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- Buccirossi, Paolo, et al.
(författare)
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Leniency and Damages: Where Is the Conflict?
- 2020
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Ingår i: Journal of Legal Studies. - : University of Chicago Press. - 0047-2530 .- 1537-5366. ; 49:2, s. 335-379
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Tidskriftsartikel (refereegranskat)abstract
- Damage actions may reduce leniency programs' attractiveness for cartel participants if their cooperation with the competition authority increases the chance that the cartel's victims will sue them. This apparent conflict between public and private antitrust enforcement led to calls for a legal compromise. We show that the conflict is due to the legislation, and a compromise is not required: limiting the victims' ability to recover their losses is not necessary to preserve the effectiveness of leniency programs and may be counterproductive. We show that damage actions will improve their effectiveness if the civil liability of the immunity recipient is minimized and full access to all evidence collected by the competition authority is granted to claimants. Our results help compare the EU and US damage systems and directly question the 2014 EU directive that tries to protect leniency programs' effectiveness by restricting access to leniency statements in subsequent damage actions.
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| 2. |
- Dorfman, Mauricio, et al.
(författare)
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Chronic-intermittent cold stress in rats induces selective ovarian insulin resistance.
- 2009
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Ingår i: Biology of reproduction. - : Oxford University Press (OUP). - 0006-3363 .- 1529-7268. ; 80:2, s. 264-71
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Tidskriftsartikel (refereegranskat)abstract
- In rat ovary chronic cold stress increases sympathetic nerve activity, modifies follicular development, and initiates a polycystic condition. To see whether there is a relationship between the previously described changes in follicular development and metabolic changes similar to those in women with polycystic ovary, we have studied the effect of chronic cold stress (4 degrees C for 3 h/day, Monday to Friday, for 4 wk) on insulin sensitivity and the effect of insulin on sympathetic ovarian activity. Although cold-stressed rats ate more than the controls, they did not gain more weight. Insulin sensitivity, determined by hyperinsulinemic-euglycemic clamp, was significantly increased in the stressed animals. Insulin in vitro increased the basal release of norepinephrine from the ovaries of control rats but not from those of stressed rats, suggesting a local neural resistance to insulin in stressed rats. The levels of mRNA and protein for IRS1 and SLC2A4 (also known as GLUT4), molecules involved in insulin signaling, decreased significantly in the ovaries but not in the muscle of stressed rats. This decrease was preferentially located in theca-interstitial cells compared with granulosa cells, indicating that theca cells (the only cells directly innervated by sympathetic nerves) are responsible for the ovarian insulin resistance found in stressed rats. These findings suggest that ovarian insulin resistance produced by chronic stress could be in part responsible for the development of the polycystic condition induced by stress.
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