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: The moral/conventional task has been widely used to study the emergence of moral understanding in children and to explore the defi cits in moral understanding in clinical populations. Previous studies have indicated that moral transgressions, particularly those in which a victim is harmed, evoke a signature pattern of responses in the moral/conventional task: they are judged to be serious, generalizable and not authority dependent. Moreover, this signature pattern is held to be pan-cultural and to emerge early in development. However, almost all the evidence for these claims comes from studies using harmful transgressions of the sort that primary school children might commit in the schoolyard. In a study conducted on the Internet, we used a much wider range of harm transgressions, and found that they do not evoke the signature pattern of responses found in studies using only schoolyard transgressions. Paralleling other recent work, our study provides preliminary grounds for skepticism regarding many conclusions drawn from earlier research using the moral/conventional task.

We first describe recent empirical research on racial cognition, particularly work on implicit racial biases that suggests they are widespread, that they can coexist with explicitly avowed anti-racist and tolerant attitudes, and that they influence behavior in a variety of subtle but troubling ways. We then consider a cluster of questions that the existence and character of implicit racial biases raise for moral theory. First, is it morally condemnable to harbor an implicit racial bias? Second, ought each of us to suspect ourselves of racial bias, and therefore correct for it in ordinary activity, such as grading student papers?

Abstract:Our primary aim in this paper is to sketch a cognitive evolutionary approach for developing explanations of social change that is anchored in the psychological mechanisms underlying normative cognition and the transmission of social norms. We throw the relevant features of this approach into relief by comparing it with the self-fulfilling social expectations account developed by Bicchieri and colleagues. After describing both accounts, we argue that the two approaches are largely compatible, but that the cognitive evolutionary approach is well suited to encompass much of the social expectations view, whose focus on a narrow range of norms comes at the expense of the breadth the cognitive evolutionary approach can provide.

We argue that work on norms provides a way to move beyond debates between proponents of individualist and structuralist approaches to bias, oppression, and injustice. We briefly map out the geography of that debate before presenting Charlotte Witt's view, showing how her position, and the normative ascriptivism at its heart, seamlessly connects individuals to the social reality they inhabit. We then describe recent empirical work on the psychology of norms and locate the notions of informal institutions and soft structures with respect to it. Finally, we argue that the empirical resources enrich Witt's ascriptivism, and that the resulting picture shows theorists need not, indeed should not, choose between either the individualist or structuralist camp.

Altered response to the intestinal microbiota strongly associates with inflammatory bowel disease (IBD); however, how commensal microbial cues are integrated by the host during the pathogenesis of IBD is not understood. Epigenetics represents a potential mechanism that could enable intestinal microbes to modulate transcriptional output during the development of IBD. Here, we reveal a histone methylation signature of intestinal epithelial cells isolated from the terminal ilea of newly diagnosed pediatric IBD patients. Genes characterized by significant alterations in histone H3-lysine 4 trimethylation (H3K4me3) showed differential enrichment in pathways involving immunoregulation, cell survival and signaling, and metabolism. Interestingly, a large subset of these genes was epigenetically regulated by microbiota in mice and several microbiota-sensitive epigenetic targets demonstrated altered expression in IBD patients. Remarkably though, a substantial proportion of these genes exhibited H3K4me3 levels that correlated with the severity of intestinal inflammation in IBD, despite lacking significant differential expression. Collectively, these data uncover a previously unrecognized epigenetic profile of IBD that can be primed by commensal microbes and indicate sensitive targets in the epithelium that may underlie how microbiota predispose to subsequent intestinal inflammation and disease.

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