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- All Subjects: psychology
- Genre: Doctoral Dissertation
- Creators: Arizona State University
Description
Family adaptation to child developmental disability is a dynamic transactional process that has yet to be tested in a longitudinal, rigorous fashion. In addition, although children with developmental delays frequently have behavior problems, not enough research has examined possible underlying mechanisms in the relation between child developmental delay, adaptation and behavior problems. In the current study, factor analysis examined how best to conceptualize the construct of family adaptation to developmental delay. Also, longitudinal growth curve modeling tested models in which child behavior problems mediated the relation between developmental risk and indices of family adaptation. Participants included 130 typically developing children and their families (Mental Development Index [MDI] > 85) and 104 children with developmental delays and their families (MDI < 85). Data were collected yearly between the ages of three and eight as part of a multi-site, longitudinal investigation examining the interrelations among children's developmental status, family processes, and the emergence of child psychopathology. Results of the current study indicated that adaptation is best conceptualized as a multi-index construct. Different aspects of adaptation changed in unique ways over time, with some facets of adaptation remaining stable while others fluctuated. Child internalizing and externalizing behavior problems were found to decrease over time for both children with developmental delays and typically developing children. Child behavior problems were also found to mediate the relation between developmental risk and family adaptation for over half of the mediation pathways. Significant mediation results indicated that children with developmental delays showed higher early levels of behavior problems, which in turn was associated with more maladaptive adaptation. These findings provide further evidence that families of children with developmental delays experience both positive and more challenging changes in their families over time. This study implies important next steps for research and clinical practice in the area of developmental disability.
ContributorsPedersen y Arbona, Anita (Author) / Crnic, Keith A (Thesis advisor) / Sandler, Irwin (Committee member) / Lemery, Kathryn (Committee member) / Enders, Craig (Committee member) / Arizona State University (Publisher)
Created2011
Description
An emerging body of literature suggests that humans likely have multiple threat avoidance systems that enable us to detect and avoid threats in our environment, such as disease threats and physical safety threats. These systems are presumed to be domain-specific, each handling one class of potential threats, and previous research generally supports this assumption. Previous research has not, however, directly tested the domain-specificity of disease avoidance and self-protection by showing that activating one threat management system does not lead to responses consistent only with a different threat management system. Here, the domain- specificity of the disease avoidance and self-protection systems is directly tested using the lexical decision task, a measure of stereotype accessibility, and the implicit association test. Results, although inconclusive, more strongly support a series of domain-specific threat management systems than a single, domain- general system
ContributorsAnderson, Uriah Steven (Author) / Kenrick, Douglas T. (Thesis advisor) / Shiota, Michelle N. (Committee member) / Neuberg, Steven L. (Committee member) / Becker, David V (Committee member) / Arizona State University (Publisher)
Created2011
Description
Alzheimer's Disease (AD) is a debilitating neurodegenerative disease. The disease leads to dementia and loss of cognitive functions and affects about 4.5 million people in the United States. It is the 7th leading cause of death and is a huge financial burden on the healthcare industry. There are no means of diagnosing the disease before neurodegeneration is significant and sadly there is no cure that controls its progression. The protein beta-amyloid or Aâ plays an important role in the progression of the disease. It is formed from the cleavage of the Amyloid Precursor Protein by two enzymes - â and ã-secretases and is found in the plaques that are deposits found in Alzheimer brains. This work describes the generation of therapeutics based on inhibition of the cleavage by â-secretase. Using in-vitro recombinant antibody display libraries to screen for single chain variable fragment (scFv) antibodies; this work describes the isolation and characterization of scFv that target the â-secretase cleavage site on APP. This approach is especially relevant since non-specific inhibition of the enzyme may have undesirable effects since the enzyme has been shown to have other important substrates. The scFv iBSEC1 successfully recognized APP, reduced â-secretase cleavage of APP and reduced Aâ levels in a cell model of Alzheimer's Disease. This work then describes the first application of bispecific antibody therapeutics to Alzheimer's Disease. iBSEC1 scFv was combined with a proteolytic scFv that enhances the "good" pathway (á-secretase cleavage) that results in alternative cleavage of APP to generate the bispecific tandem scFv - DIA10D. DIA10D reduced APP cleavage by â-secretase and steered it towards the "good" pathway thus increasing the generation of the fragment sAPPá which is neuroprotective. Finally, treatment with iBSEC1 is evaluated for reduced oxidative stress, which is observed in cells over expressing APP when they are exposed to stress. Recombinant antibody based therapeutics like scFv have several advantages since they retain the high specificity of the antibodies but are safer since they lack the constant region and are smaller, potentially facilitating easier delivery to the brain
ContributorsBoddapati, Shanta (Author) / Sierks, Michael (Thesis advisor) / Arizona State University (Publisher)
Created2011
Description
