In most Puerto Rico reservoirs, Largemouth Bass Micropterus salmoides are typically fast-growing with distributions composed of distinct year-classes. Cerrillos Reservoir, however, displays the classic characteristics of a crowded bass population common in temperate lakes and ponds with fish stockpiling into a single modal distribution of slow-growing fish. This developed shortly after stocking in 1997, with the population quickly expanding to carrying capacity. Consequently, relative weight declined from above 100 to about 80 and the population was mostly composed of fish <=350 mm. A protected slot limit (356-508 mm) was implemented; however, limited effort and angler attitudes towards harvest of small bass prevented the success of this regulation, which was subsequently removed. In this dissertation, I examined the efficacy of using targeted management harvests for improving growth, size structure, and condition of Largemouth Bass in Cerrillos Reservoir. I used bioenergetics modeling to simulate the effects of targeted harvests. I predicted annual consumption of stock and quality-sized Largemouth Bass and used these estimates to model the effects of population reduction on consumption and growth of remaining bass. To validate the model, experimental removals of Largemouth Bass from the crowded size classes (200-380 mm) were conducted in 2012 and 2013. In these two years, I removed 20% and 22% of the total biomass, respectively. Following the experimental removals, mean condition of Largemouth Bass increased from 83 to 90, and increases were observed in all Largemouth Bass size categories. The reduction in predator abundance resulted in increased prey availability and smaller size structure of sunfish (Lepomis spp.) and tilapia (Coptodon and Oreochromis spp.) populations. I concluded that reducing Largemouth Bass abundance in Cerrillos Reservoir can move population dynamics toward desired management outcomes, but these actions must continue indefinitely to achieve success and sustainability. Annual management harvests are feasible but impractical, so I recommend increasing angler harvest and implementing management efforts designed to limit recruitment (e.g., shoreline rotenone application) to achieve management goals.

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Gap junctions are highly-conserved communicating junctions composed of the connexin family of proteins. In addition to this channel function, gap junctions mediate adhesive contacts at extracellular domains, and are host to a variety of signalling metabolites at intracellular surfaces. In this thesis, I explore the emerging theme of the connexin interactome. Starting with a non-biased proteomic approach, I identified endogenous protein interactions with the predominant liver and oligodendrocyte connexin, connexin32 (Cx32). Here, I identified novel mitochondrial protein interactions suggesting that Cx32 might localize to mitochondrial membranes, as has been reported for cardiac Cx43. Following proteomic quantitation of WT and Cx32 KO membranes, I determined that loss of Cx32 specifically induces mitochondrial protein expression. Bioenergetic analysis of isolated mitochondria then confirmed that oxygen consumption and rates of reactive oxygen species (ROS) generation were elevated in Cx32 KO mitochondria. In addition to novel intracellular connexin protein interactions, we hypothesized that connexin-mediated glial cell:cell interactions were responsible for mediating fate decisions in the complex hippocampal neurogenic niche environment. We identified that Cx32-mediated glial cell:cell interactions exert significant proliferative and fate specifying pressures on hippocampal progenitor cell types, wherein the loss of Cx32 enables improved histological and functional regeneration following excitotoxic injury. Together, this thesis identifies novel connexin-mediated signalling pathways that provide mechanistic insight into both intracellular and extracellular interactomedependent functions for Cx32, and outlines a potentially transformative avenue for brain repair.

INTRODUCTION: The detection of a second inorganic phosphate (Pi) resonance, a possible marker of mitochondrial content in vivo, using phosphorus magnetic resonance spectroscopy (31P- MRS) at 3T is technically challenging, which may prevent its reproducible quantification. PURPOSE: To determine the reproducibility of resting alkaline inorganic phosphate (Pialk) measurement using 31P-MRS in human skeletal muscle at 3 tesla (T). METHODS: Resting 31P- MRS of the quadriceps muscles was acquired on two separate visits, within seven days, in 13 healthy, sedentary to moderately active young adults using a whole-body 3T MR system. Measurement variability related to coil position, shimming procedure, and spectral analysis were also quantified. 31P-MRS data were acquired with a 31P/1H dual-tuned surface coil positioned on the quadriceps using a pulse-acquire sequence. Test-retest absolute and relative reproducibility were analyzed using coefficient of variation (CV) and intra-class correlation coefficients (ICC), respectively. RESULTS: Pialk demonstrated a within-subject reproducibility marginally greater then the 10% cutoff (CV: 10.6 ± 5.4%; ICC: 0.80), but still appropriate given its small concentration in relation to other 31P metabolites. Proximo-distal change in coil positioning along the length of the quadriceps induced large variability in Pialk quantification (CV: 21.1%). In contrast, measurement variability due to repeated shims on consecutive scans from the same muscle sample (CV: 6.6%), and the automated spectral processing procedure, were minor (CV: 2.3%). Both metrics of absolute and relative reproducibility of Pialk were of similar magnitude to other well-resolved metabolites (e.g., phosphocreatine, Pi, and phosphodiester). CONCLUSION: Using multiple metrics, the present study established the high reproducibility of Pialk quantification by 31P-MRS using a surface coil on the quadriceps muscle at 3T. However, large variability in Pialk quantification can originate from positioning the coil on the most distal part of the quadriceps, which should be avoided due to shimming inhomogeneity.

