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- Creators: Barrett, The Honors College
- Creators: Gallitano, Amelia
Description
Schizophrenia risk is influenced by both genetic and environmental factors. The immediate early gene early growth response 3 (Egr3), is regulated downstream of several schizophrenia risk genes and encodes a zinc-finger transcription factor protein. Previous studies from our lab indicate that Egr3 deficient (Egr3 -/-) mice exhibit schizophrenia-like phenotypes. We also discovered decreased serotonin 2a receptors (5-HT2AR) in the Egr3 -/- mice, similar to studies that reported decreased 5-HT2ARs in schizophrenia patients. We previously reported that sleep deprivation, a mild stress, causes the over expression of Egr3 and the serotonin 2a gene (Htr2a) in the cortex. To determine whether EGR3, a transcription factor, regulates Htr2a in the prefrontal cortex after sleep deprivation, Egr3 -/-and Egr3 +/+ mice were sleep deprived for eight hours. Transgenic mice were used that expressed enhanced green fluorescent protein (EGFP) under control of the Htr2a promoter via a bacterial artificial chromosome (BAC). Immunohistochemistry was performed to identify EGFP containing cells. Data analysis revealed no significant interaction between genotype and sleep deprivation in 5-HT2AR/EGFP containing cells within the prefrontal cortex. Based on the findings of this study, more data is needed to better determine the relationship between sleep deprivation and its effect on the regulation of Htr2a through in an EGR3 dependent manner.
ContributorsReznik, Derek Lee (Author) / Wilson-Rawls, Jeanne (Thesis director) / Gallitano, Amelia (Committee member) / Anderson, Karen (Committee member) / School of Sustainability (Contributor) / School of Life Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2016-12
Description
This paper will discuss what psychological operations (PSYOP) and psychological warfare (PSYWAR) are, emphasizing the role they played in the Korean War on soldiers and POWs. It includes two dynamic, engaging personal narratives adding relevance and intrigue to the topic examined. Two types of psychological operations will be identified and discussed, the leaflet and radio broadcast. Three methods of psychological warfare in the form of bacteriological warfare allegations, brainwashing, and sleep deprivation are analyzed and the effects of these methods during wartime. All participating countries during the Korean war either used psychological operations and warfare on their enemies, or had it used on them. The key takeaway was increased understanding that PSYOP and PSYWAR are founded on truthfulness rather than falsehoods. The paper concludes with the results of the war on the players involved and the legacy of psychological operations, encompassing how it applies to our technologically advanced world today.
ContributorsGoldsteen, Elizabeth (Author) / Niebuhr, Robert (Thesis director) / Ackerman, Heather (Committee member) / Barrett, The Honors College (Contributor) / College of Integrative Sciences and Arts (Contributor)
Created2023-05
Description
Older adults tend to learn at a lesser extent and slower rate than younger individuals. This is especially problematic for older adults at risk to injury or neurological disease who require therapy to learn and relearn motor skills. There is evidence that the reticulospinal system is critical to motor learning and that deficits in the reticulospinal system may be responsible, at least in part, for learning deficits in older adults. Specifically, delays in the reticulospinal system (measured via the startle reflex) are related to poor motor learning and retention in older adults. However, the mechanism underlying these delays in the reticulospinal system is currently unknown.
Along with aging, sleep deprivation is correlated with learning deficits. Research has shown that a lack of sleep negatively impacts motor skill learning and consolidation. Since there is a link between sleep and learning, as well as learning and the reticulospinal system, these observations raise the question: does sleep deprivation underlie reticulospinal delays? We hypothesized that sleep deprivation was correlated to a slower startle response, indicating a delayed reticulospinal system. Our objectives were to observe the impact of sleep deprivation on 1) the startle response (characterized by muscle onset latency and percentage of startle responses elicited) and 2) functional performance (to determine whether subjects were sufficiently sleep deprived).
