Non-indigenous species can profoundly alter the ecosystems they invade and impact local economies. Growth and body condition declines of commercially fished Great Lakes lake whitefish coincide with the establishment of non-native dreissenid mussels and the cladoceran Bythotrephes longimanus. Declines in lake herring abundance—a key prey item for other commercially important species—have also been reported. Though additional stressors such as climate change may have contributed to changes in coregonid populations, they have not been thoroughly evaluated. Here, I present data that condition and contaminant declines in coregonids are associated with increasing density or warming climate, but growth declines in lake whitefish are likely due to ecosystem changes associated with dreissenids and Bythotrephes. In South Bay, Lake Huron, changes in lake whitefish diet composition and stable isotope signatures were consistent with increased reliance on nearshore resources after dreissenid establishment; lake whitefish occupied shallower habitats and experienced declines in mean diet energy densities post-dreissenid invasion. Growth of South Bay lake whitefish declined after environmental effects were statistically removed, whereas condition declines were explained best by changes in lake whitefish density. Among four lake whitefish populations, growth declined after dreissenids established, but not in uninvaded reference populations. Growth also declined among four lake whitefish populations after the establishment of Bythotrephes relative to reference populations. In contrast with growth, condition of lake whitefish did not change as a result of dreissenid or Bythotrephes invasion. Bioenergetic models revealed that activity rates increased and conversion efficiencies decreased in lake whitefish populations exposed to dreissenids, despite higher consumption rates in populations with dreissenids present. Condition declines among many lake whitefish and lake herring populations (and declines in mercury among herring populations) reflected regional differences and were not related to the presence of Bythotrephes or Mysis relicta. Declines in condition were more pronounced in northwest Ontario populations where climate has changed more dramatically than in southern Ontario. This work suggests that projected range expansions of dreissenid mussels and Bythotrephes will likely affect native fisheries, and their effect on these fisheries may be exacerbated by declining fish condition associated with climate change.

Non-indigenous species can profoundly alter the ecosystems they invade and impact local economies. Growth and body condition declines of commercially fished Great Lakes lake whitefish coincide with the establishment of non-native dreissenid mussels and the cladoceran Bythotrephes longimanus. Declines in lake herring abundance—a key prey item for other commercially important species—have also been reported. Though additional stressors such as climate change may have contributed to changes in coregonid populations, they have not been thoroughly evaluated. Here, I present data that condition and contaminant declines in coregonids are associated with increasing density or warming climate, but growth declines in lake whitefish are likely due to ecosystem changes associated with dreissenids and Bythotrephes. In South Bay, Lake Huron, changes in lake whitefish diet composition and stable isotope signatures were consistent with increased reliance on nearshore resources after dreissenid establishment; lake whitefish occupied shallower habitats and experienced declines in mean diet energy densities post-dreissenid invasion. Growth of South Bay lake whitefish declined after environmental effects were statistically removed, whereas condition declines were explained best by changes in lake whitefish density. Among four lake whitefish populations, growth declined after dreissenids established, but not in uninvaded reference populations. Growth also declined among four lake whitefish populations after the establishment of Bythotrephes relative to reference populations. In contrast with growth, condition of lake whitefish did not change as a result of dreissenid or Bythotrephes invasion. Bioenergetic models revealed that activity rates increased and conversion efficiencies decreased in lake whitefish populations exposed to dreissenids, despite higher consumption rates in populations with dreissenids present. Condition declines among many lake whitefish and lake herring populations (and declines in mercury among herring populations) reflected regional differences and were not related to the presence of Bythotrephes or Mysis relicta. Declines in condition were more pronounced in northwest Ontario populations where climate has changed more dramatically than in southern Ontario. This work suggests that projected range expansions of dreissenid mussels and Bythotrephes will likely affect native fisheries, and their effect on these fisheries may be exacerbated by declining fish condition associated with climate change.

