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- Creators: Smith, Brian
Description
Honey bee (Apis mellifera) colonies have experienced substantial losses due to colony collapse disorder (CCD) since the first officially reported cases in 2006. Many factors have been implicated in CCD, including pests, pathogens, malnutrition, and pesticide use, but no correlation has been found between a single factor and the occurrence of CCD. Fungicides have received less research attention compared to insecticides, despite the fact that fungicide application coincides with bloom and the presence of bees. Pristine fungicide is widely used in agriculture and is commonly found as a residue in hives. Several studies have concluded that Pristine can be used without harming bees, but reports of brood loss following Pristine application continue to surface across the country. The primary objectives of this study were to determine whether Pristine causes an aversive gustatory response in bees and whether consumption of an acute dose affects responsiveness to sucrose. An awareness of how foragers interact with contaminated food is useful to understand the likelihood that Pristine is ingested and how that may affect bees' ability to evaluate floral resources. Our results indicated that Pristine has no significant effect on gustatory response or sucrose responsiveness. There was no significant difference between bee responses to Pristine contaminated sucrose and sucrose alone, and no significant effect of Pristine on sucrose responsiveness. These results indicate that honey bees do not have a gustatory aversion to Pristine. A lack of aversion means that honey bees will continue collecting contaminated resources and dispersing them throughout the colony where it can affect brood and clean food stores.
ContributorsMcHugh, Cora Elizabeth (Co-author) / Jernigan, Christopher (Co-author, Committee member) / Burden, Christina (Co-author) / DeGrandi-Hoffman, Gloria (Co-author) / Smith, Brian (Thesis director) / Fewell, Jennifer (Committee member) / Barrett, The Honors College (Contributor) / School of Geographical Sciences and Urban Planning (Contributor) / School of Life Sciences (Contributor) / School of Art (Contributor)
Created2015-05
Description
Traumatic brain injury (TBI) most frequently occurs in pediatric patients and remains a leading cause of childhood death and disability. Mild TBI (mTBI) accounts for 70-90% of all TBI cases, yet its neuropathophysiology is still poorly understood. While a single mTBI injury can lead to persistent deficits, repeat injuries increase the severity and duration of both acute symptoms and long term deficits. In this study, to model pediatric repetitive mTBI (rmTBI) we subjected unrestrained juvenile animals (post-natal day 20) to repeat weight drop impact. Animals were anesthetized and subjected to sham or rmTBI once per day for 5 days. At 14 days post injury (PID), magnetic resonance imaging (MRI) revealed that rmTBI animals displayed marked cortical atrophy and ventriculomegaly. Specifically, the thickness of the cortex was reduced up to 46% beneath and the ventricles increased up to 970% beneath the impact zone. Immunostaining with the neuron specific marker NeuN revealed an overall loss of neurons within the motor cortex but no change in neuronal density. Examination of intrinsic and synaptic properties of layer II/III pyramidal neurons revealed no significant difference between sham and rmTBI animals at rest or under convulsant challenge with the potassium channel blocker, 4-Aminophyridine. Overall, our findings indicate that the neuropathological changes reported after pediatric rmTBI can be effectively modeled by repeat weight drop in juvenile animals. Developing a better understanding of how rmTBI alters the pediatric brain may help improve patient care and direct "return to game" decision making in adolescents.
ContributorsGoddeyne, Corey (Author) / Anderson, Trent (Thesis advisor) / Smith, Brian (Committee member) / Kleim, Jeffrey (Committee member) / Arizona State University (Publisher)
Created2014