21 young adults participated in two experimental sessions: one control session (8-10 hour time in bed opportunity for at least 3 nights prior) and one sleep deprivation session (0 hour time in bed opportunity for one night prior). The same protocol was conducted during each session. First, subjects were randomly exposed to 15 loud, startling acoustic stimuli of 120 dB. Electromyography (EMG) data measured muscle activity from the left and right sternocleidomastoid (LSCM and RSCM), biceps brachii, and triceps brachii. To assess functional performance, cognitive, balance, and motor tests were also administered. The EMG data were analyzed in MATLAB. A generalized linear mixed model was performed on LSCM and RSCM onset latencies. Paired t-tests were performed on the percentage of startle responses elicited and functional performance metrics. A p-value of less than 0.05 indicated significance.
Thirteen out of 21 participants displayed at least one startle response during their control and sleep deprived sessions and were further analyzed. No differences were found in onset latency (RSCM: control = 75.87 ± 21.94ms, sleep deprived = 82.06 ± 27.47ms; LSCM: control = 79.53 ± 17.85ms, sleep deprived = 78.48 ± 20.75ms) and percentage of startle responses elicited (control = 84.10 ± 15.53%; sleep deprived = 83.59 ± 18.58%) between the two sessions. However, significant differences were observed in reaction time, TUG with Dual time, and average balance time with the right leg up. Our data did not support our hypothesis; no significant differences were seen between subjects’ startle responses during the control and sleep deprived sessions. However, sleep deprivation was indicated with declines were observed in functional performance. Therefore, we concluded that sleep deprivation may not affect the startle response and underlie delays in the reticulospinal system.
Along with aging, sleep deprivation is correlated with learning deficits. Research has shown that a lack of sleep negatively impacts motor skill learning and consolidation. Since there is a link between sleep and learning, as well as learning and the reticulospinal system, these observations raise the question: does sleep deprivation underlie reticulospinal delays? We hypothesized that sleep deprivation was correlated to a slower startle response, indicating a delayed reticulospinal system. Our objectives were to observe the impact of sleep deprivation on 1) the startle response (characterized by muscle onset latency and percentage of startle responses elicited) and 2) functional performance (to determine whether subjects were sufficiently sleep deprived).
21 young adults participated in two experimental sessions: one control session (8-10 hour time in bed opportunity for at least 3 nights prior) and one sleep deprivation session (0 hour time in bed opportunity for one night prior). The same protocol was conducted during each session. First, subjects were randomly exposed to 15 loud, startling acoustic stimuli of 120 dB. Electromyography (EMG) data measured muscle activity from the left and right sternocleidomastoid (LSCM and RSCM), biceps brachii, and triceps brachii. To assess functional performance, cognitive, balance, and motor tests were also administered. The EMG data were analyzed in MATLAB. A generalized linear mixed model was performed on LSCM and RSCM onset latencies. Paired t-tests were performed on the percentage of startle responses elicited and functional performance metrics. A p-value of less than 0.05 indicated significance.
Thirteen out of 21 participants displayed at least one startle response during their control and sleep deprived sessions and were further analyzed. No differences were found in onset latency (RSCM: control = 75.87 ± 21.94ms, sleep deprived = 82.06 ± 27.47ms; LSCM: control = 79.53 ± 17.85ms, sleep deprived = 78.48 ± 20.75ms) and percentage of startle responses elicited (control = 84.10 ± 15.53%; sleep deprived = 83.59 ± 18.58%) between the two sessions. However, significant differences were observed in reaction time, TUG with Dual time, and average balance time with the right leg up. Our data did not support our hypothesis; no significant differences were seen between subjects’ startle responses during the control and sleep deprived sessions. However, sleep deprivation was indicated with declines were observed in functional performance. Therefore, we concluded that sleep deprivation may not affect the startle response and underlie delays in the reticulospinal system.
ContributorsGopalakrishnan, Smita (Author) / Honeycutt, Claire (Thesis director) / Petrov, Megan (Committee member) / Harrington Bioengineering Program (Contributor) / School of Mathematical and Statistical Sciences (Contributor) / Barrett, The Honors College (Contributor)
Created2020-05