived stress and feelings in past and present situations, for the control and intervention group. To measure improvement in overall mood, 10 one-hour art sessions are performed on patients over 10 weeks. A one-hour discussion analyzing the participants' artwork follows each art session. The Spielberger State-Trait Anxiety Inventory (STAI) assesses overall mood for the intervention and control groups. I created rationale and predictions based on the intended results of each experiment.
ContributorsAluri, Bineetha C. (Author) / Orchinik, Miles (Thesis director) / Davis, Mary (Committee member) / Essary, Alison (Committee member) / School of Life Sciences (Contributor) / School for the Science of Health Care Delivery (Contributor) / Barrett, The Honors College (Contributor)
Created2018-05
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 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
Description
Alzheimer’s disease (AD) is a progressive cognitive and behavior disorder that is characterized by the deposition of extracellular Aβ plaques, intracellular neurofibrillary tangles, and neuroinflammation. Aβ is generated by cleavage of the amyloid precursor protein (APP) by β-secretase (BACE1) and, subsequently, y- secretase. In recent years, there has been an increasing interest in studying and understanding inflammation as a therapeutic target for AD. Inflammation manifests in the brain in the form of activated microglia and astrocytes. These cells are able to release high levels of inflammatory cytokines such as Tumor Necrosis Factor-α (TNF-α). TNF-α is a major cytokine, which is involved in early inflammatory events and plays a role in the progression of AD pathology. There are currently no treatments that target chronic neuroinflammation. However, previous work in our laboratory with transgenic mice modeling AD suggested that the anti-cancer drug lenalidomide could lower neuroinflammation and slow AD progression, though the cellular and molecular mechanisms are yet to be elucidated. Here we hypothesized that lenalidomide can modulate TNF-α production in microglia and decrease amyloidogenesis. Using immortal cell lines mimicking several brain cell types, we discovered that lenalidomide is likely to decrease inflammation by modulating microglia cells rather than neurons or astrocytes. In addition, the drug may prevent the overexpression of BACE1 upon inflammation, thus blocking the overproduction of Aβ. If confirmed, these results could lead to a better understanding of how inflammation regulates Aβ synthesis and provide novel cellular and molecular therapeutic targets to control the progression AD.
ContributorsGujju, Manasa (Author) / DeCourt, Boris (Thesis director) / Olive, M. Foster (Committee member) / Department of Psychology (Contributor) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2018-05
Description
This paper explores the idea of xenophilia and the circumstances under which it may occur. Xenophilia is the preference for an outgroup member over an ingroup member. This preference does not have to be amicable, and in fact can be exploitative under certain circumstances. Previous research indicates that xenophobia is much more common, but a few researchers have found support for the existence of xenophilia. To experimentally test the circumstances under which xenophilia might occur, I conducted a survey-based experiment on Amazon’s Mechanical Turk. This consisted of directed visualizations that manipulated participant goal (self-protection vs. mate acquisition) and the resources offered by both a fictitious outgroup and the hometown ingroup, followed by measures of ingroup/outgroup preference. I hypothesized that when the resource offered by the group addressed the participants’ goal, they would prefer the group with the “matched” resource—even if it was the outgroup providing that resource. My hypothesis was not supported, as the univariate analysis of variance for preference for the outgroup was not significant, F (2, 423) = .723, p = .486. This may have occurred because the goal manipulations were not strong enough to counteract the strong natural preference for ingroup members.
ContributorsDrury, Margaret E. (Author) / Neuberg, Steven (Thesis director) / Davis, Mary (Committee member) / Kenrick, Douglas (Committee member) / Department of Psychology (Contributor) / School of Life Sciences (Contributor) / School of Social and Behavioral Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2018-05
Description
Cardiovascular disease is the leading cause of death in the United States, and classic risk factors only predict half of the variance of cases. In this study, parental overprotection and temperamental negative affectivity both significantly correlated with blood pressure and heart rate, which suggests the importance of examining early life factors when determining one's risk for CVD.
