Using data from the National Longitudinal Study of Adolescent to Adult Health (Add Health), I investigate the influence of adolescent friendship network on the likelihood of college enrollment, and whether and how this influence is affected by stratification factors (e.g., gender, race/ethnicity, and socioeconomic status). However, there is a challenge in evaluating this influence process since adolescents usually non-randomly select their friends. A selection process needs to be taken into consideration simultaneously with the influence process of adolescents’ friendship network on their likelihood of college enrollment. Previous research on peer effects has methodological issues and limitations. Traditional methods (e.g., multivariate regression, multilevel modeling, or propensity score matching) using limited data (e.g., cross-sectional) and measures of friendship network (e.g., one best friend) could not solve the problem of integrating selection process and influence process in one model. In addition, the dyadic and triadic (or even higher level) dependency among friends in the network makes it more difficult to estimate selection and influence processes using traditional methods. To address these concerns, I employ longitudinal network analysis with stochastic actor-based models (SABMs) to account for the influence of friendship network on adolescent college enrollment when simultaneously considering the selection of friendship. The co-evolution model of network dynamics (selection) and behavioral dynamics (influence) also addresses the problem of endogeneity between network change and behavioral change. However, the co-evolution model requires network data and behavioral data measured in multiple time points, so in the first stage of this research, I generate the predicted probability of college enrollment at three time points of Add Health using traditional logistic regression. Then in the second stage of this research, I use the transformed likelihood of college enrollment, a statistical artifact, as the behavior variable in the co-evolution model to examine how the likelihood of college enrollment affect the friendship selection and in turn friend’s average likelihood of college enrollment in the network influences an adolescent’s own likelihood of college enrollment. In the first stage, I find that there are some levels of gender, race/ethnicity, and SES inequalities in the college enrollment, even after controlling for previous academic achievement, other individual characteristics, family backgrounds, and school level variables. In the second stage, the results of dynamic network analysis indicate significant selection (partial deselection) and influence effects of adolescent friendship networks on the likelihood of college enrollment. In the selection process, adolescents have high tendency to select friends who are similar to them in the likelihood of college enrollment, or terminate friendships with other students of dissimilar likelihood of college enrollment. In the influence process, the average alter effect is found consistently significant and positive across all models and schools, which indicates that there is strong social influence of friendship network on adolescents’ likelihood of college enrollment. The higher the average friends’ likelihood of college enrollment, the more likely the adolescent will increase own likelihood of college enrollment. I also discuss the significance of results and many important policy and practical implications.

Semantic memory includes vocabulary and word meanings, conceptual information, and general facts about the world (Tulving, 1972). According to the standard view of semantic memory in cognitive neuroscience, the hippocampus is necessary to first acquire new semantic information (Gabrieli, Cohen, & Corkin, 1988), but these representations are then consolidated in the neocortex and become independent of the hippocampus with time (McClelland, McNaughton, & O'Reilly, 1995). Remote semantic memory is considered independent of the hippocampus, and the hippocampus is not thought to play a critical role in the processing and use of such representations. The current work challenges the notion that previously acquired semantic knowledge, and its use during communication, is independent of the hippocampus. A group of patients with bilateral hippocampal damage and severe impairments in declarative memory were tested. Intact naming and word-definition matching performance in amnesia, has led to the notion that remote semantic memory is intact in patients with hippocampal amnesia. Motivated by perspectives of word learning as a protracted process where additional features and senses of a word are added over time, and by recent discoveries about the time course of hippocampal contributions to on-line relational processing, reconsolidation, and the flexible integration of information, we revisit the notion that remote semantic memory is intact in amnesia. Using measures of semantic richness and vocabulary depth from psycholinguistics and first and second language-learning studies, we examined how much information is associated with previously acquired, highly familiar words in hippocampal amnesic patients. Relative to healthy demographically matched comparison participants and a group of brain-damaged comparison participants, the patients with hippocampal amnesia performed significantly worse on both productive and receptive measures of vocabulary depth and semantic richness. In the healthy brain, semantic memory appears to get richer and deeper with time. Healthy participants of all ages were tested on these measures and strong correlations are seen with age as older healthy adults displayed richer semantic knowledge than the younger adults. The patient data provides a mechanism: hippocampal relational binding supports the deepening and enrichment of knowledge over time. These findings suggest that remote semantic memory is impoverished in patients with hippocampal amnesia and that the hippocampus supports the maintenance and updating of semantic memory beyond its initial acquisition. The use of lexical and semantic knowledge during discourse was also examined. Amnesic patients displayed significantly lower levels of lexical diversity in the speech they produced, and showed a strong trend toward producing language with reduced levels of semantic detail suggesting that patients cannot use their semantic representations as richly during communication. These results add to a growing body of work detailing a role for the hippocampus in language processing more generally. By documenting a role for the hippocampus in maintaining, updating, and using semantic knowledge, this work informs theories of semantic memory and it's neural bases, advances knowledge of the role of the hippocampus in supporting human behavior, and brings more sensitive measures to the neuroscientific study of semantic memory.

