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Most of the world's marine fisheries are overexploited or endangered, including the Gulf of Maine groundfish fishery, once one of the world's most prolific. After 35 years of management, groundfish stock sizes and catches are lower than when management began. We argue that in New England, the groundfishing industry is caught in a prisoner's dilemma caused by a large number of interactive social, political, and economic variables. These factors have (1) motivated fishermen to oppose the rules promulgated by the government (which we call the “harvest game”) and (2) lowered the benefits of investing in rules to conserve fish stocks (which we call the “rule game”). In both games, fishermen are motivated to play their dominant strategy to the detriment of the industry, conservation, and fish stocks. We suggest that the dilemma will only be solved by a change in the culture of the industry that would lead to support for a conservation ethic. Unfortunately, the current institutional framework of management does not support the development of such an ethic. Rational-choice theory and concepts from evolutionary game theory add to our understanding of the dilemma facing those concerned with groundfish management in this region. Received March 3, 2010; accepted June 16, 2011 [ABSTRACT FROM PUBLISHER]

Abstract Similar to leptin, ciliary neurotrophic factor (CNTF) suppresses appetite and selectively reduces body fat in leptin-deficient ob/ob mice. To assess the relative importance of specific regions of the hypothalamus in mediating these effects, we administered a CNTF analogue (CNTFAx15 ) or leptin to mice made obese by administration of gold thioglucose (GTG), which destroys a well-defined portion of the medial basal hypothalamus. CNTFAx15 treatment reduced appetite and body weight in obese GTG-lesioned C57BL/6 mice, whereas leptin failed to effect similar changes regardless of whether treatment was initiated before or after the lesioned mice had become obese. Because leptin does not reduce food intake or body weight in most forms of obesity (a condition termed ‘leptin resistance’), we also investigated the actions of leptin in GTG-lesioned leptin-deficient (ob/ob ) mice. By contrast to C57BL/6 mice, leptin treatment reduced food intake and body weight in GTG-lesioned ob/ob mice, although the effect was attenuated. To further compare the neural substrates mediating the anorectic actions of leptin and CNTF, we determined the patterns of neurone activation induced by these proteins in the hypothalamus of intact and GTG-lesioned mice by staining for phosphorylated signal transducer and activator of transcription 3 (pSTAT3). CNTFAx15 stimulated robust pSTAT3 signalling in neurones of the medial arcuate nucleus in both intact and lesioned C57BL/6 and ob/ob mice. Leptin administration stimulated pSTAT3 signalling in only a few neurones of the medial arcuate nucleus in intact or lesioned C57BL/6 mice, but elicited a robust response in intact or lesioned ob/ob mice. By contrast to CNTFAx15 , leptin treatment also resulted in prominent activation of STAT3 in several areas of the hypothalamus outside the medial arcuate nucleus. This leptin-induced pSTAT3 signal was at least as prominent in intact and GTG-lesioned C57BL/6 mice as it was in ob/ob mice, and thus was not correlated with appetite suppression or weight loss. These results indicate that the medial arcuate nucleus is a key mediator of appetite suppression and weight loss produced by CNTF and leptin, whereas GTG-vulnerable regions play a role only in leptin-induced weight loss. Other regions of hypothalamus in which pSTAT3 signal is induced by leptin may regulate energy metabolism through mechanisms other than appetite reduction. [ABSTRACT FROM AUTHOR]