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Consistent with the hypothesis that some of the psychological, behavioral, and physiological characteristics of morning- and evening-types may represent adaptations to slow and fast life histories, respectively, this study investigated variation in time perspective (i.e., being present- vs. future-oriented), impulsivity, cooperation and competition, self-perceived social status, and cortisol and testosterone concentrations in baseline conditions and in response to psychosocial stress in relation to morningness–eveningness. Study participants were 60 male and 60 female young adults, mostly college students. Questionnaires were used to collect demographic information and to assess morningness–eveningness, impulsivity, time perspective, and self-perceived social status. Cooperative and competitive tendencies were assessed with an Ultimatum Game, an iterated Prisoner’s Dilemma Game, and a Prosocial Risk-Taking Task. Half of the study participants underwent a standardized procedure that elicits psychosocial stress (the Trier Social Stress Test) and half served as controls. Three saliva samples were obtained before and after the TSST or the control condition and later assayed for testosterone and cortisol concentrations. Consistent with our hypotheses, morning-types were more future-oriented, more cooperative in the Prisoner’s dilemma (men, not women), and perceived themselves to be of lower social status than evening-types. Furthermore, morning-types had a significantly greater cortisol response to stress than evening-types. Some of our findings support the functional interpretation of morningness–eveningness from a life history perspective. In particular, higher physiological reactivity to psychosocial stress among morning-types may be associated with their reported lower extraversion and be one of the factors contributing to some aspects of their slow life history strategy, including their avoidance of short-term mating strategies, lower sexual competitiveness, and lower social status.

Introduction Acetaminophen toxicity has been associated with elevation of microRNAs. The present study was to evaluate overall microRNA profiles and previously identified microRNAs to differentiate acetaminophen (APAP) toxicity from other causes of transaminase elevation. Methods This was an observational study of adults with presumed acetaminophen toxicity at presentation. Serum samples were collected every 12 hours during hospitalization. Total miRNAs were extracted from plasma and levels of 327 microRNAs were quantified using real-time polymerase chain reaction. A standard measure of miRNA expression (delta-delta cycle threshold) was calculated for each microRNAs. A two-level cluster analysis was performed using a random k-means algorithm. Demographic and clinical characteristics of each cluster were compared using ANOVA, Wilcoxon rank sum, Kruskal-Wallis, and chi-square tests. Performance of specific miRNAs of interest was also evaluated. Results Twenty-seven subjects were enrolled (21 with a final diagnosis of acetaminophen toxicity), and a total of 61 samples were analyzed. Five clusters were identified, two of which demonstrated clear clinical patterns and included specific elevated miRNAs previously reported to be elevated in APAP toxicity patients. Features associated with clusters 1 and 5 included confirmed acetaminophen toxicity, high peak alanine aminotransferase, and late presentation. Clusters 2-4 contained lower peak microRNAs, lower peak alanine aminotransferase, and heterogeneous clinical characteristics. Conclusions Severe cases of acetaminophen toxicity showed two distinct patterns of microRNA elevation which were similar to previous work, while less severe cases were difficult to distinguish from non-acetaminophen-associated cases. Further work is needed to incorporate microRNA profiles into the diagnostic algorithm of acetaminophen toxicity.

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