Background: A positive relationship between problematic gaming and escapism motivation to play video games has been well established, suggesting that problematic gaming may result from attempts to deal with negative emotions. However, to date, no study has examined how emotion dysregulation affects both escapism motives and problematic gaming patterns. Methods: Difficulties in emotion regulation, escapism, and problematic involvement with video games were assessed in a sample of 390 World of Warcraft players. A structural equation modeling framework was used to test the hypothesis that escapism mediates the relationship between emotion dysregulation and problematic gaming. Results: Statistical analyses showed that difficulties in emotion regulation predicted both escapism motives and problematic gaming, and that escapism partially mediated this relationship. Conclusion: Our findings support the view that problematic players are likely to escape in online games as a maladaptive coping strategy for dealing with adverse emotional experiences.
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In order to investigate the 4-hydroxy-1,2,5-oxadiazol-3-yl moiety as a carboxylic acid bioisoster at ionotropic glutamate receptors (iGluRs), a series of acidic R-aminocarboxylic acids in which the distal carboxy group was replaced by the 4-hydroxy-1,2,5-oxadiazol-3-yl group was synthesized. Ionization constants were determined. All target compounds, except the Asp analogue 12, were resolved using chiral HPLC. Whereas 12 showed good affinity exclusively at NMDA receptors, the Glu analogue, (þ)-10, was an unselective, though potent AMPA receptor preferring agonist (EC 50 = 10 μM at iGluR2) showing only low stereoselectivity. The two higher Glu homologues, (þ)-15 and (þ)-18, turned out to be weak agonists at iGluR2 as well as weak antagonists at NR1/NR2A, whereas the corresponding (-)-isomers were selective NR1/NR2A antagonists with somewhat higher potency. The results proved the 4-hydroxy-1,2,5-oxadiazol-3-yl moiety to be a useful bioisoster at all three classes of iGluRs, capable of being integrated into agonists as well as antagonists.
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