Respiratory syncytial virus (RSV) is the most common cause of bronchiolitis-induced hospitalization in young children. A natural RSV infection fails to elicit long-lasting immunity, further increasing the need for an effective vaccine. Despite the significant healthcare burden, there is no licensed RSV vaccine currently available. While most RSV vaccine strategies focus on the induction of humoral immunity, high antibody titers do not prevent RSV infection. It remains unclear if protective immunity can be achieved through robust cellular immunity. Previous work has indicated that a relatively low frequency of virus-specific CD8 T cells is induced following an RSV infection in human infants. In addition, RSV-specific memory CD8 T cells diminish to almost undetectable frequencies in the blood of the elderly. The lack of long-lasting immunity against RSV may be explained by an absence or low frequency of memory CD8 T cells within the lung following infection. However, I determined that the majority of effector CD8 T cells reside within the lung tissue following infection with either RSV or influenza A virus (IAV), both of which replicate primarily in the airways. In addition, approximately 70% of antigen-experienced memory CD8 T cells persist in the lung tissue at day 30 following RSV infection. In contrast, the majority of CD8 T cells remain in the pulmonary vasculature following intranasal infection with either of the systemically replicating viruses lymphocytic choriomeningitis virus or vaccinia virus. Therefore, the tissue tropism of a virus will determine if CD8 T cells preferentially accumulate in the lung tissue following infection of the respiratory tract. An experimental formalin-inactivated RSV (FI-RSV) vaccine caused enhanced respiratory disease in vaccinated children following a natural RSV infection. Incomplete knowledge of the underlying immunological mechanisms that were responsible for mediating the enhanced disease has greatly hampered vaccine development. Previous studies have indicated that eosinophils, non-neutralizing antibodies, and CD4 T cells may be required to elicit FI-RSV vaccine-enhanced disease. I determined that distinct CD4 T cell subsets mediate individual disease parameters. The Th2-biased immune response, but not eosinophils specifically, was responsible for induction of airway hyperresponsiveness and mucus hypersecretion. On the other hand, the Th1-associated pro-inflammatory cytokine TNF-α was required to mediate baseline pulmonary dysfunction and weight loss. Lastly, while depletion of CD4 T cells ameliorated all disease parameters evaluated, the antibody titers remained unaltered in depleted mice. Thus, antibodies induced by FI-RSV immunization were not required for vaccine-enhanced disease. My data demonstrate that discrete disease manifestations associated with FI-RSV immunization are orchestrated by distinct subsets of CD4 T cells. The CD8 T cell response is believed to contribute to both pathogen clearance and immunopathology following an acute RSV infection. However, it is unclear if robust memory CD8 T cell responses will protect against an RSV infection. I determined that induction of a high-magnitude, epitope-specific memory CD8 T cell pool mediated increased viral clearance following RSV challenge. However, mice with robust secondary CD8 T cell responses exhibit increased airway dysfunction, weight loss, and mortality as compared to mock-immunized mice undergoing an acute RSV infection. The enhanced disease severity was unique to the context of an RSV infection as similarly immunized mice were protected from chge with a lethal dose of a recombinant IAV engineered to express an RSV-derived epitope. In addition, the increased morbidity and mortality was associated with an elevated amount of both IFN-γ and TNF-α in the serum of immunized mice. Neutralization of either IFN-γ or TNF-α led to a significant reduction in disease severity and survival of all mice. These results demonstrate that robust memory CD8 T cell responses enhance viral clearance, but also lead to severe pulmonary immunopathology following RSV infection. Overall, I establish that the majority of effector CD8 T cells are localized within the lung tissue following a respiratory infection, and determine that either memory CD4 or CD8 T cell responses elicits severe immunopathology following a RSV infection.