Mercury poses significant challenges to human health and fisheries management. Historical industrial practices in Waynesboro, Virginia left portions of the Shenandoah River basin contaminated with mercury and stringent health advisories for fish consumption. I investigated processes affecting the bioaccumulation of mercury in Catostomus commersoni, Ictalurus punctatus, Lepomis auritus, and Micropterus dolomieu by studying food habits, total mercury and methylmercury in common prey items, and bioaccumulation dynamics of methylmercury in the mercury contaminated South River and South Fork of the Shenandoah River and uncontaminated North River. Additionally, I evaluated sexual and seasonal variations of total mercury in M. dolomieu in the South Fork of the Shenandoah River. Algae, aquatic insects, crayfish, detritus, and fish accounted for 75-97% of the diet. Total mercury in aquatic invertebrates and forage fish in contaminated rivers ranged from 66.7-398.3 and 198.0-594.9 ng/g wet weight, while total mercury in aquatic invertebrates and forage fish in the reference river were 4.4 and 29.3 ng/g. Model simulations indicated that dietary pathways accounted for 87% of methylmercury uptake by fish in contaminated rivers, but only 57% in the reference river. Total mercury in M. dolomieu was 19-20% higher in females than males and 14-21% higher during spring than summer and fall. Results of this study indicate that bioenergetics-based bioaccumulation models are valuable tools for evaluating field data, identifying processes critical to contaminant accumulation, and comparing outcomes of alternative management options associated with pollution control, ecosystem management, and/or restoration activities for management guidance prior to costly expenditures. / Master of Science

Annual energy budgets of dominant benthic macro-invertebrates were examined during November 1973 to October 1974 from the benthos of a small pond ecosystem in north-central Texas. Estimates of annual secondary production (Hynes and Coleman 1968) were Procladius s. (Diptera, Chironimidae), 2.4 g m^-2 y^-1 (13 kcal m^-2 y^-1 ); Tendipes decorus (Diptera, Chironomidae), 6.0 g m^-2 y^-1 (40 kcal m^-2 y^-1 ); Brachycercus sp. (Ephemeroptera, Caenidae), 1.9 g m^-2 y^-1 (11 kcal m^-2 y^-1). Energy metabolism was measured in the laboratory at six seasonally encountered temperatures (5, 10, 15, 20, 25, and 30 C) on an acclimatization basis, and then extrapolated to the field. Estimates of annual energy metabolism are Procladius sp., 5.0 kcal m^-2 y^-1 ; Tendipes decorus, 17.2 kcal m^-2 y^-1 ; Brachycercus sp. 40.0 kcal m^-2 y^-1.

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Dans les années 20, Otto Warburg émit l’hypothèse que l’altération des mitochondries est la cause du développement du cancer bien qu’il reconnaissait l’existence de tumeurs oxydatives. Egalement, Weinhouse (1950) parmi d’autres, a établi qu’une respiration mitochondriale défectueuse n’était pas une caractéristique systématique du cancer et Peter Vaupel a suggéré dans les années 90 que l’oxygénation de la tumeur était le facteur limitant de la production énergétique de la mitochondrie dans le cancer plutôt que la capacité mitochondriale elle-même. Cette thèse ainsi que des études récentes montrent clairement que les mitochondries sont fonctionnelles dans les tumeurs et la discipline d’oncobioénergétique a identifié Myc, Src, Oct1 et Ras comme des oncogènes pro-OXPHOS. De plus, l’adaptation des cellules cancéreuses à l’aglycémie, la symbiose métabolique entre les régions hypoxiques et normoxiques des tumeurs ainsi que l’hypothèse de Reverse Warburg effect supportent le rôle crucial des mitochondries dans la survie d’un groupe de tumeurs. Par conséquent, les mitochondries sont maintenant considérées come des cibles potentielles pour la thérapie anti-cancéreuse et des tentatives incluant la modulation bioénergétique pourraient être considéré pour tuer les cellules cancéreuses. Nous montrons l’effet anti-cancéreux de deux modulateurs mitochondriaux et disséquons leur mécanisme d’action. / In the 1920s, Otto Warburg first hypothesized that mitochondrial impairment is a leading cause of cancer although he recognized the existence of oxidative tumors. Likewise, Weinhouse (1950) and others found that deficient mitochondrial respiration is not an obligatory feature of cancer and Peter Vaupel suggested in the 90s that tumor oxygenation rather than OXPHOS capacity was the limiting factor of mitochondrial energy production in cancer. This thesis and recent studies now clearly indicate that mitochondria are highly functional in tumors and the field of oncobioenergetic identified Myc, Src, Oct1 and RAS as pro-OXPHOS oncogenes. In addition, cancer cells adaptation to aglycemia, metabolic symbiosis between hypoxic and non-hypoxic tumor regions as well the reverse Warburg hypothesis support the crucial role of mitochondria in the survival of a subclass of tumors. Therefore, mitochondria are now considered as potential targets for anti-cancer therapy and tentative strategies including a bioenergetic profile characterization of the tumor and the subsequent adapted bioenergetic modulation could be considered for cancer killing. We show anti-cancer effects of two mitochondrial modulators and dissect their mechanism of action.

