Inferring emotion from amygdala activation alone is problematic

Cook et al. investigated neural responses in domestic dogs in an experiment designed to elicit jealousy. Relative to a control condition, watching the dogs’ caregivers feed a fake dog activated the amygdala bilaterally. Dogs rated higher in dog-directed aggressiveness showed larger initial amygdala activation. Amygdala activity in this context is insufficient evidence to infer that the dogs experienced jealousy or even negative affect. The experimental design does not provide an adequate level of control to infer the presence of jealousy

A functional polymorphism of the MAOA gene is associated with neural responses to induced anger control

Aggressiveness is highly heritable. Recent experimental work has linked individual differences in a functional polymorphism of the monoamine oxidase-A gene (MAOA) to anger-driven aggression. Other work has implicated the dorsal ACC (dACC) in cognitive-emotional control and the amygdala in emotional arousal. The present imaging genetics study investigated dACC and amygdala reactivity to induced anger control as a function of MAOA genotype. A research assistant asked 38 healthy male undergraduates to control their anger in response to an insult by a rude experimenter. Men with the low-expression allele showed increased dACC and amygdala activation after the insult, but men with the high-expression allele did not. Both dACC and amygdala activation independently mediated the relationship between MAOA genotype and self-reported anger control. Moreover, following the insult, men with the high-functioning allele showed functional decoupling between the amygdala and dACC, but men with the low-functioning allele did not. These results suggest that heightened dACC and amygdala activation and their connectivity are neuroaffective mechanisms underlying anger control in participants with the low-functioning allele of the MAOA gene

Brief Report: Evidence of Ingroup Bias on the Shooter Task in a Saudi Sample

When predominantly White participants in Western countries are asked to shoot individuals in a computer game who may carry weapons, they show a greater bias to shoot at outgroup members and people stereotyped as dangerous. The goal was to determine the extent to which shooter biases in the Middle East would vary as a function of target ethnicity and culturally appropriate or inappropriate headgear. Within a sample of 37 male Saudi Arabian residents, we examined shooter biases outside of Western nations for the first time. Targets in this task were either White or Middle Eastern in appearance, and wore either American style baseball caps or a Saudi Arabian style shemagh and igal. Our results replicated the bias to shoot racial outgroup members observed in Western samples; we found a bias to shoot White over Middle Eastern targets. Unexpectedly, we also found a bias for Saudi participants to shoot at people wearing culturally appropriate traditional Saudi headgear over Western style baseball caps. To explain this latter finding, we cautiously speculate that relative perceptions of dangerousness in the Middle East may be influenced by media exposure and changing social conditions in the region

The angry brain: neural correlates of anger, angry rumination, and aggressive personality

Abstract & Very little is known about the neural circuitry guiding anger, angry rumination, and aggressive personality. In the present fMRI experiment, participants were insulted and induced to ruminate. Activity in the dorsal anterior cingulate cortex was positively related to self-reported feelings of anger and individual differences in general aggression. Activity in the medial prefrontal cortex was related to self-reported rumination and individual differences in displaced aggression. Increased activation in the hippocampus, insula, and cingulate cortex following the provocation predicted subsequent self-reported rumination. These findings increase our understanding of the neural processes associated with the risk for aggressive behavior by specifying neural regions that mediate the subjective experience of anger and angry rumination as well as the neural pathways linked to different types of aggressive behavior. &amp

The feeling of anger: From brain networks to linguistic expressions.

This review of the neuroscience of anger is part of The Human Affectome Project, where we attempt to map anger and its components (i.e., physiological, cognitive, experiential) to the neuroscience literature (i.e., genetic markers, functional imaging of human brain networks) and to linguistic expressions used to describe anger feelings. Given the ubiquity of anger in both its normative and chronic states, specific language is used in humans to express states of anger. Following a review of the neuroscience literature, we explore the language that is used to convey angry feelings, as well as metaphors reflecting inner states of anger experience. We then discuss whether these linguistic expressions can be mapped on to the neural circuits during anger experience and to distinct components of anger. We also identify relationships between anger components, brain networks, and other affective research relevant to motivational states of dominance and basic needs for safety

Multi-omics of the gut microbial ecosystem in inflammatory bowel diseases.

Inflammatory bowel diseases, which include Crohn's disease and ulcerative colitis, affect several million individuals worldwide. Crohn's disease and ulcerative colitis are complex diseases that are heterogeneous at the clinical, immunological, molecular, genetic, and microbial levels. Individual contributing factors have been the focus of extensive research. As part of the Integrative Human Microbiome Project (HMP2 or iHMP), we followed 132 subjects for one year each to generate integrated longitudinal molecular profiles of host and microbial activity during disease (up to 24 time points each; in total 2,965 stool, biopsy, and blood specimens). Here we present the results, which provide a comprehensive view of functional dysbiosis in the gut microbiome during inflammatory bowel disease activity. We demonstrate a characteristic increase in facultative anaerobes at the expense of obligate anaerobes, as well as molecular disruptions in microbial transcription (for example, among clostridia), metabolite pools (acylcarnitines, bile acids, and short-chain fatty acids), and levels of antibodies in host serum. Periods of disease activity were also marked by increases in temporal variability, with characteristic taxonomic, functional, and biochemical shifts. Finally, integrative analysis identified microbial, biochemical, and host factors central to this dysregulation. The study's infrastructure resources, results, and data, which are available through the Inflammatory Bowel Disease Multi'omics Database ( http://ibdmdb.org ), provide the most comprehensive description to date of host and microbial activities in inflammatory bowel diseases

Pothead or pot smoker? a taxometric investigation of cannabis dependence

BACKGROUND: Taxometric methods were used to discern the latent structure of cannabis dependence. Such methods help determine if a construct is categorical or dimensional. Taxometric analyses (MAXEIG and MAMBAC) were conducted on data from 1,474 cannabis-using respondents to the 2001–2002 National Epidemiologic Survey on Alcohol and Related Conditions (NESARC). Respondents answered questions assessing DSM-IV criteria for cannabis dependence. RESULTS: Both taxometric methods provided support for a dimensional structure of cannabis dependence. CONCLUSION: Although the MAMBAC results were not entirely unequivocal, the majority of evidence favored a dimensional structure of cannabis dependence

Prediction of complicated disease course for children newly diagnosed with Crohn's disease: a multicentre inception cohort study

Stricturing and penetrating complications account for substantial morbidity and health-care costs in paediatric and adult onset Crohn’s disease. Validated models to predict risk for complications are not available, and the effect of treatment on risk is unknown

Acute mountain sickness.

Acute mountain sickness (AMS) is a clinical syndrome occurring in otherwise healthy normal individuals who ascend rapidly to high altitude. Symptoms develop over a period ofa few hours or days. The usual symptoms include headache, anorexia, nausea, vomiting, lethargy, unsteadiness of gait, undue dyspnoea on moderate exertion and interrupted sleep. AMS is unrelated to physical fitness, sex or age except that young children over two years of age are unduly susceptible. One of the striking features ofAMS is the wide variation in individual susceptibility which is to some extent consistent. Some subjects never experience symptoms at any altitude while others have repeated attacks on ascending to quite modest altitudes. Rapid ascent to altitudes of 2500 to 3000m will produce symptoms in some subjects while after ascent over 23 days to 5000m most subjects will be affected, some to a marked degree. In general, the more rapid the ascent, the higher the altitude reached and the greater the physical exertion involved, the more severe AMS will be. Ifthe subjects stay at the altitude reached there is a tendency for acclimatization to occur and symptoms to remit over 1-7 days