Complex behaviors require selectively attending to task-relevant items, and ignoring conspicuous, irrelevant items. For example, driving requires selectively attending to other cars on the road while ignoring flashing billboards. Dominant models of attentional control posit that we avoid distraction by biasing attention towards task-relevant items, and our ability to avoid distraction depends on the strength and specificity of this bias. I find that a strong, specific bias towards task-relevant items is insufficient for preventing distraction. Instead, preventing distraction also requires past experience ignoring distractors. I also find that long-term memory systems, rather than visual short-term memory or priming memory systems, maintain this experience. Based upon these findings, I propose that effective attentional control not only demands a strong, specific bias towards task-relevant items, but also requires that observers learn to ignore conspicuous, irrelevant items.

Person-Environment (PE) Fit has been a subject of research interest for over 100 years, and although much is know about the consequences PE fit and the types of PE fit, the actions that people take in pursuit of this desirable condition are less well understood. This dissertation develops and tests a model that explains how personality traits influence individuals' choice of coping mechanisms used in pursuit of PE Fit and their ability to use them effectively. Achievement and anxiety motivations influence the choice of coping mechanisms used in pursuit of fit. The efficacy of these coping mechanisms to change the level of PE fit is determined by individuals' ability to respond to feedback from the environment, indicated by narcissism. I also explore the influence of aspects of change in the environment that drive individuals to cope with uncertainty during times of change. Finally, the level of fit achieved and the changes in fit made over time influence individuals' well-being and organizational commitment. I test this model using a pilot study sample of student teams assessed over the course of 5 time periods and a field study sample of working adults assess over the course of 4 time periods. I analyzed this data using Regression, Structural Equation Modeling, Random Coefficient Modeling, and Latent Growth Modeling.

Prostaglandins (PG) are ubiquitous lipid mediators that play key roles in pathophysiological responses to infections. They are considered to have both pro and anti-inflammatory roles depending upon the time of inflammation, the receptors that they bind to and the tissues that they act upon. Hence given their pleiotropic effects, a perfect balance between the pro and anti-inflammatory functions of PGs are required to ensure that a controlled timely immune response is elicited to mediate protection and to avoid immunopathology. PGD2 is one such PG that was reported to increase with age in the lungs of mice and to mediate an anti-inflammatory effect thereby blunting the immune response following Severe Acute Respiratory Syndrome – Coronavirus (SARS-CoV). Increase in PGD2 with age incapacitates respiratory dendritic cells (rDC) to migrate from lungs to the draining lymph node following SARS-CoV infection due to down regulation of CCR7 (a receptor for chemokines CCL19/21). Migration of rDCs to draining lymph nodes requires high expression of CCR7 and it's binding to CCL19/21, a chemokine that mediates migration of dendritic cells along its gradient. Although increase in levels of PGD2 might prove beneficial in high inflammatory conditions, it should be noted that high levels of such a potent anti-inflammatory mediator during the initiation of an immune response could prove detrimental. In chapter II of this thesis I show that age-related increases in oxidative stress result in the upregulation of a single phospholipase (PLA2) group II D (G2D) (PLA2G2D) with anti-inflammatory roles. PLA2G2D functions by releasing Arachidonic acid (AA) from the lipid membrane, which will be further metabolized to other pro-resolving/ anti-inflammatory lipid mediators including PGD2. I show that inducing oxidative stress in young mice as well as in human peripheral blood macrophages, results in the upregulation of PLA2G2D (probably as a counter mechanism against oxidative stress). Also increase in the expression levels of this gene during the course of SARS-CoV infection results in the upregulation of PGD2, which is completely abrogated in Pla2g2d-/- mice. I also show Pla2g2d/- middle-aged mice have low levels of PGD2 and that they are capable of mounting a strong immune response and survive the otherwise lethal SARS-CoV infection. PGD2 is also a major PG in the brain and its role has been investigated in many non-infectious setting such as stroke and Alzheimer' disease. The PGD2 binding to one of its receptors DP1 has been shown to have primarily a neuro-protective role. In chapter III, I show that PGD2/DP1 signaling has beneficial effects in the brain of mice infected with a neurotropic strain of murine hepatitis virus (MHV) (rj2.2). In agreement with the neuro-protective role of PGD2, at least 60% of DP1-/- mice succumb to a sublethal dose of rj2.2. rj2.2 infection in these mice is characterized by a delay in the induction of IFN I response and lower activation status of microglia and macrophages in the brain. I also show that abrogation of DP1 signaling results in global defects in the immune system response to infection. Notably, a genome wide expression analysis using microarray, shows that a gene, Pydc3 with putative inflammasome inhibiting function is upregulated in WT mice compared to DP1-/- mice in the CD11b population of cells which primarily comprises microglia and macrophages. In line with the predicted function of Pydc3, DP1-/- mice have higher frequency and number of IL-1β+ producing microglia in the brain. Studies are underway to determine the exact role of DP1 signaling in Pydc3 expression as well as the role of this gene in inflammasome function. Overall these studies emphasize the immuno-modulatory roles of PGs in the context of a viral infection. Thus, altering the levels of these lipid mediators at appropriate times during the course of infection might prove useful as an effective therapeutic strategy to decide the fate of an infection.

