The effects of stereotype activation on behavior: a review of possible mechanisms.

Considerable recent research has examined the effects that activated stereotypes have on behavior. Research on both self-stereotype activation and other-stereotype activation has tended to show that people behave in ways consistent with the stereotype (e.g., walking more slowly if the elderly stereotype is activated). Interestingly, however, the dominant account for the behavioral effects of self-stereotype activation involves a hot motivational factor (i.e., stereotype threat), whereas the dominant account for the behavioral effects of other-stereotype activation focuses on a rather cold cognitive explanation (i.e., ideomotor processes). The current review compares and contrasts the behavioral research on self- and other-stereotype activation and concludes that both motivational and cognitive explanations might account for effects in each domain.

Fictional narratives change beliefs: replications of Prentice, Gerrig, and Bailis (1997) with mixed corroboration.

We report three exact replications of experiments aimed at iluminating how fictional narratives influence beliefs (Prentice, Gerrig, & Bailis, 1997). Students read fictional stories that contained weak, unsupported assertions and which took place either at their home school or at an away school. Prentice et al. found that students were influenced to accept the assertions, even those blatantly false, but that this effect on beliefs was limited to the away-school setting. We questioned the limiting of the narrative effect to remote settings. Our studies consistently reproduced the first finding, heightened acceptance of statements occurring in the conversations of narrative protagonists, but we failed to reproduce the moderating effect of school location. In an attempt to understand these discrepancies, we measured likely moderating factors such as readers' need for cognition and their extent of scrutiny of the narratives.

Concomitant etodolac affects neither the unbound clearance nor the pharmacologic effect of warfarin.

Potential interactions between the nonsteroidal anti-inflammatory etodolac and the anticoagulant warfarin were studied in 18 healthy subjects by use of a randomized, three-period crossover design. Each treatment lasted 2 1/2 days and consisted of warfarin, etodolac, or both drugs. Prothrombin time was determined daily during each warfarin period to measure pharmacologic effect. Total serum concentration and unbound fraction of both drugs were determined over the dose interval after the last dose of the study drug(s). Concomitant etodolac did not affect the prothrombin time response or the unbound clearance of warfarin. During concomitant etodolac administration, the median peak concentration of total warfarin was significantly decreased by 19% (p = 0.005), median total clearance was significantly increased by 13% (p = 0.0123), and the unbound fraction tended to increase (median unbound fraction of warfarin, 1.245% with etodolac and 1.045% without etodolac; p = 0.0979; not statistically significant). These observations suggest a small displacement of warfarin from serum protein by etodolac or a metabolite of etodolac. No etodolac pharmacokinetic parameter was significantly affected by concomitant warfarin administration. Thus etodolac does not appear to alter the unbound clearance of warfarin or augment its pharmacologic effect. Nevertheless, it is prudent that clinical monitoring be done for individuals taking these two compounds concomitantly.

Norfloxacin does not alter warfarin's disposition or anticoagulant effect.

Drug interactions related to inhibition of hepatic drug metabolism have been identified for some fluoroquinolone antibiotics. This study was designed to investigate whether the fluoroquinolone norfloxacin at the usual clinical dosage interacts with the anticoagulant agent warfarin. Ten healthy male subjects were administered a single oral dose of 30 mg warfarin sodium alone or during multiple-dose treatment with norfloxacin, 400 mg bid, in a randomized, crossover fashion. Plasma warfarin concentrations and prothrombin times were measured for 6 days after each of the two warfarin doses. The pharmacokinetic parameters of warfarin were comparable in the absence and presence of norfloxacin, including no significant differences in warfarin's elimination half-life, apparent total clearance, apparent volume of distribution, or peak plasma concentration. Norfloxacin also had no significant effect on the anticoagulant effect of warfarin, as assessed by the area under the prothrombin time versus time curve and the maximum response for prothrombin time. The lack of pharmacokinetic or pharmacodynamic interaction observed in this study suggests that a clinically important interaction of norfloxacin and warfarin is unlikely to occur in patients requiring both drugs.

Tolerance to fluphenazine and supersensitivity to apomorphine in central dopaminergic systems after chronic fluphenazine decanoate treatment.

Fluphenazine decanoate was administered chronically to rats on a schedule for which marked tolerance developed to acute fluphenazine effects on several parameters of dopaminergic neuronal function. DOPAC and HVA levels, indicators of dopaminergic activity, were quantitated in terminal areas of the mesocortical, mesolimbic and nigrostriatal systems. With this fluphenazine regimen tolerance developed not only in the nigrostriatal and mesolimbic but also in the mesocortical dopamine system to the elevation of metabolite levels induced by acute fluphenazine administration. Evidence was obtained that tolerance was functional rather than metabolic and was characterized by a large reduction in the accumulation of metabolites which normally follows a challenge dose of fluphenazine. Other experiments suggested that the results were not due to the effects of chronic fluophenazine on the noradrenergic innervation of the cortex and were not explained by altered catabolism or clearance of the dopamine metabolites. During withdrawal from chronic fluphenazine decanoate treatment supersensitivity to apomorphine developed in the striatum. The time courses of the disappearance of apomorphine supersensitivity and of the reversal of tolerance to a fluphenazine challenge were different.