ContributorsCarter, Steven Cross (Author) / Luecken, Linda (Thesis director) / Presson, Clark (Committee member) / Davis, Mary (Committee member) / Barrett, The Honors College (Contributor) / Department of Psychology (Contributor) / School of Life Sciences (Contributor)
Created2013-05
Description
Use of psychostimulants, such as cocaine, is associated with an increased risk of human immunodeficiency virus (HIV) infection. Dopaminergic signaling within the nucleus accumbens (NAc) is critically implicated in both disease states, mediating the addictive and reinforcing effects of cocaine and perpetuating HIV replication throughout the central nervous system (CNS). Cocaine and HIV induce neurobehavioral deficits separately; however, little is known regarding how they interact to dysregulate neuroimmune function or how this impacts relapse vulnerability. We have previously shown that inhibition of dopamine D3 receptor (D3R) signaling using MC-25-41, a novel and highly selective D3R partial agonist, attenuates cocaine-seeking behavior. Here, we sought to characterize changes in neuroimmune function in a rat model of combined HIV and cocaine use disorders across abstinence and examined the therapeutic efficacy of MC-25-41 in the presence of this comorbidity. Male rats were systemically treated with the HIV protein gp120 after establishing a history of cocaine self-administration and then, following 21 days of abstinence, were administered a systemic injection of MC-25-41 (10 mg/kg) prior to cue reactivity testing. Glial fibrillary acidic protein (GFAP) and ionized calcium-binding adapter molecule 1 (Iba1) immunoreactivity were analyzed after 5 or 21 days of cocaine abstinence as an index of glial cell levels. We demonstrate that inhibition of D3R signaling significantly attenuates cue-induced cocaine seeking among control rats but not gp120-exposed rats. Moreover, we show that NAc core GFAP and Iba1 expression is impaired by 5 days of abstinence, which persists into protracted abstinence and cue reactivity testing. However, we also demonstrate that neither gp120 nor D3R inhibition significantly altered NAc core GFAP or Iba1 expression. Altogether, these results reveal significant changes in glial cell function across cocaine abstinence and unique behavioral interactions with gp120 may inhibit the effectiveness of medication regimens, which highlights the need to consider these comorbidities when treating HIV infection.
ContributorsPhillips, Megan (Author) / Neisewander, Janet (Thesis director) / Olive, M. Foster (Committee member) / Namba, Mark (Committee member) / Barrett, The Honors College (Contributor) / School of Life Sciences (Contributor)
Created2021-12
Description
Hand-coding systems of measuring facial expressions were developed to study and analyze human emotions, but they are time-intensive and thus seldom used. As technology has advanced, new computer software programs, such as Affectiva, were developed to code facial expressions automatically using artificial intelligence and machine learning. Since this technology is still new, Affectiva and its validity remain understudied, and no psychological research has been conducted to compare Affectiva computer coding and hand coding of children’s emotions. The purpose of this study was to compare hand and computer coding of children’s expressions of emotion during a videotaped parent-child interaction. The study answered the following questions: 1) Do hand and computer coding agree?; and 2) Are hand and computer coding in higher agreement for some emotions than others? The sample included 25 pairs of twins from the Arizona Twin Project. Facial expressions were coded from videotape by a trained and reliable human coder and using the software Affectiva. The results showed that hand and computer coded emotion were in agreement for positive, but not negative emotions. Changing the context of the interaction to elicit more negative emotion, and using the same indicators of each emotion in computer and hand coding are suggested to improve the comparison of computer and hand coding.
