To resolve these discrepancies, we examined recognition memory and event-related potentials (ERPs) for young and old faces in young participants and two elderly groups, who either reported high or low degrees of daily contact with elderly relative to younger persons. As expected, young

adults showed more accurate memory for young versus old faces. While no OAB was found in old/low contact participants, old/high contact participants were more accurate with old versus ICG-001 in vivo young faces. ERPs in young adults revealed a parietal old/new effect from 500 to 800 ms (hits > correct rejections) for young but not old faces. Whereas no old/new effect was seen in the old/low contact group, the old/high contact participants exhibited a prominent reversed old/new effect (hits < correct rejections) for old faces. These results suggest that contact may account for earlier discrepant results with regard to the OAB in elderly participants. A behavioral OAB selleck screening library in elderly participants may depend on high degrees of contact towards old people. The finding of ERP old/new effects specific to own-age faces suggests enhanced recollection of study phase detail in young participants,

whereas it may reflect increased engagement in processes aiming at compensating for a deficit in recollection in elderly participants. (C) 2012 Elsevier Ltd. All rights reserved.”
“Clinical use of nonsteroidal anti-inflammatory drugs (NSAIDs) like diclofenac (DCLF) is limited by multiple adverse effects, including renal toxicity leading to acute kidney injury. In mice with DCLF-induced nephrotoxicity, TDZD-8, a selective glycogen synthase kinase (GSK)3 beta inhibitor, improved acute kidney dysfunction and ameliorated tubular necrosis and apoptosis associated with induced cortical expression of cyclooxygenase-2 (COX-2) and

prostaglandin E2. This renoprotective effect was blunted but still largely preserved in COX-2-null mice, suggesting that other GSK3 beta targets beyond COX-2 functioned in renal protection. Indeed, TDZD-8 diminished the mitochondrial permeability transition in DCLF-injured kidneys. In vitro, GSK3 beta inhibition reinstated viability and suppressed necrosis and apoptosis in DCLF-stimulated tubular epithelial cells. DCLF elicited Farnesyltransferase oxidative stress, enhanced the activity of the redox-sensitive GSK3 beta, and promoted a mitochondrial permeability transition by interacting with cyclophilin D, a key component of the mitochondrial permeability transition pore. TDZD-8 blocked GSK3 beta activity and prevented GSK3 beta-mediated cyclophilin D phosphorylation and the ensuing mitochondrial permeability transition, concomitant with normalization of intracellular ATP. Conversely, ectopic expression of a constitutively active GSK3 beta abolished the effects of TDZD-8.