Sharks, turtles, billfish, and marine mammals are frequently caught accidentally in commercial fisheries. Although conservationists and fisheries managers encourage the release of these nontarget species, the long-term outcome of released animals is uncertain. Using blue sharks Prionace glauca, we developed a model to predict the long-term survival of released animals based on analysis of small blood samples. About 5% of the sharks were landed in obviously poor condition (lethargic and unresponsive to handling); these moribund sharks were sampled and euthanized. A subset of the remaining sharks was sampled and tagged with pop-up satellite archival tags (PSATs). Each of the PSATs that reported data (11 tags) showed that the sharks roamed at sea for at least 3 weeks postrelease. Five variables differentiated moribund sharks from survivors: plasma Mg 2þ (moribund, 1.57 6 0.08 mM; survivor, 0.98 6 0.05 mM; P , 0.00001), plasma lactate (moribund, 27.7 6 4.1 mM; survivor, 5.80 6 2.96 mM; P , 0.001), erythrocyte heat shock protein 70 (Hsp70) mRNA (relative levels: moribund, 3.96 6 0.53; survivor, 1.00 6 0.29; P , 0.005), plasma Ca 2þ (moribund, 3.70 6 0.14 mM; survivor, 3.13 6 0.11; P , 0.005), and plasma K þ (moribund, 7.01 6 0.66 mM; survivor, 5.12 6 0.44 mM; P , 0.05). These analyses were used to develop logistic regression models that could ''predict'' the long-term survival of captured sharks, including a larger group of sharks that we sampled but did not tag. The best logistic model, which incorporated Mg 2þ and lactate, successfully categorized 95% of fish of known outcome (19 of 20). These analyses suggest that sharks landed in an apparently healthy condition are likely to survive long term if released (95% survival based on biochemical analyses; 100% based on PSATs).

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Hummingbirds in flight display the highest rates of aerobic metabolism known among vertebrates. Their flight muscles possess sufficient maximal activities of hexokinase and carnitine palmitoyltransferase to allow the exclusive use of either glucose or long-chain fatty acids as metabolic fuels during flight. Respiratory quotients (RQ = VCO2/VO2) indicate that fatty acid oxidation serves as the primary energy source in fasted resting birds, while subsequent foraging occurs with a rapid shift towards the use of carbohydrate as the metabolic fuel. We suggest that hummingbirds building up fat deposits in preparation for migration behave as carbohydrate maximizers (or fat minimizers) with respect to the metabolic fuels selected to power foraging flight.

Cortical spreading depression (CSD) is closely associated with important pathologies including stroke, seizures and migraine. The mechanisms underlying SD in its various forms are still incompletely understood. Here we describe SD-like events in an invertebrate model, the ventilatory central pattern generator (CPG) of locusts. Using K+ -sensitive microelectrodes, we measured extracellular K+ concentration ([K+]o) in the metathoracic neuropile of the CPG while monitoring CPG output electromyographically from muscle 161 in the second abdominal segment to investigate the role K+ in failure of neural circuit operation induced by various stressors. Failure of ventilation in response to different stressors (hyperthermia, anoxia, ATP depletion, Na+/K+ ATPase impairment, K+ injection) was associated with a disturbance of CNS ion homeostasis that shares the characteristics of CSD and SD-like events in vertebrates. Hyperthermic failure was preconditioned by prior heat shock (3 h, 45°C) and induced-thermotolerance was associated with an increase in the rate of clearance of extracellular K+ that was not linked to changes in ATP levels or total Na+/K+ ATPase activity. Our findings suggest that SD-like events in locusts are adaptive to terminate neural network operation and conserve energy during stress and that they can be preconditioned by experience. We propose that they share mechanisms with CSD in mammals suggesting a common evolutionary origin.

SUMMARYIn mammals, the peroxisome proliferator-activated receptor (PPAR) γ coactivator-1 (PGC-1) family members and their binding partners orchestrate remodelling in response to diverse challenges such as diet, temperature and exercise. In this study, we exposed goldfish to three temperatures (4, 20 and 35°C) and to three dietary regimes (food deprivation, low fat and high fat) and examined the changes in mitochondrial enzyme activities and transcript levels for metabolic enzymes and their genetic regulators in red muscle, white muscle, heart and liver. When all tissues and conditions were pooled, there were significant correlations between the mRNA for the PGC-1 coactivators (both α and β) and mitochondrial transcripts (citrate synthase), metabolic gene regulators including PPARα, PPARβ and nuclear respiratory factor-1 (NRF-1). PGC-1β was the better predictor of the NRF-1 axis, whereas PGC-1α was the better predictor of the PPAR axis (PPARα, PPARβ, medium chain acyl CoA dehydrogenase). In contrast to these intertissue/developmental patterns, the response of individual tissues to physiological stressors displayed no correlations between mRNA for PGC-1 family members and either the NRF-1 or PPAR axes. For example, in skeletal muscles, low temperature decreased PGC-1α transcript levels but increased mitochondrial enzyme activities (citrate synthase and cytochrome oxidase) and transcripts for COX IV and NRF-1. These results suggest that in goldfish, as in mammals, there is a regulatory relationship between (i) NRF-1 and mitochondrial gene expression and (ii) PPARs and fatty acid oxidation gene expression. In contrast to mammals, there is a divergence in the roles of the coactivators, with PGC-1α linked to fatty acid oxidation through PPARα, and PGC-1β with a more prominent role in mediating NRF-1-dependent control of mitochondrial gene expression, as well as distinctions between their respective roles in development and physiological responsiveness.

