Previous studies on fishes exposed to effluent from the Key Lake uranium mill in northern Saskatchewan have demonstrated elevated lipids in young-of-the-year pike (Esox lucius), deformities in larval pike and decreased survival of fathead minnows (Pimephales promelas). The objectives of this thesis were to evaluate possible factors that could be contributing to altered bioenergetics of juvenile northern pike inhabiting lakes receiving effluent from the Key Lake operation and to examine the effects of effluent exposure on biomarkers of oxidative stress and histopathology of target organs. Although glycogen and triglycerides stores were significantly greater in pike from exposure lakes compared to the reference, triglycerides stores of juvenile pike prey items showed no overall differences among lakes. Measures of parasitism, however, were negatively correlated with pike bioenergetics thereby reflecting a possible energetic cost of parasitism on reference lake fish. The degree of infection by intestinal parasites and gill monogeneans was greatest in reference pike and intermediate in low exposure pike, whereas high exposure pike harboured no parasites. <p>Arsenic, nickel and selenium are elevated in lakes downstream of the Key Lake mill and have been shown to be associated with increased reactive oxygen species (ROS) in biological systems causing oxidative stress. The potential for oxidative stress was assessed in pike liver and kidney using several biomarkers. Overall, the concentrations of total, reduced and oxidized glutathione and the ratio of oxidized to reduced glutathione did not differ significantly among exposure and reference pike. The activity of glutathione peroxidase was greater in high exposure than reference liver whereas, contrary to predictions, lipid peroxidation was greater in reference than exposure pike tissues. <p>Histopathological evaluations revealed greater kidney and gill pathology in reference lake pike, whereas for liver, hepatocyte morphology differed among lakes without any clear signs of pathology. Trace metal analyses of muscle showed that eight elements (arsenic, cobalt, copper, iron, molybdenum, selenium, thallium, uranium) were significantly elevated in exposure pike. These results provide only limited evidence of oxidative stress in exposure pike tissues and no evidence of histopathology despite indications that metals are bioaccumulating in tissue. Overall, the results from this thesis suggest that the health and condition of juvenile northern pike living downstream of the Key Lake uranium mill may not be compromised by effluent exposure.

Thesis (Ph. D.)--University of Missouri-Columbia, 2001. / No leaf vii so pagination is misnumbered. Typescript. Vita. Includes bibliographical references. Also available on the Internet.

Thesis (Ph. D.)--University of Missouri-Columbia, 2001. / No leaf vii so pagination is misnumbered. Typescript. Vita. Includes bibliographical references. Also available on the Internet.

The black-ribbed mussel, Septifer virgatus, is a northern species which forms dominant bands in the mid-low levels of exposed rocky shores along the Northwest Pacific coast. S. virgatus is thought to reach its southern distributional limits just south of Hong Kong. In Hong Kong, mass mortalities of S. virgatus were recorded with the onset of the hot and wet season, with mussel cover decreasing at the upper limit of the mussel bed at Shek O from 82 % (~1746 ind m-2) in May to 9 % (~ 38 ind m-2) in August 2012. Elevated temperatures played an important role in driving physiological responses of the mussel, including heart rate, oxygen consumption and mantle water and haemolymph osmotic concentrations. The upper thermal limit in water (36 °C, as indicated by the Arrhenius breakpoint temperature, ABT), was unlikely to be reached by local seawater, but the ABT in air (~ 41 °C) was often lower than rock temperatures on Hong Kong shores, suggesting S. virgatus is living at its thermal limit. When immersed, both heart rates and oxygen consumption increased from 25 – 35 °C and dropped beyond 35 °C; whilst in air, haemolymph and mantle water osmolalities increased with duration (0 vs 6 hrs) and temperature (30 vs 40 °C) and 60 % of individuals died at 40 °C after 6 hours. Mortality of S. virgatus is, therefore, linked to the high temperatures and desiccation stress experienced on the shore, which are likely to impose high energetic costs. To better understand the performance of S. virgatus under natural conditions, and the energetic implications of thermal stress on its survival and fitness and hence potential distribution, a Dynamic Energy Budget (DEB) model was constructed. The model had a high goodness of fit. Mussels were predicted to live 5 years, and their main growth and energy reserves were derived from high assimilation during the hot and wet season when food was most abundant, while another slower growth period and reproduction occurred during the cool and dry season. Energy stored in the reserve during growth periods was likely to be allocated to combat thermal stress during the hot and wet season and reproduction during the cool and dry season. The DEB model was used to investigate the energy allocation strategies of S. virgatus under the most conservative and extreme scenarios associated with climate change as projected by the IPCC. The model predicted that reproductive events throughout the mussels’ life-span would be reduced by 30 – 70 %, despite an increase (18 – 470 %) in number of eggs per event. This reduction in the number of reproductive events might not be able to sustain local populations due to the high annual mortality. Such a decrease in performance and fitness, associated with not being able to reach the energy threshold necessary for somatic maintenance, suggests that S. virgatus may be limited to living lower on the shore, where conditions and duration of exposure are more benign, and ultimately experience a northwards range shift as environmental temperatures increase. / published_or_final_version / Biological Sciences / Master / Master of Philosophy

