Publications by authors named "Sandra M Troxell-Smith"

Humans are a constant in the lives of captive animals, but the effects of human-animal interactions vary. Research on the welfare impacts of human-animal interactions focus predominantly on mammals, whereas fish have been overlooked. To address this lack of research, we assessed the impacts of aquarium visitors on the behaviors of ten members of four elasmobranch species: an Atlantic stingray (), four southern stingrays (), two blue-spotted maskrays (), and three fiddler rays ().

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Foraging is a three-stage process during which animals visit patches, consume food and quit. Foraging theory exploring relative patch quality has mostly focused on patch use and quitting decisions, ignoring the first crucial step for any forager: finding food. Yet, the decision to visit a patch is just as important as the decision to quit, as quitting theories can only be used if animals visit patches in the first place.

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What does domestication select for in terms of foraging and anti-predator behaviors? We applied principles of patch use and foraging theory to test foraging strategies and fear responses of three strains of Mus musculus: wild-caught, control laboratory, and genetically modified strains. Foraging choices were quantified using giving-up densities (GUDs) under three foraging scenarios: (1) patches varying in microhabitat (covered versus open), and initial resource density (low versus high); (2) daily variation in auditory cues (aerial predators and control calls); (3) patches with varying seed aggregations. Overall, both domestic strains harvested significantly more food than wild mice.

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Spinal and bulbar muscular atrophy (SBMA) is a late-onset, progressive neurodegenerative disease linked to a polyglutamine (polyQ) expansion in the androgen receptor (AR). Men affected by SBMA show marked muscle weakness and atrophy, typically emerging midlife. Given the androgen-dependent nature of this disease, one might expect AR antagonists to have therapeutic value for treating SBMA.

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Background: Spinal bulbar muscular atrophy (SBMA) is caused by a CAG repeat expansion mutation in the androgen receptor (AR) gene, and mutant AR is presumed to act in motoneurons to cause SBMA. However, we found that mice overexpressing wild-type (wt) AR solely in skeletal muscle fibers display the same androgen-dependent disease phenotype as when mutant AR is broadly expressed, challenging the assumptions that only an expanded AR can induce disease and that SBMA is strictly neurogenic. We have previously reported that AR toxicity was ligand dependent in our model, and that very few transgenic (tg) males survived beyond birth.

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