Rainbow trout, Oncorhynchus mykiss, were exercise trained for 28–52 days. Trained fish were 13% larger and swam 12% faster in an aerobic swimming test. Training induced cardiac growth that was isometric with body growth, since ventricle mass relative to body mass was constant. The proportions of compact and spongy myocardia in the ventricle were also unchanged by training. Trained fish had significantly higher levels of citrate synthase, β-hydroxyacyl CoA dehydrogenase, and hexokinase in both compact and spongy myocardium. Ligation of a 0.5- to 1.0-cm section of the coronary artery produced only a temporary interruption of coronary flow to the compact myocardium because new vessels grew around the ligation site in the majority of fish during the 28- to 52-day experiment. Nonetheless, coronary ligation resulted in a significantly smaller (17%) proportion of compact myocardium with lower levels of citrate synthase, β-hydroxyacyl CoA dehydrogenase, and hexokinase. Exercise-induced increases in the levels of these enzymes in the compact myocardium were prevented by coronary ligation. The decrease of enzymes in the compact myocardium as a result of coronary ligation was compensated for by a 30% increase in the levels of the aerobic enzymes citrate synthase and β-hydroxyacyl CoA dehydrogenase and a 32% increase in the mass of spongy myocardium. As a result of these compensations and coronary regrowth, chronic coronary ligation did not affect maximum prolonged swimming speed. These experiments clearly reveal that cardiac plasticity allows compensatory changes that are necessary for the heart to maintain adequate oxygen delivery to exercising skeletal muscle. The compensatory changes were isometric increases in heart mass or proportionately larger increases in heart mass and compact tissue if the coronary artery was ligated and an increase in metabolic enzymes associated with ATP generation, namely, citrate synthase, β-hydroxyacyl CoA dehydrogenase, and hexokinase.

The International Study of Asthma and Allergies in Childhood (ISAAC) Phase One showed large worldwide variations in the prevalence of symptoms of asthma, rhinoconjunctivitis and eczema, up to 10 to 20 fold between countries. Ecological analyses were undertaken with ISAAC Phase One data to explore factors that may have contributed to these variations, and are summarised and reviewed here.In ISAAC Phase One the prevalence of symptoms in the past 12 months of asthma, rhinoconjunctivitis and eczema were estimated from studies in 463,801 children aged 13 - 14 years in 155 centres in 56 countries, and in 257,800 children aged 6-7 years in 91 centres in 38 countries. Ecological analyses were undertaken between symptom prevalence and the following: Gross National Product per capita (GNP), food intake, immunisation rates, tuberculosis notifications, climatic factors, tobacco consumption, pollen, antibiotic sales, paracetamol sales, and outdoor air pollution.Symptom prevalence of all three conditions was positively associated with GNP, trans fatty acids, paracetamol, and women smoking, and inversely associated with food of plant origin, pollen, immunisations, tuberculosis notifications, air pollution, and men smoking. The magnitude of these associations was small, but consistent in direction between conditions. There were mixed associations of climate and antibiotic sales with symptom prevalence.The potential causality of these associations warrant further investigation. Factors which prevent the development of these conditions, or where there is an absence of a positive correlation at a population level may be as important from the policy viewpoint as a focus on the positive risk factors. Interventions based on small associations may have the potential for a large public health benefit.

We used expression and reporter gene analysis to understand how changes in transcription factors impinge on mitochondrial gene expression during myogenesis of cultured murine myoblasts (C2C12 and Sol8). The mRNA levels for nuclear respiratory factor-1 (NRF-1) and NRF-2alpha increased 60% by the third day of myogenesis, whereas NRF-1 and NRF-2 reporter gene activity increased by fivefold over the same period. Although peroxisome proliferator activated receptor (PPARalpha) mRNA levels increased almost 10-fold, the activity of a PPAR reporter was unchanged during myogenesis. The PPAR coactivator PPAR-gamma coactivator-1alpha (PGC1alpha), a master controller of mitochondrial biogenesis, was not expressed at detectable levels. However, the mRNA for both PGC1alpha-related coactivator and PGC1beta was abundant, with the latter increasing by 50% over 3 days of differentiation. We also conducted promoter analysis of the gene for citrate synthase (CS), a common mitochondrial marker enzyme. The proximal promoter ( approximately 2,100 bp) of the human CS lacks binding sites for PPAR, NRF-1, or NRF-2. Deletion mutants, a targeted mutation, and an Sp1 site-containing reporter construct suggest that changes in Sp1 regulation also participate in mitochondrial biogenesis during myogenesis. Because most mitochondrial genes are regulated by PPARs, NRF-1, and/or NRF-2, we conducted inhibitor studies to further support the existence of a distinct pathway for CS gene regulation in myogenesis. Although both LY-294002 (a phosphatidylinositol 3-kinase inhibitor) and SB-203580 (a p38-MAPK inhibitor) blocked myogenesis (as indicated by creatine phosphokinase activity), only SB-203580 prevented the myogenic increase in cytochrome oxidase activity, whereas only LY-294002 blocked the increase in CS (enzyme and reporter gene activities). Collectively, these studies help delineate the roles of some transcriptional regulators involved in mitochondrial biogenesis associated with myogenesis and underscore an import role for posttranscriptional regulation of transcription factor activity.