Background: As modern nations undergo demographical and epidemiological transitions, infectious diseases are replaced by non-communicable and chronic illnesses as the main source of ill-health. In particular, the obesity epidemic is of important public health concern as the prevalence of overweight and obesity continues to increase at an alarming rate globally. The trend in childhood and adolescent obesity is also escalating rapidly as people are gaining excess weight at younger ages, representing a growing threat as obesity is linked to a myriad of detrimental psychosocial and physical health consequences which may persist through adulthood. The fundamental cause of obesity is energy imbalance with energy intake exceeding energy expenditure within the human body. Total daily energy expenditures can vary substantially among individuals due to non-exercise activity thermogenesis (NEAT), which accounts for the energy expended from activities we do in daily living, including spontaneous behaviours such as fidgeting. Cumulatively, trivial activities such as fidgeting may accrue to have a significant impact on total daily energy expenditure. Studies have shown that NEAT levels increase or decrease in response to over- and under-feeding, respectively, to counterbalance changes in energy homeostasis. Therefore, fidgeting and NEAT may be an important component in maintaining weight. Decreased levels of fidgeting and NEAT has been hypothesized to be more common among obese individuals as the body fails to activate NEAT in response to over-eating, leading to weight gain. Understanding the correlates of fidgeting and non-exercise physical activity will be helpful in supplementing the design and implementation of effective strategies against obesity. Objective: To investigate the correlates of fidgeting among Hong Kong adolescents, including the association between fidgeting and weight status. Methods: Post hoc statistical analysis was conducted using secondary data from the Hong Kong Student Obesity Surveillance (HKSOS) Project from 2006-2007, which surveyed 34 678 students across 42 secondary schools in Hong Kong. Multivariate logistic regression analyses yielded crude and adjusted odds ratios for the associations of background characteristics, lifestyle characteristics, and dietary intake on fidgeting. Multinomial logistic regression analyses estimated crude and adjusted odds ratios to evaluate the associations between weight status and fidgeting/non-exercise physical activity. Results: Among the sample of Hong Kong adolescents, subjects who were male, older, born outside of Hong Kong, and had daily consumption of fresh fruits, fresh vegetables, and protein were associated with having lower odds of fidgeting. In contrast, high paternal control, high maternal control, smoking, alcohol consumption, elevated levels of daily screen time, exercise time, non-exercise physical activity time, and increased intake in deep fried/fatty foods, snacks/fizzy drinks, coffee, and tea were all associated with having higher odds of fidgeting. Fidgeting did not appear to have any significant relationships with weight status. However, non-exercise physical activity was associated with increased odds of being both underweight and overweight. Conclusions: The results from this study indicate that there are meaningful associations between fidgeting and various correlates, including background demographic characteristics and modifiable behavioural factors. Further studies are required to gain a better understanding of the correlates of fidgeting and their implications to public health. / published_or_final_version / Public Health / Master / Master of Public Health