When people pick up the phone to call a telephone quitline, they are taking an important step towards changing their smoking behavior. The current study investigated the role of a critical cognition in the cessation process--self-efficacy. Self-efficacy is thought to be influential in behavior change processes including those involved in the challenging process of stopping tobacco use. By applying basic principles of self-efficacy theory to smokers utilizing a telephone quitline, this study advanced our understanding of the nature of self-efficacy in a "real-world" cessation setting. Participants received between one and four intervention calls aimed at supporting them through their quit attempt. Concurrent with the initiation of this study, three items (confidence, stress, and urges) were added to the standard telephone protocol and assessed at each call. Two principal sets of hypotheses were tested using a combination of ANCOVAs and multiple regression analyses. The first set of hypotheses explored how self-efficacy and changes in self-efficacy within individuals were associated with cessation outcomes. Most research has found a positive linear relation between self-efficacy and quit outcomes, but this study tested the possibility that excessively high self-efficacy may actually reflect an overconfidence bias, and in some cases be negatively related to cessation outcomes. The second set of hypotheses addressed several smoking-related factors expected to affect self-efficacy. As predicted, higher baseline self-efficacy and increases in self-efficacy were associated with higher rates of quitting. However, contrary to predictions, there was no evidence that overconfidence led to diminished cessation success. Finally, as predicted, shorter duration of quit attempts, shorter time to relapse, and stronger urges all were associated with lower self-efficacy. In conclusion, understanding how self-efficacy and changes in self-efficacy affect and are affected by cessation outcomes is useful for informing both future research and current quitline intervention procedures.
ContributorsGoesling, Jenna (Author) / Barrera, Manuel (Thesis advisor) / Shiota, Lani (Committee member) / Enders, Craig (Committee member) / Presson, Clark (Committee member) / Arizona State University (Publisher)
Created2011
Description
Intuitive decision making refers to decision making based on situational pattern recognition, which happens without deliberation. It is a fast and effortless process that occurs without complete awareness. Moreover, it is believed that implicit learning is one means by which a foundation for intuitive decision making is developed. Accordingly, the present study investigated several factors that affect implicit learning and the development of intuitive decision making in a simulated real-world environment: (1) simple versus complex situational patterns; (2) the diversity of the patterns to which an individual is exposed; (3) the underlying mechanisms. The results showed that simple patterns led to higher levels of implicit learning and intuitive decision-making accuracy than complex patterns; increased diversity enhanced implicit learning and intuitive decision-making accuracy; and an embodied mechanism, labeling, contributes to the development of intuitive decision making in a simulated real-world environment. The results suggest that simulated real-world environments can provide the basis for training intuitive decision making, that diversity is influential in the process of training intuitive decision making, and that labeling contributes to the development of intuitive decision making. These results are interpreted in the context of applied situations such as military applications involving remotely piloted aircraft.
ContributorsCovas-Smith, Christine Marie (Author) / Cooke, Nancy J. (Thesis advisor) / Patterson, Robert (Committee member) / Glenberg, Arthur (Committee member) / Homa, Donald (Committee member) / Arizona State University (Publisher)
Created2011
Description
In the present research, two interventions were developed to increase sun protection in young women. The purpose of the study was to compare the effects of intervention content eliciting strong emotional responses to visual images depicting photoaging and skin cancer, specifically fear and disgust, coupled with a message of self-efficacy and benefits of sun protection (the F intervention) with an intervention that did not contain an emotional arousal component (the E intervention). Further, these two intervention conditions were compared to a control condition that contained an emotional arousal component that elicited emotion unrelated to the threat of skin cancer or photoaging (the C control condition). A longitudinal study design was employed, to examine the effects of condition immediately following the intervention, and to examine sun protection behavior 2 weeks after the intervention. A total of 352 undergraduate women at Arizona State University were randomly assigned to one of the three conditions (F n = 148, E n = 73, C n = 131). Several psychosocial constructs, including benefits of sun protection, susceptibility to and severity of photoaging and sun exposure, self-efficacy beliefs of making sun protection a daily habit, and barriers to sun protection were measured before and immediately following the intervention. Sun protection behavior was measured two weeks later. Those in the full intervention reported higher self-efficacy and severity of photoaging at immediate posttest than those in the efficacy only and control conditions. The fit of several path models was tested to explore underlying mechanisms by which the intervention affected sun protection behavior. Experienced emotion, specifically fear and disgust, predicted susceptibility and severity, which in turn predicted anticipated regret of failing to use sun protection. The relationship between this overall threat component (experienced emotion, susceptibility, severity, and anticipated regret) and intentions to engage in sun protection behavior was mediated by benefits. The present research provided evidence of the effectiveness of threat specific emotional arousal coupled with a self-efficacy and benefits message in interventions to increase sun protection. Further, this research provided additional support for the inclusion of both experienced and anticipated emotion in models of health behavior.