ContributorsKwok, Connie (Author) / Lemery-Chalfant, Kathryn (Thesis director) / Davis, Mary (Committee member) / Miadich, Samantha (Committee member) / Department of Psychology (Contributor) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2020-05
Description
With opioid use disorder (OUD) being an epidemic, it is important to investigate the mechanisms as to why this is so. This study established a self-administration paradigm to model and investigate the mechanisms of polysubstance, sequential use in conjunction with the analysis of withdrawal symptomatology driven by opioid withdrawal. The independent variables were dichotomized into the control group (food/cocaine) and the experimental group (oxycodone/cocaine). We hypothesized that more cocaine would be self-administered on the first day of oxycodone withdrawal. In addition, we hypothesized that somatic signs of withdrawal would increase at 16 hours post-oxycodone self-administration. Finally, we hypothesized that cocaine intake during oxycodone withdrawal would potentiate subsequent oxycodone self-administration. Our findings revealed that animals readily discriminated between the active (food or oxycodone) and inactive levers - but will however require more animals to achieve the appropriate power. Further, the average cocaine infusions across phases exhibited significance between the oxycodone/cocaine and food/cocaine group, with the average cocaine infusions being lower in food than in oxycodone-experienced animals. This implies that the exacerbation of the sequential co-use pattern in this case yields an increase in cocaine infusions that may be driven by oxycodone withdrawal. Further, to characterize withdrawal from oxycodone self-administration, somatic signs were examined at either 0 or 16 hrs following completion of oxycodone self-administration. The oxycodone/cocaine group exhibited significantly lower body temperature at 16 hrs of oxycodone withdrawal compared to 0 hrs. No differences in somatic signs of withdrawal in the food/cocaine group was found between the two timepoints. Oxycodone withdrawal was not found to potentiate any subsequent self-administration of oxycodone. Future research is needed to uncover neurobiological underpinnings of motivated polysubstance use in order to discover novel pharmacotherapeutic treatments to decrease co-use of drugs of abuse. Overall, this study is of importance as it is the first to establish a working preclinical model of a clinically-relevant pattern of polysubstance use. By doing so, it enables an exceptional opportunity to examine co-use in a highly-controlled setting.
ContributorsUlangkaya, Hanaa Corsino (Author) / Gipson-Reichardt, Cassandra (Thesis director) / Olive, M. Foster (Committee member) / Department of Psychology (Contributor) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2020-05
Description
Major Depressive Disorder (MDD) affects over 300 million people worldwide, with the hippocampus showing decreased volume and activity in patients with MDD. The current study investigated whether a novel preclinical model of depression, unpredictable intermittent restraint (UIR), would decrease hippocampal neuronal dendritic complexity. Adult Sprague Dawley rats (24 male, 24 female) were equally divided into 4 groups: control males (CON-M), UIR males (UIR-M), control females (CON-F) and UIR females (UIR-F). UIR groups received restraint and shaking on an orbital shaker on a randomized schedule for 30 or 60 minutes/day for two to six days in a row for 26 days (21 total UIR days) before behavioral testing commenced. UIR continued and was interspersed between behavioral test days. At the end of behavioral testing, brains were processed. The behavior is published and not part of my honor’s thesis; my contribution involved quantifying and analyzing neurons in the hippocampus. Several neuronal types are found in the CA3 subregion of the hippocampus and I focused on short shaft (SS) neurons, which show different sensitivities to stress than the more common long shaft (LS) variety. Brains sections were mounted to slides and Golgi stained. SS neurons were drawn using a microscope with camera lucida attachment and quantified using the number of bifurcations and dendritic intersections as metrics for dendritic complexity in the apical and basal areas separately. The hypothesis that SS neurons in the CA3 region of the hippocampus would exhibit apical dendritic simplification in both sexes after UIR was not supported by our findings. In contrast, following UIR, SS apical dendrites were more complex in both sexes compared to controls. Although unexpected, we believe that the UIR paradigm was an effective stressor, robust enough to illicit neuronal adaptations. It appears that the time from the end of UIR to when the brain tissue was collected, or the post-stress recovery period, and/or repeated behavioral testing may have played a role in the observed increased neuronal complexity. Future studies are needed to parse out these potential effects.
ContributorsAcuna, Amanda Marie (Author) / Conrad, Cheryl (Thesis director) / Corbin, William (Committee member) / Olive, M. Foster (Committee member) / School of Life Sciences (Contributor) / Department of Psychology (Contributor) / Barrett, The Honors College (Contributor)
Created2020-12