published_or_final_version / Zoology / Doctoral / Doctor of Philosophy

Species invasions are regarded as one of the most serious threats to biodiversity and native ecosystems and our ability to predict and quantify the impacts of invasive species has been an arduous task. Since the 1840s, the Laurentian Great Lakes have experienced an exponential increase in the number of identified invasive species. The most recent, Hemimysis anomala, is a littoral freshwater mysid native to the Ponto-Caspian region of Eastern Europe. They have been identified in all of the Great Lakes (except Lake Superior), the St. Lawrence River downstream to Québec City, and inland lakes in New York State and have the potential to destabilize energy flow in aquatic food webs. Using stable isotopes of carbon (13C) and nitrogen (15N), I evaluated nearshore food web structure at four sites along Lake Ontario’s north shore spanning a gradient of Hemimysis density to determine: 1) if dominant nearshore food web pathways change seasonally, and 2) whether fish exhibit a dietary shift towards consumption of Hemimysis. Also, the effects of Hemimysis consumption on the growth of yellow perch (Perca flavescens) were quantified using bioenergetics modeling and four predictive feeding scenarios simulating Hemimysis incorporation into yellow perch diets. My results suggest Hemimysis are being incorporated into diets of round gobies, alewife and small yellow perch, which has resulted in a trophic lengthening of the food web. As Hemimysis populations continue to establish and stabilize, fish may incorporate this species into their diets at a higher rate. Based on the bioenergetic modeling, the incorporation of Hemimysis into the diets of yellow perch will have a negative impact on their growth. These negative impacts on fish growth will likely be exacerbated when the limited seasonal availability of Hemimysis, patchy distribution and predator avoidance behaviours, are considered. These results have implications surrounding the sustainability of the Great Lakes fishery as Hemimysis will likely increase competition with young fish for food and fish consumption of this new invasive may lead to reduced fish growth. / Thesis (Master, Biology) -- Queen's University, 2012-04-03 23:04:18.612

Glutamate is the primary excitatory neurotransmitter in the central nervous system. Extracellular glutamate concentrations are tightly regulated to avoid over-stimulation of glutamate receptors, which leads to a cascade of deleterious processes collectively known as excitotoxicity. Excitotoxicity is common to several neurodegenerative disorders and CNS injuries, including stroke and Alzheimer’s disease (AD). The projects described in this thesis were designed to uncover novel protective pathways in excitotoxic neurodegeneration. Excessive activation of the DNA repair enzyme, poly(ADP-ribose) polymerase-1 (PARP-1), is a convergence point for neuron death signaling in excitotoxic pathways. In AD, the peptide amyloid-β1-42 (Aβ1-42) is aberrantly produced, leading to excitotoxic neuron death in vitro. To investigate links between Aβ1-42 and PARP, we treated cultured cortical neurons with Aβ1-42 and determined whether PARP-1 contributes to neuron death. Increased neuron death was observed after Aβ1-42 exposure. A non-selective PARP-1/2 inhibitor significantly reduced Aβ1-42-induced death while elimination of PARP-1 alone was not neuroprotective. This suggests that PARP-2 or combined effects of PARP-1 and PARP-2 are required for Aβ1-42-induced neuron death. A hallmark of PARP over-activation is depletion of intracellular NAD+ and ATP levels, yet nearly all studies examining adenine nucleotide levels use separate biochemical samples to measure nucleotides individually. We developed two HPLC methods for simultaneous separation of NAD+, ATP, ADP and AMP. We determined that PARP-1 activation in astrocytes leads to near complete NAD+ depletion, followed by partial loss of ATP pools and total adenine nucleotide pools. Finally, we hypothesized that conjugated linoleic acid (CLA), a naturally occurring polyunsaturated fatty acid, is capable of enhancing neuron survival after an excitotoxic insult. Cultured cortical neurons were exposed to glutamate in the presence and absence of CLA. CLA levels likely achievable in human plasma and brain tissue during dietary supplementation regimens, protected neurons against glutamate excitotoxicity when given during or up to five hours after glutamate exposure. Several markers of mitochondrial damage and intrinsic apoptosis were examined. CLA stabilized mitochondrial membrane potential and permeability, shedding light on the mechanism of CLA neuroprotection. Overall, our research suggests a role for PARP in Aβ1-42 toxicity and identifies a novel role for CLA in neuroprotection following excitotoxicity.

