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Notes: 1. The present review focuses on the gene regulatory mechanisms involved in the control of cardiac mitochondrial energy production in the developing heart and following the onset of pathological cardiac hypertrophy. Particular emphasis has been given to the mitochondrial fatty acid oxidation (FAO) pathway and its control by members of the nuclear receptor transcription factor superfamily.2. During perinatal cardiac development, the heart undergoes a switch in energy substrate preference from glucose in the fetal period to fatty acids following birth. This energy metabolic switch is paralleled by changes in the expression of the enzymes and protein involved in the respective pathways.3. The postnatal activation of the mitochondrial energy production pathway involves the induced expression of nuclear genes encoding FAO enzymes, as well as other proteins important in mitochondrial energy transduction/production pathways. Recent evidence indicates that this postnatal gene regulatory effect involves the actions of the nuclear receptor peroxisome proliferator-activated receptor α (PPARα) and its coactivator the PPARγ coactivator 1 (PGC-1).4. The PGC-1 not only activates PPARα to induce FAO pathway enzymes in the postnatal heart, but it also plays a pivotal role in the control of cardiac mitochondrial number and function. Thus, PGC-1 plays a master regulatory role in the high-capacity mitochondrial energy production system in the adult mammalian heart.5. During the development of pathological forms of cardiac hypertrophy, such as that due to pressure overload, the myocardial energy substrate preference shifts back towards the fetal pattern, with a corresponding reduction in the expression of FAO enzyme genes. This metabolic shift is due to the deactivation of the PPARα/PGC-1 complex.6. The deactivation of PPARα and PGC-1 during the development of cardiac hypertrophy involves regulation at several levels, including a reduction in the expression of these genes, as well as post-translational effects due to the mitogen-activated protein kinase pathway. Future studies aim at defining whether this transcriptional ‘switch’ and its effects on myocardial metabolism are adaptive or maladaptive in the hypertrophied heart.

Notes: SUMMARY. We describe a model of zooplankton population dynamics that accounts for differences in mortality and physiology among animals of different ages or sizes. The model follows changes in numbers of individuals and changes in individual and egg biomass through time and it expresses mortality and net assimilation as functions of animal size.We investigated the effect of egg size, age at first reproduction, and size at first reproduction on the per capita growth rates of populations growing under different conditions. In the absence of predation or when exposed to vertebrate predators that prefer large prey, populations achieve maximum growth rates when animals hatch from small eggs and reach maturity quickly at small sizes. Populations exposed to invertebrate predators that concentrate on small animals may increase r in two different ways. One way is for animals to increase juvenile survivorship by hatching from large eggs and by shortening the juvenile period. An alternative strategy is for animals to hatch from small eggs and to postpone maturity until they grow beyond the range of sizes available to their predators. Certain life history strategies maximize r if animals continue to grow after they reach maturity. By growing larger, non-primiparous females are able to hatch larger clutches and thereby increase the overall rate of population growth.The model analysis shows how to assess age-dependent mortality rates from field data. The net rate of population increase and the age distribution of eggs together provide specific, quantitative information about mortality.

Notes: 1. Rates of embryonic and post-embryonic development for Bythotrephes cederstroemi from Lakes Erie, Huron and Michigan are represented almost equally well by three empirical models across water temperatures ranging from about 12–22 °C, but at lower temperatures two of the competing models fail and an exponential development rate model proves most robust.2. Clutch masses of parthenogenic females can greatly exceed the tissue mass of the mother. Clutch size is strongly correlated with the mass of reproductive adults, accounting for over 90% of the variation among individuals. Hence, the mass gain from neonate to reproductive adult can be estimated directly from clutch size.3. Tissue stoichiometries, respiration quotients and stoichiometries of C and N metabolism were determined experimentally, extending the predictions of existing respiration and growth models.4. A predictive model for growth and production by the invertebrate predator has advantages over previous model formulations owing to our expanded calibration data base. The model is presented in a modular design that is easily upgraded as additional calibration data become available.

Notes: 1. Seasonal termination of the vernal clear-water phase in Long Lake, Grand Traverse Co., Michigan coincided with severe size-selective predation on juvenile Daphnia pulicaria from 0.8 to 1.8 mm in length. This could be caused by predation by age-0 yellow perch (Perca flavescens) or by the exotic predatory zooplankter Bythotrephes cederstroemi.2. During the initial decline of Daphnia, Ivlev’s electivity coefficient for yellow perch from 15.0 to 20.0 mm in length was 0.50 for copepods and −0.75 for D. pulicaria.3. Bioenergetics modelling of both yellow perch and Bythotrephes demonstrates that, during the initial Daphnia decline, Bythotrephes consumed 1.5–5 times greater total mass than yellow perch. Furthermore, models in which Bythotrephes consumed juvenile Daphnia were more consistent with the timing of the Daphnia decline than those in which yellow perch consumed juvenile Daphnia.4. The invasion of Bythotrephes into Long Lake seems to be a significant perturbation, introducing effects that propagate throughout the food chain. Bythotrephes created a possible bottleneck for age-0 yellow perch in late June by suppressing Daphnia.