N,N,N\',N \'-tetrametil-p-fenilenodiamina (TMPD) catalisa a autoxidação de coenzimas piridínicos (NADH, NADPH) e modelos (ClBCH ,ClPCH ) ao cátion piridínico com rendimentos de 80-100%. A velocidade destas reações mostrou dependência de primeira ordem com respeito à concentração da 1,4-dihidronicotinamida e de meia ordem em relação às concentrações de O2 e TMPD. Estes dados cinéticos e testes com captadores de ion superóxido e superóxido dismutase indicam que os radicais HO&#8226;2 oriundos da autoxidação lenta do TMPD promovem a oxidação da dihidronicotinamida numa reação em cadeia; no término os radicais HO&#8226;2 se aniquilam por dismutação. O mecanismo proposto também é confirmado (1º) pela razão kC-H/kC-D=2,3 quando se substitui um dos hidrogênios do C4 de ClBCH por deutério, (2º) pelas idênticas velocidades iniciais em H2O e D2O, (3º) pelo valor da Ea = 10 kcal/mol na autoxidação do NADH e (4º) pelo aumento da velocidade de pH = 7,8 a pH 6,5. TMPD também promove a autoxidação do derivado 5, 6-hidratado (PHTN) da dihidronicotinamida ao cátion piridínico (ClPC+) apenas de fosfato ou arsenato estão presentes. O ClPC+ nã o se forma a partir do ClPCH em equilíbrio com o PHTN. Muito provavelmente se forma a partir do intermediário fosforilado no C6 por oxidação no C4 seguida de eliminação de fosfato. Quando PHTN e ClPCH foram oxidados pelo sistema O2/TMPD na presença de fosfato de piridínio ou de tetra-n-butilamônio em meio piridínico houve formação de pirofosfato, isolado por cromatografia de papel e por resina de troca aniônica. Adicionando-se ADP de tetra-n-butilamôneo ao sistema, constatou-se a formação de pirofosfato e de ATP com rendimentos mínimos de 5% e 3% , respectivamente. Por outro lado se a mistura de reação contém AMP de tetra-n-butilamôneo pôde-se verificar a formação de pirofosfato, ADP e ATP com rendimento total de 28% de \"ligações ricas\". A reação estudada foi proposta como modelo para síntese de ATP no sítio I da cadeia respiratória. / N,N,N\',N\'-tetramethyl-p-phenylenediamine (TMPD) catalyses the autoxidation of the pyridine coenzymes and of their models to the pyridinium form (80-100% yields). The first arder dependence of the rate upon the dihidronicotinamide concentration and half order upon both the O2 and TMPD concentrations, indicates that the relatively slow autoxidation of TMPD is the source of free radicals: dihydronicotinamide autoxidizes by the HO&#8226;2 chain mechanism and in the termination step the HO&#8226;2 radicals decay by dismutation. Such a mechanis is also supported by the inhibitory effects of cathecol, a scavenger of the HO&#8226;2 radical, and of superoxide dismutase, an enzyme which accelerates the dismutation of the O-2/ HO&#8226;2 species. The mecanism is further supported by (1) kC-H/kC-D=2,3 for substitution in 1-benzyl-1,4-dihydronicotinamide (ClBCH), (2) identical rates in H2O and D2O buffers, (3) Ea = 10 kcal/mole in the autoxidation of NADH and (4) the increase in rate from pH 7,8 to 6,5. TMPD promotes also the autoxidation of 1-n-propyl-6-hydroxy-1,4,5,6 - tetrahydronicotinamide (PHTN) to the 1-propyl-3-carboxamidopyridinium cation (ClPC+) provided phosphate ar arsenate are present. ClPC+ originates not from 1-n-propyl-1,4-dihydronicotinamide (ClPCH) in equilibrium with PHTN but most certainly from a C6 phosphorylated intermediate by oxidation at C4 and loss of phosphate. When PHTN an ClPCH were oxidated by the system O2/TMPD in the presence of pyridinium phosphate or tetra-n-butylammonium phosphate in pyridineas solvent, formation of pyrophosphate occurred. Pyrophosphate was isolated and identified by paper and ionic exchange resin chromatography. If tetra-n-butylammonium ADP is also present in the system, one can observe the formation of both pyrophosphate and ATP (5% and 3% minimum yields, respectively). In the presence of tetra-n-butylammonium AMP there, formation of pyrofosphate, ADP and ATP occurs. The total yield of energy rich bond is 28%. We suggest that the reaction is a model for the generation of the first ATP in the respiratory chain.