Temple University

About: Temple University is a education organization based out in Philadelphia, Pennsylvania, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 32154 authors who have published 64375 publications receiving 2219828 citations.

Temperamental Vulnerability and Negative Parenting as Interacting Predictors of Child Adjustment

Abstract: This study examines parenting by temperament interactions in predicting child adjustment. Participants included 40 first and second graders, their mothers, and teachers. Child report of maternal psychological control and hostility was assessed using the Child Puppet Interview. Mothers completed temperament scales from the Child Behavior Questionnaire, and teachers provided information on child adjustment. As expected, among children high in irritable distress, maternal psychological control was associated with internalizing problems and maternal hostility was associated with externalizing problems. Among children with poor effortful control, maternal hostility was associated with externalizing behavior. This study offers evidence that the effects of negative parenting are accentuated among children with temperamental vulnerabilities.

Many analysts, one dataset: Making transparent how variations in analytical choices affect results

Abstract: Twenty-nine teams involving 61 analysts used the same data set to address the same research question: whether soccer referees are more likely to give red cards to dark-skin-toned players than to light-skin-toned players. Analytic approaches varied widely across the teams, and the estimated effect sizes ranged from 0.89 to 2.93 (Mdn = 1.31) in odds-ratio units. Twenty teams (69%) found a statistically significant positive effect, and 9 teams (31%) did not observe a significant relationship. Overall, the 29 different analyses used 21 unique combinations of covariates. Neither analysts’ prior beliefs about the effect of interest nor their level of expertise readily explained the variation in the outcomes of the analyses. Peer ratings of the quality of the analyses also did not account for the variability. These findings suggest that significant variation in the results of analyses of complex data may be difficult to avoid, even by experts with honest intentions. Crowdsourcing data analysis, a strategy in which numerous research teams are recruited to simultaneously investigate the same research question, makes transparent how defensible, yet subjective, analytic choices influence research results.

More information from fewer questions: the factor structure and item properties of the original and brief fear of negative evaluation scale.

Abstract: Statistical methods designed for categorical data were used to perform confirmatory factor analyses and item response theory (IRT) analyses of the Fear of Negative Evaluation scale (FNE; D. Watson & R. Friend, 1969) and the Brief FNE (BFNE; M. R. Leary, 1983). Results suggested that a 2-factor model fit the data better for both the FNE and the BFNE, although the evidence was less strong for the FNE. The IRT analyses indicated that although both measures had items with good discrimination, the FNE items discriminated only at lower levels of the underlying construct, whereas the BFNE items discriminated across a wider range. Convergent validity analyses indicated that the straightforwardly-worded items on each scale had significantly stronger relationships with theoretically related measures than did the reverse-worded items. On the basis of all analyses, usage of the straightforwardly-worded BFNE factor is recommended for the assessment of fear of negative evaluation.

Pharmacokinetics and pharmacodynamics of oral oxycodone in healthy human subjects: Role of circulating active metabolites

Abstract: Background In vitro experiments suggest that circulating metabolites of oxycodone are opioid receptor agonists. Clinical and animal studies to date have failed to demonstrate a significant contribution of the O-demethylated metabolite oxymorphone toward the clinical effects of the parent drug, but the role of other putative circulating active metabolites in oxycodone pharmacodynamics remains to be examined. Methods Pharmacokinetics and pharmacodynamics of oxycodone were investigated in healthy human volunteers; measurements included the time course of plasma concentrations and urinary excretion of metabolites derived from N-demethylation, O-demethylation, and 6-keto-reduction, along with the time course of miosis and subjective opioid side effects. The contribution of circulating metabolites to oxycodone pharmacodynamics was analyzed by pharmacokinetic-pharmacodynamic modeling. The human study was complemented by in vitro measurements of opioid receptor binding and activation studies, as well as in vivo studies of the brain distribution of oxycodone and its metabolites in rats. Results Urinary metabolites derived from cytochrome P450 (CYP) 3A-mediated N-demethylation of oxycodone (noroxycodone, noroxymorphone, and α- and β-noroxycodol) accounted for 45% ± 21% of the dose, whereas CYP2D6-mediated O-demethylation (oxymorphone and α- and β-oxymorphol) and 6-keto-reduction (α- and β-oxycodol) accounted for 11% ± 6% and 8% ± 6% of the dose, respectively. Noroxycodone and noroxymorphone were the major metabolites in circulation with elimination half-lives longer than that of oxycodone, but their uptake into the rat brain was significantly lower compared with that of the parent drug. Pharmacokinetic-pharmacodynamic modeling indicated that the time course of pupil constriction is fully explained by the plasma concentration of the parent drug, oxycodone, alone. The metabolites do not contribute to the central effects, either because of their low potency or low abundance in circulation or as a result of their poor uptake into the brain. Conclusions CYP3A-mediated N-demethylation is the principal metabolic pathway of oxycodone in humans. The central opioid effects of oxycodone are governed by the parent drug, with a negligible contribution from its circulating oxidative and reductive metabolites. Clinical Pharmacology & Therapeutics (2006) 79, 461–479; doi: 10.1016/j.clpt.2006.01.009