8 resultados para Krohn, Julius,

em CentAUR: Central Archive University of Reading - UK


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Although it is well known that Lucan’s Libya is a wild and threatening place, its threat is not restricted to indigenous people, places and things, such as Hannibal, Cleopatra, the Syrtes, or the desert with its catalogue of horrifying snakes. He also associates Libya with anti-Republican Romans, above all Julius Caesar, who endangers the Republic with his excessive, animalistic energy and resembles the continent where he is trapped in the final book. Although the gods as characters are removed from the world of the Bellum Civile, Lucan allows supernatural traces to linger in particular locations such as the Gallic grove in Book 3 or Thessaly in Book 6. Libya is by far the greatest of these reservoirs of frightening myth and fantasy, which do violence to the historical credibility of the narrative, just as Libya itself is presented as the origin or conduit of a number of historical characters who assault Italy and Europe. Lucan’s two mythic narratives (Antaeus in Book 4 and Medusa in Book 9) are essential parts of the hostile Libyan landscape, but in very different ways. The male Antaeus, associated with lions, is connected with a region of solid rock where he was destroyed. The female Medusa, associated with snakes, is connected with a region of shifting sands where she left a deadly, everlasting legacy. To complicate matters further, even though Medusa’s snakes represent the annihilation of the Republican self, the logic of the narrative is undermined and there is even a sympathetic subtext. As part of Libya’s historical and mythical legacy, these stories reveal that for Lucan, historical epic is linked with Republicanism, but mythical epic is in the service of dictatorship.

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TRPA1 is an excitatory ion channel expressed by a subpopulation of primary afferent somatosensory neurons that contain substance P and calcitonin gene-related peptide. Environmental irritants such as mustard oil, allicin, and acrolein activate TRPA1, causing acute pain, neuropeptide release, and neurogenic inflammation. Genetic studies indicate that TRPA1 is also activated downstream of one or more proalgesic agents that stimulate phospholipase C signaling pathways, thereby implicating this channel in peripheral mechanisms controlling pain hypersensitivity. However, it is not known whether tissue injury also produces endogenous proalgesic factors that activate TRPA1 directly to augment inflammatory pain. Here, we report that recombinant or native TRPA1 channels are activated by 4-hydroxy-2-nonenal (HNE), an endogenous alpha,beta-unsaturated aldehyde that is produced when reactive oxygen species peroxidate membrane phospholipids in response to tissue injury, inflammation, and oxidative stress. HNE provokes release of substance P and calcitonin gene-related peptide from central (spinal cord) and peripheral (esophagus) nerve endings, resulting in neurogenic plasma protein extravasation in peripheral tissues. Moreover, injection of HNE into the rodent hind paw elicits pain-related behaviors that are inhibited by TRPA1 antagonists and absent in animals lacking functional TRPA1 channels. These findings demonstrate that HNE activates TRPA1 on nociceptive neurons to promote acute pain, neuropeptide release, and neurogenic inflammation. Our results also provide a mechanism-based rationale for developing novel analgesic or anti-inflammatory agents that target HNE production or TRPA1 activation.

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We let subjects take risky decisions that affect themselves and a passive recipient. Adding a requirement to justify their choices significantly reduces loss aversion. This indicates that such an accountability mechanism may be effective at debiasing loss aversion in agency relations.

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We systematically explore decision situations in which a decision maker bears responsibility for somebody else's outcomes as well as for her own in situations of payoff equality. In the gain domain we confirm the intuition that being responsible for somebody else's payoffs increases risk aversion. This is however not attributable to a 'cautious shift' as often thought. Indeed, looking at risk attitudes in the loss domain, we find an increase in risk seeking under responsibility. This raises issues about the nature of various decision biases under risk, and to what extent changed behavior under responsibility may depend on a social norm of caution in situations of responsibility versus naive corrections from perceived biases. To further explore this issue, we designed a second experiment to explore risk-taking behavior for gain prospects offering very small or very large probabilities of winning. For large probabilities, we find increased risk aversion, thus confirming our earlier finding. For small probabilities however, we find an increase of risk seeking under conditions of responsibility. The latter finding thus discredits hypotheses of a social rule dictating caution under responsibility, and can be explained through flexible self-correction models predicting an accentuation of the fourfold pattern of risk attitudes predicted by prospect theory. An additional accountability mechanism does not change risk behavior, except for mixed prospects, in which it reduces loss aversion. This indicates that loss aversion is of a fundamentally different nature than probability weighting or utility curvature. Implications for debiasing are discussed.