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Student Name: Balazs Martonffy
Graduate Level: PhD
Field of Study/Major: SIS
Committee Chairs: Boaz Atzili (SIS, Dissertation Chair), James Goldgeier (SIS), Aaron Boesenecker (SIS)
Date of Presentation: March 22, 2019
Presentation Location: SIS 348
Time of Presentation: 12 pm
Title of Dissertation: Analysis Paralysis: Threat Perception and Incohesion in NATO, 1960 - 1980
Current international relations scholarship argues that increased threat perception results in increased alliance cohesion, but historical evidence demonstrates that alliances, when facing increasing threat, may experience a decrease in cohesion. Under what condition do these decreases in cohesion occur? This dissertation seeks to answer this puzzle by looking at a novel level of analysis and uses the alliance as an actor in examining incohesion. The dissertation argues that alliance cohesion only increases when the threat is perceived to be specific. In contrast, when the threat is only perceived as general, the alliance undergoes “analysis paralysis” resulting in losses of cohesion. This analysis paralysis occurs because the alliance’s threat perception is not homogeneous, i.e. alliance members interpret the general threat rises differently, and have different methods of response, leading to incohesion within the alliance. The dissertation demonstrate this argument through a multimethod research design, initially through the statistical analysis of three hundred twenty-five decisions NATO made between 1960 and 1980, using multivariate, binomial logistical, and multinomial logistical regressions, with statistically significant findings on four of the five proposed models. The dissertation then uses process-tracing of a single case, the 1962-1963 incohesion over the sea-based MRBM nuclear force proposal, to examine the member-state level causal mechanism underpinning the alliance-level causal argument.
Student Name: Sabrina Jones
Graduate Level: PhD
Field of Study/Major: Behavior, Cognition, and Neuroscience (BCaN)
Committee Chairs: Terry Davidson
Date of Presentation: 4/5/19
Presentation Location: Asbury 336
Time of Presentation: 1-3
Title of Dissertation: THE EFFECTS OF LIRAGLUTIDE ON THE LEARNED CONTROL OF APPETITIVE BEHAVIOR
The GLP-1 analogue liraglutide has recently received attention as being a potential therapeutic treatment for obesity as it has been associated with decreases in consumption, body adiposity, and body weight. The purpose of the present set of experiments was to assess the mechanisms underlying the ability for liraglutide to alter appetitive behavior in both male and female rats. Experiment 1 found that 12d of peripheral liraglutide injections (10 μg/kg) was able to suppress body fat accumulation and increase hippocampal-dependent inhibition. Liraglutide injections did not alter responding on hippocampal-independent excitation. Findings from Experiment 1 did not vary by sex or diet consumed. Experiment 2 found that 10 μg/kg of liraglutide was able to alter body composition without inducing taste avoidance in both male and female rats. Experiment 3 extended these findings by showing that a single pre-diet exposure to 10 μg/kg of liraglutide can blunt the effectiveness of later chronic injections at suppressing body fat accumulation. Changes in body adiposity were correlated with changes in GLUT-1 levels in the hippocampus. GLUT-1 expression was upregulation in rats chronically injected with 10 μg/kg of liraglutide, but this upregulation did not occur when rats were pre-treated with a single dose of liraglutide. Experiment 4 used the parameters identified in Experiments 2 and 3 and extended findings from Experiment 1. Liraglutide did not alter responding on a hippocampal-independent simple discrimination task, even in rats that showed changes in hippocampal-dependent behavior. Taken together, the findings from this dissertation indicate that, in doses that suppress body fat gain, liraglutide does not globally alter hippocampal-independent excitation or discrimination, but rather specifically enhances hippocampal-dependent behavioral inhibition. These results provide evidence for the conceptualization that liraglutide acts to suppress appetitive behavior via hippocampal-dependent associative mechanisms.