Social learning models of the intergenerational transmission of aggression were tested for an at-risk sample of young adult men who entered a longitudinal study (Oregon Youth Study) in Grade 4 and were assessed with a female partner in young adulthood (17-20 years old). The associations of 2 family process variables--parental dyadic aggression and unskilled parenting, assessed both in late childhood and early adolescence with the son's later aggression toward a partner--were examined. Parental antisocial behavior was hypothesized to be associated with both family process variables. Unskilled parenting was hypothesized to play a key role in the son's later aggression toward an intimate partner, mediated by his development of antisocial behavior by adolescence. Fully prospective structural equation models were tested with multimethod, multiagent data, including both observed and reported aggression toward the partner. Findings indicate that the major hypothesized pathways through unskilled parenting practices and the boys' antisocial behavior were implicated in the intergenerational transmission of aggression.

We present a disease-on-a-chip model in which cancer grows within phenotypically normal breast luminal epithelium on semicircular acrylic support mimicking portions of mammary ducts. The cells from tumor nodules developing within these hemichannels are morphologically distinct from their counterparts cultured on flat surfaces. Moreover, tumor nodules cocultured with the luminal epithelium in hemichannels display a different anticancer drug sensitivity compared to nodules cocultured with the luminal epithelium on a flat surface and to monocultures of tumor nodules. The mimicry of tumor development within the epithelial environment of mammary ducts provides a framework for the design and test of anticancer therapies.

The GPR30 is a novel estrogen receptor (ER) that is a candidate membrane ER based on its binding to 17β estradiol and its rapid signaling properties such as activation of the extracellular-regulated kinase (ERK) pathway. Its distribution in the mouse limbic system predicts a role for this receptor in the estrogenic modulation of anxiety behaviors in the mouse. A previous study showed that chronic administration of a selective agonist to the GPR30 receptor, G-1, in the female rat can improve spatial memory, suggesting that GPR30 plays a role in hippocampal-dependent cognition. In this study, we investigated the effect of a similar chronic administration of G-1 on behaviors that denote anxiety in adult ovariectomized female mice, using the elevated plus maze (EPM) and the open field test as well as the activation of the ERK pathway in the hippocampus. Although estradiol benzoate had no effect on behaviors in the EPM or the open field, G-1 had an anxiolytic effect solely in the open field that was independent of ERK signaling in either the ventral or dorsal hippocampus. Such an anxiolytic effect may underlie the ability of G-1 to increase spatial memory, by acting on the hippocampus.

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