This dissertation centers on the under-researched construct of interactional competence, which refers to features of jointly constructed discourse. When applied to the testing of speaking skills in a second language, interactional competence refers to features of the discourse that the two students produce together; rather than the speaking ability or performance of each person individually. This dissertation describes the construct of interactional competence in a low-stakes, paired speaking test setting targeted at students in their second year of German instruction at the college level. The purpose of this study is two-fold. First, the study analyzes the conversational resources that are co-constructed in the test discourse to maintain mutual understanding, which is considered the basis for interactional competence. Second, the study examines the impact of task (jigsaw task and discussion task) and speaking ability-level combination (same and different ability) in the test-taker pair on the co-constructed test discourse and thus on the deployment of the conversational resources to maintain intersubjectivity. In that respect, this study also seeks to analyze how the identified conversational resources are involved in establishing and negotiating language ability identities that are displayed in the test discourse. Conversation analytic conventions were used to investigate the interactional resources that test takers deploy to maintain mutual understanding. The procedures of repair (self-repair in response to other-initiated repair, inter-turn delays, and misunderstandings as well as other-repair in conjunction with word search activities) that emerged from the inductive analysis of the test discourse have broadened the conceptualization of interactional competence in the context of paired speaking assessments. Frequency distributions of the interactional resources were created to provide a better understanding of the impact of task and ability-level combination on the co-constructed repair procedures. The rationale behind this analysis is the general understanding of language testers that both resources and context influence test performance. The findings from the quantitative analysis suggest that there are more similarities than differences in repair use across the jigsaw task and the discussion task. In addition, even though some trends in the co-construction of repair procedures may be attributed to the higher or lower speaking ability of the test takers, the relationship between the ability-level combination in the pair and the use of repair seems to be rather variable. Finally, to learn more about the interrelationship between test takers’ speaking ability and interactional competence, this dissertation also approached speaking ability in terms of test takers’ co-constructed language ability identities that are displayed in the test discourse. By means of single case analyses, the study provided a detailed picture of the relationship between language ability identities and the procedures of repair, both of which are co-constructed at the discourse level. The findings from the conversation analysis show that the speaker who provides the repair is usually able to position himself or herself as the more competent or proficient speaker in the test discourse.