Glutamate is the primary excitatory neurotransmitter in the central nervous system. Extracellular glutamate concentrations are tightly regulated to avoid over-stimulation of glutamate receptors, which leads to a cascade of deleterious processes collectively known as excitotoxicity. Excitotoxicity is common to several neurodegenerative disorders and CNS injuries, including stroke and Alzheimer’s disease (AD). The projects described in this thesis were designed to uncover novel protective pathways in excitotoxic neurodegeneration. Excessive activation of the DNA repair enzyme, poly(ADP-ribose) polymerase-1 (PARP-1), is a convergence point for neuron death signaling in excitotoxic pathways. In AD, the peptide amyloid-β1-42 (Aβ1-42) is aberrantly produced, leading to excitotoxic neuron death in vitro. To investigate links between Aβ1-42 and PARP, we treated cultured cortical neurons with Aβ1-42 and determined whether PARP-1 contributes to neuron death. Increased neuron death was observed after Aβ1-42 exposure. A non-selective PARP-1/2 inhibitor significantly reduced Aβ1-42-induced death while elimination of PARP-1 alone was not neuroprotective. This suggests that PARP-2 or combined effects of PARP-1 and PARP-2 are required for Aβ1-42-induced neuron death. A hallmark of PARP over-activation is depletion of intracellular NAD+ and ATP levels, yet nearly all studies examining adenine nucleotide levels use separate biochemical samples to measure nucleotides individually. We developed two HPLC methods for simultaneous separation of NAD+, ATP, ADP and AMP. We determined that PARP-1 activation in astrocytes leads to near complete NAD+ depletion, followed by partial loss of ATP pools and total adenine nucleotide pools. Finally, we hypothesized that conjugated linoleic acid (CLA), a naturally occurring polyunsaturated fatty acid, is capable of enhancing neuron survival after an excitotoxic insult. Cultured cortical neurons were exposed to glutamate in the presence and absence of CLA. CLA levels likely achievable in human plasma and brain tissue during dietary supplementation regimens, protected neurons against glutamate excitotoxicity when given during or up to five hours after glutamate exposure. Several markers of mitochondrial damage and intrinsic apoptosis were examined. CLA stabilized mitochondrial membrane potential and permeability, shedding light on the mechanism of CLA neuroprotection. Overall, our research suggests a role for PARP in Aβ1-42 toxicity and identifies a novel role for CLA in neuroprotection following excitotoxicity.

Migratory and resident forms of salmonid fishes, including brook trout (Salvelinus fontinalis), coexist in many river systems, but little is known about the ecological basis of these important variations in life history. This thesis elucidates the bioenergetic basis of anadromy (migration from freshwater spawning sites to the sea) in populations of brook trout. By focusing on the early stages, I provide support for the idea that variation in energy allocation leads to the adoption of migratory or resident strategies. More specifically, I demonstrate that juvenile anadromous brook trout, in the year(s) prior to migration, exhibit higher food consumption rates but lower growth efficiencies compared to residents indicating that they have higher metabolic costs. Higher metabolic costs of migratory fish are associated with the exploitation of higher current velocity habitats that provide more food but at a higher cost. This conclusion is supported by differences in delta13C (migrants have more negative delta13 C compared to residents), morphology (migrants are more streamlined than residents), and field observations (brook trout inhabiting streams with both forms exploit a wider range of habitats than those inhabiting 'pure' resident streams). Brook trout thus appear to migrate in response to energetic limitations in their local habitat. The estuary to which they migrate has better feeding opportunities, as the prey spectrum at sea is both larger and wider than that found in freshwater. This permits them to undergo diet shifts to larger prey, reducing their foraging costs, and thus most likely contributes to the trout's rapid growth rates experienced at sea. Importantly, the results of this thesis indicate that the persistence of migrant and resident strategies in the same system suggest a trade-off between local adaptability and the ability to exploit large-scale environmental heterogeneity.