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- Jagers, Sverker C., 1967, et al.
(author)
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On the preconditions for large-scale collective action
- 2020
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In: Ambio. - : Springer Science and Business Media LLC. - 0044-7447 .- 1654-7209. ; 49:7, s. 1282-1296
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Journal article (peer-reviewed)abstract
- The phenomenon of collective action and the origin of collective action problems have been extensively and systematically studied in the social sciences. Yet, while we have substantial knowledge about the factors promoting collective action at the local level, we know far less about how these insights travel to large-scale collective action problems. Such problems, however, are at the heart of humanity's most pressing challenges, including climate change, large-scale natural resource depletion, biodiversity loss, nuclear proliferation, antibiotic resistance due to overconsumption of antibiotics, and pollution. In this paper, we suggest an analytical framework that captures the theoretical understanding of preconditions for large-scale collective action. This analytical framework aims at supporting future empirical analyses of how to cope with and overcome larger-scale collective action problems. More specifically, we (i) define and describe the main characteristics of a large-scale collective action problem and (ii) explain why voluntary and, in particular, spontaneous large-scale collective action among individual actors becomes more improbable as the collective action problem becomes larger, thus demanding interventions by an external authority (a third party) for such action to be generated. Based on this, we (iii) outline an analytical framework that illustrates the connection between third-party interventions and large-scale collective action. We conclude by suggesting avenues for future research.
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- Méquinion, M., et al.
(author)
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Ghrelin: Central and peripheral implications in anorexia nervosa
- 2013
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In: Frontiers in Endocrinology. - : Frontiers Media SA. - 1664-2392 .- 1664-2392. ; 4:FEB
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Journal article (peer-reviewed)abstract
- Increasing clinical and therapeutic interest in the neurobiology of eating disorders reflects their dramatic impact on health. Chronic food restriction resulting in severe weight loss is a major symptom described in restrictive anorexia nervosa (AN) patients, and they also suffer from metabolic disturbances, infertility, osteopenia, and osteoporosis. Restrictive AN, mostly observed in young women, is the third largest cause of chronic illness in teenagers of industrialized countries. From a neurobiological perspective, AN-linked behaviors can be considered an adaptation that permits the endurance of reduced energy supply, involving central and/or peripheral reprograming. The severe weight loss observed in AN patients is accompanied by significant changes in hormones involved in energy balance, feeding behavior, and bone formation, all of which can be replicated in animals models. Increasing evidence suggests that AN could be an addictive behavior disorder, potentially linking defects in the reward mechanism with suppressed food intake, heightened physical activity, and mood disorder. Surprisingly, the plasma levels of ghrelin, an orexigenic hormone that drives food-motivated behavior, are increased. This increase in plasma ghrelin levels seems paradoxical in light of the restrained eating adopted by AN patients, and may rather result from an adaptation to the disease. The aim of this review is to describe the role played by ghrelin in AN focusing on its central vs. peripheral actions. In AN patients and in rodent AN models, chronic food restriction induces profound alterations in the « ghrelin » signaling that leads to the development of inappropriate behaviors like hyperactivity or addiction to food starvation and therefore a greater depletion in energy reserves. The question of a transient insensitivity to ghrelin and/or a potential metabolic reprograming is discussed in regard of new clinical treatments currently investigated. © 2013 Méquinion, Langlet, Zgheib, Dickson, Dehouck, Chauveau and Viltart.
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- Shirazi, Rozita H., et al.
(author)
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Glucagon-like peptide 1 receptor induced suppression of food intake, and body weight is mediated by central IL-1 and IL-6
- 2013
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In: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 0027-8424. ; 110:40, s. 16199-16204
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Journal article (peer-reviewed)abstract
- Glucagon-like peptide 1 (GLP-1), produced in the intestine and the brain, can stimulate insulin secretion from the pancreas and alleviate type 2 diabetes. The cytokine interleukin-6 (IL-6) may enhance insulin secretion from beta-cells by stimulating peripheral GLP-1 production. GLP-1 and its analogs also reduce food intake and body weight, clinically beneficial actions that are likely exerted at the level of the CNS, but otherwise are poorly understood. The cytokines IL-6 and interleukin 1 beta (IL-1 beta) may exert an anti-obesity effect in the CNS during health. Here we found that central injection of a clinically used GLP-1 receptor agonist, exendin-4, potently increased the expression of IL-6 in the hypothalamus (11-fold) and the hindbrain (4-fold) and of IL-1 beta in the hypothalamus, without changing the expression of other inflammation-associated genes. Furthermore, hypothalamic and hindbrain interleukin-associated intracellular signals [phosphorylated signal transducer and activator of transcription-3 (pSTAT3) and suppressor of cytokine signaling-1 (SOCS1)] were also elevated by exendin-4. Pharmacologic disruption of CNS IL-1 receptor or IL-6 biological activity attenuated anorexia and body weight loss induced by central exendin-4 administration in a rat. Simultaneous blockade of IL-1 and IL-6 activity led to a more potent attenuation of exendin-4 effects on food intake. Mice with global IL-1 receptor gene knockout or central IL-6 receptor knockdown showed attenuated decrease in food intake and body weight in response to peripheral exendin-4 treatment. GLP-1 receptor activation in the mouse neuronal Neuro2A cell line also resulted in increased IL-6 expression. These data outline a previously unidentified role of the central IL-1 and IL-6 in mediating the anorexic and body weight loss effects of GLP-1 receptor activation.
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