Acid-sensing ion channel 1A (ASIC1A) is abundant in the nucleus accumbens (NAc), a region known for its role in addiction. Because ASIC1A has been previously suggested to promote associative learning, we hypothesized that disrupting ASIC1A in the NAc would reduce drug-associated learning and memory. However, contrary to this hypothesis, we found that disrupting ASIC1A in the NAc increased cocaine-conditioned place preference, suggesting an unexpected role for ASIC1A in addiction-related behavior. Investigating the underlying mechanisms, we identified a novel postsynaptic current during neurotransmission mediated by ASIC1A and ASIC2 and thus well-positioned to regulate synapse structure and function. Consistent with this possibility, disrupting ASIC1A altered dendritic spine density and glutamate receptor function, and increased cocaine-evoked plasticity in AMPA-to-NMDA ratio, all resembling changes previously associated with cocaine-induced behavior. Together, these data suggest ASIC1A inhibits plasticity underlying addiction-related behavior, and raise the possibility of therapies for drug addiction by targeting ASIC-dependent neurotransmission. The amygdala plays critical roles in the learning and expression of fear-related behavior. Previous studies have implicated the amygdala in CO2-evoked fear-like behavior in mice; however, a more recent study demonstrated that humans lacking the amygdala bilaterally experience fear and panic with CO2-inhalation. Because all subjects lacking the amygdala had panic attacks after inhaling CO2 compared to only 25% of controls, this data suggests the amygdala may play an inhibitory role in CO2-evoked panic. To assess the role of the amygdala in CO2-evoked behaviors in mice, we lesioned the amygdala and optogenetically stimulated different amygdalar nuclei. We found that large unilateral and bilateral amygdala lesions caused the emergence of escape-like jumping behavior in mice exposed to CO2 and a relative deficit in CO2-evoked freezing. This jumping behavior depended on the dorsal periaqueductal gray, a brain area previously associated with panic attacks. Additionally, the putative CO2 chemosensor ASIC1A and ASIC2 are not necessary for CO2-evoked jumping, and may even play an inhibitory role in this behavior. Optogenetic manipulation of the amygdala revealed that stimulation of the basolateral amygdala enhanced jumping behavior and inhibited freezing behavior. This may be due to the basolateral amygdala's ability to inhibit the main output center of the amygdala, the central nucleus. Together, these results suggest that different amygdalar nuclei differentially modulate CO2-evoked behavior by regulating the switch between mobile and immobile defense responses. Additionally, they provide additional evidence that amygdalar dysfunction may contribute to panic disorder.

This is a qualitative, mixed-methods study that focuses on the experiences of pre-service teachers in an art methods for non-majors class. The purpose of this study is to describe the process of transforming pre-service elementary teachers’ apprehensive feelings and experiences about creating art. An examination of play, Thirdspace pedagogy, and contextual exploration within a humanistic approach all inform this study. The dataset exposed themes of apprehension and reluctance to art-making, community building, preconceptions about art and art-making, exploration, non-prescribed outcomes, learning from mistakes, and identity. The results of this study show evidence that explorative methods can alter the conceptions and approaches to art of pre-service teachers in an art methods for non-majors course. As a researcher, it is my hope that this study will impact art educators’ views of teaching art methods courses to non-majors.

The purpose of the study was to identify teacher perception regarding the effects of NCLB on the development of knowledge among elementary school students in two school districts in a Midwestern state. I applied a case-study design to address the research questions, with data obtained from interviews with eight experienced school teachers, who reported on the state of the cognitive development of their students. Epistemology, specifically social and virtue epistemology, served as the theoretical framework for the analysis of the data, thus filling a gap in the literature for an epistemological study of the effects of NCLB. The hypothesis for the study was that NCLB is detrimental to the development of knowledge among elementary students by placing too much emphasis on mandated standardized testing, and by limiting the curriculum to the subjects that are under the requirements for Adequate Yearly Progress (YAP). The analysis of teacher input indicates that NCLB hinders the development of knowledge among elementary school students. This is because educators are constrained by excessive testing requirements, and are thus not able to foster in their students the intellectual virtues necessary for the development of the lifelong learner, the student who is capable of and understands that learning continuous throughout one’s life. Future research is needed to link the scholarship on intellectual virtues to the education of school children, making of the virtues a central and intrinsic part of the educational effort.