The maintenance of a functional energy balance in ectothermic fauna could be challenging in a thermally disparate environment. Biochemical adaptations at the enzyme and membrane levels allows for a set compensatory mechanism that allow the individual to maintain an energetic surplus, thus allocating energy for growth and reproduction. The present work describes how the energetic machinery in the cell, particularly the mitochondrion, could be affected by temperature changes. More specifically, this work aimed to determine how environmental temperature affects the mitochondria energetic performance of fishes from disparate thermal regimes. Mitochondrial ATP production efficiency was evaluated in fishes from polar, tropical and subtropical regions. In polar fishes, mitochondria remained functional at temperatures well beyond whole organismal critical temperatures. On the other hand, tropical and subtropical teleosts exhibited a decrease in mitochondrial efficiency at temperatures commonly found during summer seasons. This remarkable variability of mitochondrial thermal sensitivity may restrict the energy allocated for growth and reproduction during the summer months in tropical and subtropical regions. The observed variation in the thermal window of tolerance of mitochondrial function in fishes provides further insight into how the energetic machinery responds to thermal changes, like those associated with warming trends in marine ecosystems. In addition, the reduced efficiency in mitochondrial function among teleosts from latitudinal gradients suggest that warm-adapted species are close to their upper tolerance range, and further warming trends could severely impact the energy budget of fishes.

Changes in intracellular redox homeostasis are implicated in both normal cell signaling and as pathophysiological mechanisms contributing to a variety of age-related diseases, including diabetes, atherosclerosis, neurodegenerative conditions, and cancer. Though a variety of well described mechanisms exist to counterbalance the overproduction of cellular oxidants and maintain optimal intracellular redox poise, the understanding of the mechanism(s) through which cellular redox homeostasis regulates cell signaling functions is less well understood. Here, we demonstrate that signaling by the immediate early gene / orphan nuclear hormone receptor NGFI-B (Nur77, TR3), which functions pleiotropically in the regulation of cell growth, metabolism, differentiation and death in diverse tissues, is redox-regulated at both the level of induction and NGFI-B-dependent gene transcription. Using co-immunoprecipitation experiments in cells, we also identified a novel interaction between NGFI-B and the cytoplasmic thiol-reducing catalyst thioredoxin1 (Trx1), that, similar to DTT, blocks NGFI-B-dependent gene expression in a manner that depends on the Trx1 active site cysteines. Together these observations add NGFI-B-dependent gene expression to a growing portfolio of transcription factor pathways that are redox-regulated. NGFI-B, in addition, appears to regulate the mitochondrial membrane potential in L6 skeletal myoblasts. NGFI-B is indispensible for T-cell receptor-mediated apoptosis and induces cell death in a variety of cell types in response to diverse pro-apoptotic stimuli. Like p53, translocation of NGFI-B from the nucleus to the mitochondria may be a critical aspect of its pro-apoptotic function. Interestingly, we found that enforced NGFI-B expression in L6 skeletal muscle myoblasts led to a significant decrease of MMP that peaked 48hr after transfection and did not require a cell death-inducing stimulus. Moreover, NGFI-B transfected cells had no increase in mitochondrial cytochrome C release despite loss of MMP at 48 hr. Combined, these data suggest that loss of MMP in muscle cells may be an early event in the apoptotic process regulated by NGFI-B. This, along with the redox regulation of NGFI-B, provides unique evidence of a relationship between the mitochondria, mitochondrial by-products, ROS, and the regulation of and by the transcription factor NGFI-B. / text