ContributorsMoser, Stephanie E (Author) / Aiken, Leona S. (Thesis advisor) / Shiota, Michelle N. (Committee member) / Kwan, Sau (Committee member) / Castro, Felipe (Committee member) / Arizona State University (Publisher)
Created2011
Description
Externalizing behaviors are pervasive, widespread, and disruptive across a multitude of settings and developmental contexts. While the conventional diathesis-stress model typically measures the disordered end of the spectrum, studies that span the range of behavior, from externalizing to competence behaviors, are necessary to see the full picture. To that end, this study examined the additive and nonadditive relations of a dimension of parenting (ranging from warm to rejecting), and variants in dopamine, vasopressin, and neuropeptide-y receptor genes on externalizing/competence in a large sample of predominantly Caucasian twin children in toddlerhood, middle childhood, and early adolescence. Variants within each gene were hypothesized to increase biological susceptibility to both negative and positive environments. Consistent with prediction, warmth related to lower externalizing/higher competence at all ages. Earlier levels of externalizing/competence washed out the effect of parental warmth on future externalizing/competence with the exception of father warmth in toddlerhood marginally predicting change in externalizing/competence from toddlerhood to middle childhood. Warmth was a significant moderator of the heritability of behavior in middle childhood and early adolescence such that behavior was less heritable (mother report) and more heritable (father report) in low warmth environments. Interactions with warmth and the dopamine and vasopressin genes in middle childhood and early adolescence emphasize the moderational role gene variants play in relations between the rearing environment and child behavior. For dopamine, the long variant related to increased sensitivity to parent warmth such that the children displayed more externalizing behaviors when exposed to rejection but they also displayed more competence behaviors when exposed to high warmth. Vasopressin moderation was only present under conditions of parental warmth, not rejection. Interactions with neuropeptide-y and warmth were not significant. The picture that emerges is one of gene-environment interplay, wherein the influence of both parenting and child genotype each depend on the level of the other. As genetic research moves forward, gene variants previously implicated as conferring risk for disorder should be reexamined in conjunction with salient aspects of the environment on the full range of the behavioral outcome of interest.
ContributorsO'Brien, T. Caitlin (Author) / Lemery-Chalfant, Kathryn (Thesis advisor) / Eisenberg, Nancy (Committee member) / Enders, Craig (Committee member) / Nagoshi, Craig (Committee member) / Arizona State University (Publisher)
Created2011
Description
Neurostimulation methods currently include deep brain stimulation (DBS), optogenetic, transcranial direct-current stimulation (tDCS), and transcranial magnetic stimulation (TMS). TMS and tDCS are noninvasive techniques whereas DBS and optogenetic require surgical implantation of electrodes or light emitting devices. All approaches, except for optogenetic, have been implemented in clinical settings because they have demonstrated therapeutic utility and clinical efficacy for neurological and psychiatric disorders. When applied for therapeutic applications, these techniques suffer from limitations that hinder the progression of its intended use to treat compromised brain function. DBS requires an invasive surgical procedure that surfaces complications from infection, longevity of electrical components, and immune responses to foreign materials. Both TMS and tDCS circumvent the problems seen with DBS as they are noninvasive procedures, but they fail to produce the spatial resolution required to target specific brain structures. Realizing these restrictions, we sought out to use ultrasound as a neurostimulation modality. Ultrasound is capable of achieving greater resolution than TMS and tDCS, as we have demonstrated a ~2mm lateral resolution, which can be delivered noninvasively. These characteristics place ultrasound superior to current neurostimulation methods. For these reasons, this dissertation provides a developed protocol to use transcranial pulsed ultrasound (TPU) as a neurostimulation technique. These investigations implement electrophysiological, optophysiological, immunohistological, and behavioral methods to elucidate the effects of ultrasound on the central nervous system and raise questions about the functional consequences. Intriguingly, we showed that TPU was also capable of stimulating intact sub-cortical circuits in the anesthetized mouse. These data reveal that TPU can evoke synchronous oscillations in the hippocampus in addition to increasing expression of brain-derived neurotrophic factor (BDNF). Considering these observations, and the ability to noninvasively stimulate neuronal activity on a mesoscale resolution, reveals a potential avenue to be effective in clinical settings where current brain stimulation techniques have shown to be beneficial. Thus, the results explained by this dissertation help to pronounce the significance for these protocols to gain translational recognition.
