Are Some Negotiators Better Than Others? Individual Differences in Bargaining Outcomes

The authors address the long-standing mystery of stable individual differences in negotiation performance, on which intuition and conventional wisdom have clashed with inconsistent empirical findings. The present study used the Social Relations Model to examine individual differences directly via consistency in performance across multiple negotiations and to disentangle the roles of both parties within these inherently dyadic interactions. Individual differences explained a substantial 46% of objective performance and 19% of subjective performance in a mixed-motive bargaining exercise. Previous work may have understated the influence of individual differences because conventional research designs require specific traits to be identified and measured. Exploratory analyses of a battery of traits revealed few reliable associations with consistent individual differences in objective performance—except for positive beliefs about negotiation, positive affect, and concern for one’s outcome, each of which predicted better performance. Findings suggest that the field has large untapped potential to explain substantial individual differences. Limitations, areas for future research, and practical implications are discussed

Clinical Variability in a Family with an Ectodermal Dysplasia Syndrome and a Nonsense Mutation in the TP63 Gene

Item does not contain fulltextMutations in the TP63 gene have been associated with a variety of ectodermal dysplasia syndromes, among which the clinically overlapping Ankyloblepharon-Ectodermal defects-Cleft lip/palate (AEC) and the Rapp-Hodgkin syndromes. We report a multiplex nonconsanguineous family of Ashkenazi-Jewish descent, in which the index patient presented with a persistent scalp skin lesion, dystrophic nails and light thin hair. Further evaluation revealed over 10 affected individuals in the kindred, over four generations, exhibiting varying degrees of ectodermal involvement. Analysis of the TP63 gene from four of the patients and from two healthy individuals of the same family was performed. Gene sequencing of the patients revealed a nonsense mutation leading to a premature termination codon (PTC) (p.Gln16X). The same mutation was found in all tested affected individuals in the family, but gave rise to marked phenotypic variability with minor clinical manifestations in some individuals, underscoring the clinical heterogeneity associated with the recently described PTC-causing mutations