This thesis is a series of investigations into the regulation of skeletal muscle mitochondrial metabolism. Novel regulatory mechanisms regarding mitochondrial fatty acid oxidation are continually being identified and alterations in skeletal muscle mitochondrial metabolism have been implicated in the pathogenesis of type II diabetes (T2DM). Therefore, advancing our basic understanding of mitochondrial regulatory processes is required to provide insight into the progression of T2DM. In study one, the utilization of knockout mice for the putative mitochondrial fatty acid transport protein FAT/CD36, showed that mitochondrial FAT/CD36 plays a functional role in mitochondrial long chain fatty acid (LCFA) oxidation. Specifically, FAT/CD36 was found to be located on the outer mitochondrial membrane (OMM) upstream of acyl-CoA synthetase. In study two, it was observed that in rat muscle, malonyl-CoA (M-CoA) inhibition kinetics of carnitine palmitoyltransferase I (CPT-I) display a more physiological IC50 in permeabilzed muscle fibre bundles (PmFB) compared to isolated mitochondria. These data suggest that the cytoskeleton may have a role in regulating M-CoA inhibition. Additionally, a significant effect of LCFA-CoA on M-CoA inhibition kinetics was observed. These data indicate that M-CoA content does not need to decrease to promote an increase in CPT-I flux. Finally, in a model of T2DM (ZDF rat), submaximal ADP-stimulated respiration rates and the content of adenine nucleotide translocase 2 (ANT2) content were depressed compared to lean control animals. Resveratrol treatment in ZDF rats recovered these declines concomitantly with improving insulin-stimulated skeletal muscle glucose uptake and the cellular redox state. A number of novel findings are presented, specifically, 1) a functional role for mitochondrial FAT/CD36 in mitochondrial LCFA oxidation was confirmed and the topology of this protein along the OMM is expanded upon, 2) M-CoA inhibition kinetics of CPT-I were re-evaluated in PmFB and a regulatory role of LCFA-CoA on M-CoA inhibition kinetics is established, and 3) submaximal ADP-stimulated respiration rates and ANT2 content are depressed in the ZDF rat and resveratrol supplementation prevents these decrements.

On the forefront of the recent expansion in biofuels research is the production of cellulosic ethanol, or ethanol produced from a cellulose containing feedstock. Cellulose is a six-carbon polysaccharide found in most plant life and is one of the most abundant organic compounds on the planet. While the first generation of ethanol facilities uses sugar and starch based (corn kernels) plants as their feedstock, the next generation will use cellulosic sources such as wood chips, switchgrass, and forest residues. These cellulosic sources require far less energy and resources to grow and harvest, and are also much more abundant. A cellulosic source widely available in Georgia and much of the southeastern US is southern pine. This study involves the modeling of a complete 2000 dry ton per day pine to ethanol production facility with the AspenTech3 software Aspen Plus, which outputs a mass and energy balance as well as the capital cost of the equipment. A key parameter which affects the competitiveness of cellulosic ethanol is the internal processing energy required to convert the pine to ethanol. As a result, the heat and electrical load of every component within the facility is modeled and then quantified through the Aspen Plus simulation. After this base case energy analysis is developed, various alternate plant configurations are integrated in an attempt to reduce this process energy requirement. The material that is not fermented into ethanol is burned on-site to provide steam and electricity to the plant, as well as excess electricity to be sold to the grid as a byproduct. As the facility processing energy requirement is decreased, more excess electricity is available for sale. The implementation of the alternate distillation scenarios effectively reduce the internal processing energy in a manner as to increase the amount of excess electricity sold to the grid by 13.5%. The additional equipment required in this alternate scenario returns a simple payback period of 1.1 years through the additional revenue of the increased electricity sale.

Thesis (Ph.D.)--Victoria University (Melbourne, Vic.), 2007.

Thesis (Ph.D.)--Københavns universitet, 2005. / Abstract in Danish. Title from title screen (viewed on July 10, 2008). Title from document title page. Includes bibliographical references. Available in PDF format via the World Wide Web.

Thesis (M.S.)--Humboldt State University, 2005. / Includes bibliographical references (leaves 77-82).

Thesis (Ph. D.)--University of Missouri-Columbia, 1996. / Typescript. Vita. Includes bibliographical references (leaves 81-90). Also available on the Internet.