Conscientiousness is a personality construct that is a core determinant of health, positive aging, and human capital. A large body of work has contributed to our understanding of this important aspect of personality, but there are multiple conceptual and methodological issues that complicate our understanding of conscientiousness. Toward this end, we review (a) the conceptual standing of conscientiousness as a personality trait, (b) past research focusing on the underlying dimensions of conscientiousness, (c) the nomological network in which conscientiousness is embedded, and (d) the diverse methods that have been used to assess dimensions of conscientiousness. We conclude with recommendations for improving our understanding of the construct of conscientiousness, methods of assessment, and etiological underpinnings of conscientiousness. We believe this article can serve an important role in the larger goal of better understanding conscientiousness and its core role in the health of our society.

The neural systems underlying reward-related behaviors across development have recently generated a great amount of interest. Yet, the neurodevelopmental literature on reward processing is marked by inconsistencies due to the heterogeneity of the reward paradigms used, the complexity of the behaviors being studied, and the developing brain itself as a moving target. The present review will examine task design as one source of variability across findings by compiling this literature along three dimensions: (1) task structures, (2) cognitive processes, and (3) neural systems. We start with the presentation of a heuristic neural systems model, the Triadic Model, as a way to provide a theoretical framework for the neuroscience research on motivated behaviors. We then discuss the principles guiding reward task development. Finally, we review the extant developmental neuroimaging literature on reward-related processing, organized by reward task type. We hope that this approach will help to clarify the literature on the functional neurodevelopment of reward-related neural systems, and to identify the role of the experimental parameters that significantly influence these findings.

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Theories of addiction implicate stress as a crucial mechanism underlying initiation, maintenance, and relapse to cigarette smoking. Examinations of the biological stress systems, including functioning of the hypothalamic-pituitary-adrenal (HPA) axis and the autonomic nervous system (ANS), have provided additional insights into the relationship between stress and smoking. To date, convergent data suggests that chronic cigarette smoking is associated with alterations in HPA and ANS functioning; however, less is known about the role of HPA and ANS functioning in smoking initiation and relapse following cessation. In order to organize existing findings and stimulate future research, the current paper summarizes the available literature on the roles of HPA axis and ANS functioning in the relationship between stress and cigarette smoking, highlights limitations within the existing literature, and suggests directions for future research to address unanswered questions in the extant literature on the biological mechanisms underlying the relationship between stress and smoking.

The aromatase enzyme complex, located primarily in the stromal cells of breast tumors, catalyzes estrogen biosynthesis and is fundamental to hormone-dependent growth of breast cancer. Although an important pharmacological target, the mechanisms by which aromatase is regulated are poorly understood. Thus, regulation of aromatase activity and expression in human breast stromal cells by prostaglandin E(2) (PGE(2)) was investigated. PGE(2) exerts its actions via four transmembrane receptors, EP(1), EP(2), EP(3), and EP(4), which coordinate different signal transduction pathways. Using selective receptor agonists and antagonists, the involvement of the EP(1), EP(2), and EP(3) subtypes was assessed. Enzyme activity levels in cultures of disease-free stromal cells were determined using a tritiated water-release assay. PGE(2) and agonists of EP(1) and EP(2) significantly increased aromatase activity levels, which were decreased by the corresponding antagonists. An agonist of EP(3), an inhibitory pathway, antagonized activity levels induced by PGE(2). These results were generally reflective of changes in aromatase protein expression, determined by Western blotting analysis and the pattern of mRNA expression determined by a competitive RT-PCR method. Collectively, the results demonstrate that regulation of aromatase by PGE(2) is complex and may influence the development and progression of hormone-dependent breast cancer.