Matching Items (6)
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- All Subjects: Resilience
- Creators: Luecken, Linda J.
Description
The primary aim of this study was to investigate resilient profiles in low-income Mexican American (MA) mothers. MA mothers are part of an under researched population, the fastest growing ethnic minority group, and have the highest birth rate in the United States, presenting a significant public health concern. The transition to motherhood can be an emotionally and physically complex time for women, particularly in the context of a stressful low-income environment. Although most low-income women navigate this transition well, a significant number of mothers develop moderate to severe depressive symptoms. The proposed research investigated profiles of resilience during the prenatal period using a person-centered approach via latent profile analysis. In alignment with current resilience theories, several domains of resilience were investigated including psychological, social, and cultural adherence (e.g., maintaining specific cultural traditions). Concurrent prenatal depressive symptoms and stress were correlated with the profiles in order to establish validity. Six week postpartum depressive symptoms and physiological processes (e.g., overall cortisol output, heart rate variability, and sleep) were also predicted by the prenatal resilient profiles. The resulting data revealed three separate profiles: low-resource, high-resource Anglo, and high-resource Mexican. These resilience profiles had differential associations with concurrent depressive symptoms and stress, such that women in the high-resource profiles reported less depressive symptoms and stress prenatally. Further, profile differences regarding cortisol output, resting heart rate variability, were also found, but there were no differences in insomnia symptoms. Profile classification also moderated the effects of prenatal economic stress on postpartum depressive symptoms, such that women in the high-resource Mexican profile were at risk for higher postpartum depressive symptoms under high economic stress compared to the high-resource Anglo group, which demonstrated a more resilient response. Overall, the results suggest the presence of multiple clusters of prenatal resilience within a sample of MA mothers facing health disparities, with various effects on perinatal mental health and postpartum physiological processes. The results also highlight the need for multi-dimensional models of resilience and the possible implications for interventions.
ContributorsGress Smith, Jenna L (Author) / Luecken, Linda J. (Thesis advisor) / Gonzales, Nancy (Committee member) / Okun, Morris (Committee member) / Zautra, Alex (Committee member) / Arizona State University (Publisher)
Created2014
Description
Female infertility can present a significant challenge to quality of life. To date, few, if any investigations have explored the process by which women adapt to premature ovarian insufficiency (POI), a specific type of infertility, over time. The current investigation proposed a bi-dimensional, multi-factor, model of adjustment characterized by the identification of six latent factors representing personal attributes (resilience resources and vulnerability), coping (adaptive and maladaptive) and outcomes (distress and wellbeing). Measures were collected over the period of one year; personal attributes were assessed at Time 1, coping at Time 2 and outcomes at Time 3. It was hypothesized that coping factors would mediate associations between personal attributes and outcomes. Confirmatory Factor Analysis (CFA), simple regressions and single mediator models were utilized to test study hypotheses. Overall, with the exception of coping, the factor structure was consistent with predictions. Two empirically derived coping factors, and a single standalone strategy, avoidance, emerged. The first factor, labeled "approach coping" was comprised of strategies directly addressing the experience of infertility. The second was comprised of strategies indicative of "letting go /moving on." Only avoidance significantly mediated the association between vulnerability and distress.
ContributorsDriscoll, Mary (Author) / Davis, Mary C. (Thesis advisor) / Aiken, Leona S. (Committee member) / Luecken, Linda J. (Committee member) / Zautra, Alex J. (Committee member) / Arizona State University (Publisher)
Created2011
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 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
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 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
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
Over 35% of multiracial college students fail to earn a degree, which can have significant economic and health costs over their lifespan. This study aimed to better understand college and psychological adjustment among multiracial college students of Hispanic/Latinx and White non-Hispanic descent by examining students’ racial identities and use of resilience resources. Latent profiles of identity were identified to better understand how different aspects of racial identity are clustered in this population. Multiracial college students (N=221) reported on racial identity as measured on multiple dimensions: Hispanic/Latinx identity, Hispanic/Latinx cultural orientation, White identity, identity integration, shifting expressions of identity, and identity malleability. Students also reported on their use of multiple resilience resources (personal mastery, social competence, perspective taking, coping flexibility, familism support values) and both college and psychological adjustment. Through regression and SEM analyses, results indicated that, of the resilience resources, only personal mastery was positively related to both college and psychological adjustment, while social competence was positively related to college adjustment. More shifting expressions of identity was related to poorer college and psychological adjustment, which was partially mediated via personal mastery. Stronger Hispanic/Latinx identity was related to higher perspective taking and coping flexibility, while stronger White identity was related to higher familism support values. Latent profiles of identity indicated a four-class solution, consisting of 1) “low identity”, 2) “integrated, low shifting”, 3) “integrated, shifting”, and 4) “high shifting, low integration”. Findings highlight the need for person-centered and ecological approaches to understanding identity development and resilience among multiracial college students, and can inform prevention and intervention efforts for multiracial college students of Hispanic/Latinx and White non-Hispanic descent. Results also demonstrate the importance of assessing multiracial identity via multiple dimensions including factors such as identity integration, shifting expressions of identity, and identity malleability.
ContributorsJewell, Shannon (Author) / Luecken, Linda J. (Thesis advisor) / Jackson, Kelly (Committee member) / Doane, Leah (Committee member) / Edwards, Michael (Committee member) / Arizona State University (Publisher)
Created2020