Human dimensions of bycatch reduction technology: Current assumptions and directions for future research

Bycatch reduction technology (BRT) modifies fishing gear to increase selectivity and avoid capture of non-target species, or to facilitate their non-lethal release. As a solution to fisheries-related mortality of non-target species, BRT is an attractive option; effectively implemented, BRT presents a technical 'fix' that can reduce pressure for politically contentious and economically detrimental interventions, such as fisheries closures. While a number of factors might contribute to effective implementation, our review of BRT literature finds that research has focused on technical design and experimental performance of individual technologies. In contrast, and with a few notable exceptions, research on the human and institutional context of BRT, and more specifically on how fishers respond to BRT, is limited. This is not to say that fisher attitudes are ignored or overlooked, but that incentives for fisher uptake of BRT are usually assumed rather than assessed or demonstrated. Three assumptions about fisher incentives dominate: (1) economic incentives will generate acceptance of BRT; (2) enforcement will generate compliance with BRT; and (3) 'participation' by fishers will increase acceptance and compliance, and overall support for BRT. In this paper, we explore evidence for and against these assumptions and situate our analysis in the wider social science literature on fisheries. Our goal is to highlight the need and suggest focal areas for further research. © Inter-Research 2008.

Eco-evolutionary trophic dynamics: loss of top predators drives trophic evolution and ecology of prey.

Ecosystems are being altered on a global scale by the extirpation of top predators. The ecological effects of predator removal have been investigated widely; however, predator removal can also change natural selection acting on prey, resulting in contemporary evolution. Here we tested the role of predator removal on the contemporary evolution of trophic traits in prey. We utilized a historical introduction experiment where Trinidadian guppies (Poecilia reticulata) were relocated from a site with predatory fishes to a site lacking predators. To assess the trophic consequences of predator release, we linked individual morphology (cranial, jaw, and body) to foraging performance. Our results show that predator release caused an increase in guppy density and a "sharpening" of guppy trophic traits, which enhanced food consumption rates. Predator release appears to have shifted natural selection away from predator escape ability and towards resource acquisition ability. Related diet and mesocosm studies suggest that this shift enhances the impact of guppies on lower trophic levels in a fashion nuanced by the omnivorous feeding ecology of the species. We conclude that extirpation of top predators may commonly select for enhanced feeding performance in prey, with important cascading consequences for communities and ecosystems.

Harvesting life's energy: increase in the aerotolerence of the electrogenic anaerobe geobacter sulfurreducens due to over-expression of superoxide dismutase and catalase

Gemstone Team iGEM

The Emergence of Access Controls in Small-Scale Fishing Commons: A Comparative Analysis of Individual Licenses and Common Property-Rights in Two Mexican Communities

Addressing global fisheries overexploitation requires better understanding of how small-scale fishing communities in developing countries limit access to fishing grounds. We analyze the performance of a system based on individual licenses and a common property-rights regime in their ability to generate incentives for self-governance and conservation of fishery resources. Using a qualitative before-after-control-impact approach, we compare two neighbouring fishing communities in the Gulf of California, Mexico. Both were initially governed by the same permit system, are situated in the same ecosystem, use similar harvesting technology, and have overharvested similar species. One community changed to a common property-right regime, enabling the emergence of access controls and avoiding overexploitation of benthic resources, while the other community, still relies on the permit system. We discuss the roles played by power, institutions, socio-historic, and biophysical factors to develop access controls. © 2012 The Author(s).

Overexpression of the cardiac beta(2)-adrenergic receptor and expression of a beta-adrenergic receptor kinase-1 (betaARK1) inhibitor both increase myocardial contractility but have differential effects on susceptibility to ischemic injury.

Cardiac beta(2)-adrenergic receptor (beta(2)AR) overexpression is a potential contractile therapy for heart failure. Cardiac contractility was elevated in mice overexpressing beta(2)ARs (TG4s) with no adverse effects under normal conditions. To assess the consequences of beta(2)AR overexpression during ischemia, perfused hearts from TG4 and wild-type mice were subjected to 20-minute ischemia and 40-minute reperfusion. During ischemia, ATP and pH fell lower in TG4 hearts than wild type. Ischemic injury was greater in TG4 hearts, as indicated by lower postischemic recoveries of contractile function, ATP, and phosphocreatine. Because beta(2)ARs, unlike beta(1)ARs, couple to G(i) as well as G(s), we pretreated mice with the G(i) inhibitor pertussis toxin (PTX). PTX treatment increased basal contractility in TG4 hearts and abolished the contractile resistance to isoproterenol. During ischemia, ATP fell lower in TG4+PTX than in TG4 hearts. Recoveries of contractile function and ATP were lower in TG4+PTX than in TG4 hearts. We also studied mice that overexpressed either betaARK1 (TGbetaARK1) or a betaARK1 inhibitor (TGbetaARKct). Recoveries of function, ATP, and phosphocreatine were higher in TGbetaARK1 hearts than in wild-type hearts. Despite basal contractility being elevated in TGbetaARKct hearts to the same level as that of TG4s, ischemic injury was not increased. In summary, beta(2)AR overexpression increased ischemic injury, whereas betaARK1 overexpression was protective. Ischemic injury in the beta(2)AR overexpressors was exacerbated by PTX treatment, implying that it was G(s) not G(i) activity that enhanced injury. Unlike beta(2)AR overexpression, basal contractility was increased by betaARK1 inhibitor expression without increasing ischemic injury, thus implicating a safer potential therapy for heart failure.