Reasoning supports utilitarian resolutions to moral dilemmas across diverse measures.

Sacrificial moral dilemmas elicit a strong conflict between the motive to not personally harm someone and the competing motive to achieving the greater good, which is often described as the "utilitarian" response. Some prior research suggests that reasoning abilities and deliberative cognitive style are associated with endorsement of utilitarian solutions, but, as has more recently been emphasized, both conceptual and methodological issues leave open the possibility that utilitarian responses are due instead to a reduced emotional response to harm. Across 8 studies, using self-report, behavioral performance, and neuroanatomical measures, we show that individual differences in reasoning ability and cognitive style of thinking are positively associated with a preference for utilitarian solutions, but bear no relationship to harm-relevant concerns.

The behavioral and neural basis of empathic blame.

Mature moral judgments rely both on a perpetrator's intent to cause harm, and also on the actual harm caused-even when unintended. Much prior research asks how intent information is represented neurally, but little asks how even unintended harms influence judgment. We interrogate the psychological and neural basis of this process, focusing especially on the role of empathy for the victim of a harmful act.

Neuroanatomical correlates of forgiving unintentional harms.

Mature moral judgments rely on the consideration of a perpetrator's mental state as well as harmfulness of the outcomes produced. Prior work has focused primarily on the functional correlates of how intent information is neurally represented for moral judgments, but few studies have investigated whether individual differences in neuroanatomy can also explain variation in moral judgments. In the current study, we conducted voxel-based morphometry analyses to address this question.

Congenital hyperinsulinism: clinical and molecular analysis of a large Italian cohort.

Congenital hyperinsulinism (CHI) is a genetic disorder characterized by profound hypoglycemia related to an inappropriate insulin secretion. It is a heterogeneous disease classified into two major subgroups: "channelopathies" due to defects in ATP-sensitive potassium channel, encoded by ABCC8 and KCNJ11 genes, and "metabolopathies" caused by mutation of several genes (GLUD1, GCK, HADH, SLC16A1, HNF4A and HNF1A) and involved in different metabolic pathways. To elucidate the genetic etiology of CHI in the Italian population, we conducted an extensive sequencing analysis of the CHI-related genes in a large cohort of 36 patients: Twenty-nine suffering from classic hyperinsulinism (HI) and seven from hyperinsulinism-hyperammonemia (HI/HA).