ContributorsTufail, Yusuf Zahid (Author) / Tyler, William J (Thesis advisor) / Duch, Carsten (Committee member) / Muthuswamy, Jitendran (Committee member) / Santello, Marco (Committee member) / Tillery, Stephen H (Committee member) / Arizona State University (Publisher)
Created2011
Description
Patients with Alzheimer's disease (AD) exhibit a significantly higher incidence of unprovoked seizures compared to age-matched non-AD controls, and animal models of AD (i.e., transgenic human amyloid precursor protein, hAPP mice) display neural hyper-excitation and epileptic seizures. Hyperexcitation is particularly important because it contributes to the high incidence of epilepsy in AD patients as well as AD-related synaptic deficits and neurodegeneration. Given that there is significant amyloid-β (Aβ) accumulation and deposition in AD brain, Aβ exposure ultimately may be responsible for neural hyper-excitation in both AD patients and animal models. Emerging evidence indicates that α7 nicotinic acetylcholine receptors (α7-nAChR) are involved in AD pathology, because synaptic impairment and learning and memory deficits in a hAPPα7-/- mouse model are decreased by nAChR α7 subunit gene deletion. Given that Aβ potently modulates α7-nAChR function, that α7-nAChR expression is significantly enhanced in both AD patients and animal models, and that α7-nAChR play an important role in regulating neuronal excitability, it is reasonable that α7-nAChRs may contribute to Aβ-induced neural hyperexcitation. We hypothesize that increased α7-nAChR expression and function as a consequence of Aβ exposure is important in Aβ-induced neural hyperexcitation. In this project, we found that exposure of Aβ aggregates at a nanomolar range induces neuronal hyperexcitation and toxicity via an upregulation of α7-nAChR in cultured hippocampus pyramidal neurons. Aβ up-regulates α7-nAChRs function and expression through a post translational mechanism. α7-nAChR up-regulation occurs prior to Aβ-induced neuronal hyperexcitation and toxicity. Moreover, inhibition of α7-nAChR or deletion of α7-nAChR prevented Aβ induced neuronal hyperexcitation and toxicity, which suggests that α7-nAChRs are required for Aβ induced neuronal hyperexcitation and toxicity. These results reveal a profound role for α7-nAChR in mediating Aβ-induced neuronal hyperexcitation and toxicity and predict that Aβ-induced up-regulation of α7-nAChR could be an early and critical event in AD etiopathogenesis. Drugs targeting α7-nAChR or seizure activity could be viable therapies for AD treatment.
ContributorsLiu, Qiang (Author) / Wu, Jie (Thesis advisor) / Lukas, Ronald J (Committee member) / Chang, Yongchang (Committee member) / Sierks, Michael (Committee member) / Smith, Brian (Committee member) / Vu, Eric (Committee member) / Arizona State University (Publisher)
Created2011
Description
Systemic lupus erytematosus (SLE) is an autoimmune disease where the immune system is reactive to self antigens resulting in manifestations like glomerulonephritis and arthritis. The immune system also affects the central nervous system (known as CNS-SLE) leading to neuropsychiatric manifestations such as depression, cognitive impairment, psychosis and seizures. A subset of pathogenic brain-reactive autoantibodies (BRAA) is hypothesized to bind to integral membrane brain proteins, affecting their function, leading to CNS-SLE. I have tested this BRAA hypothesis, using our lupus-mouse model the MRL/lpr mice, and have found it to be a reasonable explanation for some of the manifestations of CNS-SLE. Even when the MRL/lpr had a reduced autoimmune phenotype, their low BRAA sera levels correlated with CNS involvement. The correlation existed between BRAA levels to integral membrane protein and depressive-like behavior. These results were the first to show a correlation between behavioral changes and BRAA levels from brain membrane antigen as oppose to cultured neuronal cells. More accurate means of predicting and diagnosing lupus and CNS-SLE is necessary. Using microarray technology I was able to determine peptide sets that could be predictive and diagnostic of lupus and each specific CNS manifestation. To knowledge no test currently exists that can effectively diagnose lupus and distinguish between each CNS manifestations. Using the peptide sets, I was able to determine possible natural protein biomarkers for each set as well as for five monoclonal BRAA from one MRL/lpr. These biomarkers can provide specific targets for therapy depending on the manifestation. It was necessary to investigate how these BRAA enter the brain. I hypothesized that substance P plays a role in altering the blood-brain barrier (BBB) allowing these BRAA to enter and affect brain function, when bound to its neurokinin-1 receptor (NK-1R). Western blotting results revealed an increase in the levels of NK-1R in the brain of the MRL/lpr compared to the MRL/mp. These MRL/lpr with increased levels of both NK-1R and BRAA displayed CNS dysfunction. Together, these results demonstrate that NK-1R may play a role in CNS manifestations. Overall, the research conducted here, add to the role that BRAA are playing in CNS-lupus.
ContributorsWilliams, Stephanie (Author) / Hoffman, Steven A (Thesis advisor) / Conrad, Cheryl (Committee member) / Chen, Julian (Committee member) / Orchinik, Miles (Committee member) / Arizona State University (Publisher)
Created2011