A fundamental issue in cognitive neuroscience is how the brain encodes others’ actions and intentions. In recent years, a potential advance in our knowledge on this issue is the discovery of mirror neurons in the motor cortex of the nonhuman primate. These neurons fire to both execution and observation of specific types of actions. Researchers use this evidence to fuel investigations of a human mirror system, suggesting a common neural code for perceptual and motor processes. Among the methods used for inferring mirror system activity in humans are changes in a particular frequency band in the electroencephalogram (EEG) called the mu rhythm. Mu frequency appears to decrease in amplitude (reflecting cortical activity) during both action execution and action observation. The current meta-analysis reviewed 85 studies (1,707 participants) of mu that infer human mirror system activity. Results demonstrated significant effect sizes for mu during execution (Cohen’s d = 0.46, N = 701) as well as observation of action (Cohen’s d = 0.31, N = 1,508), confirming a mirroring property in the EEG. A number of moderators were examined to determine the specificity of these effects. We frame these meta-analytic findings within the current discussion about the development and functions of a human mirror system, and conclude that changes in EEG mu activity provide a valid means for the study of human neural mirroring. Suggestions for improving the experimental and methodological approaches in using mu to study the human mirror system are offered.

In the present study we examined the neural correlates of facial emotion processing in the first year of life using ERP measures and cortical source analysis. EEG data were collected cross-sectionally from 5-(N = 49), 7-(N = 50), and 12-month-old (N = 51) infants while they were viewing images of angry, fearful, and happy faces.The N290 component was found to be larger in amplitude in response to fearful and happy than angry faces in all posterior clusters and showed largest response to fear than the other two emotions only over the right occipital area. The P400 and Nc components were found to be larger in amplitude in response to angry than happy and fearful faces over central and frontal scalp. Cortical source analysis of the N290 component revealed greater cortical activation in the right fusiform face area in response to fearful faces. This effect started to emerge at 5 months and became well established at 7 months, but it disappeared at 12 months. The P400 and Nc components were primarily localized to the PCC/Precuneus where heightened responses to angry faces were observed. The current results suggest the detection of a fearful face in infants' brain can happen shortly (~200-290 ms) after the stimulus onset, and this process may rely on the face network and develop substantially between 5 to 7 months of age. The current findings also suggest the differential processing of angry faces occurred later in the P400/Nc time window, which recruits the PCC/ Precuneus and is associated with the allocation of infants' attention. K E Y W O R D S cortical source analysis, ERPs, infant facial emotion processing S U PP O RTI N G I N FO R M ATI O N Additional supporting information may be found online in the Supporting Information section at the end of the article. How to cite this article: Xie W, McCormick SA, Westerlund A, Bowman LC, Nelson CA. Neural correlates of facial emotion processing in infancy. Dev Sci. 2019;22:e12758.

Pulmonary arterial hypertension (PAH) is an obstructive pulmonary vasculopathy, characterized by excess proliferation, apoptosis-resistance, inflammation, fibrosis and vasoconstriction. While PAH therapies target some of these vascular abnormalities (primarily vasoconstriction) most do not directly benefit the right ventricle (RV). This is suboptimal since a patient’s functional state and prognosis are largely determined by the success of the adaptation of the RV to the increased afterload. The RV initially hypertrophies but may ultimately decompensate, becoming dilated, hypokinetic and fibrotic. A number of pathophysiologic abnormalities have been identified in the PAH RV, including: ischemia and hibernation (partially reflecting RV capillary rarefaction), autonomic activation (due to GRK2-mediated down-regulation and desensitization of β-adrenergic receptors), mitochondrial-metabolic abnormalities (notably increased uncoupled glycolysis and glutaminolysis), and fibrosis. Many RV abnormalities are detectable by molecular imaging and may serve as biomarkers. Some molecular pathways, such as those regulating angiogenesis, metabolism and mitochondrial dynamics, are similarly deranged in the RV and pulmonary vasculature, offering the possibility of therapies that treat both the RV and pulmonary circulation. An important paradigm in PAH is that the RV and pulmonary circulation constitute a unified cardiopulmonary unit. Clinical trials of PAH pharmacotherapies should assess both components of the cardiopulmonary unit.

Objective Behavioral inhibition (BI) is a temperament identified in early childhood that is a risk factor for later social anxiety. However, mechanisms underlying development of social anxiety remain unclear. To better understand the emergence of social anxiety, longitudinal studies investigating changes at both behavioral neural levels are needed. Method BI was assessed in the laboratory at ages 2 and 3 (N = 268). Children returned at age 12, and electroencephalography (EEG) was recorded while performing a flanker task under two conditions: once while believing they were being observed by peers, and once while not being observed. This methodology isolated changes in error monitoring (error-related negativity; ERN) and behavior (post-error reaction time [RT] slowing) as a function of social context. At age 12, current social anxiety symptoms and lifetime diagnoses of social anxiety were obtained. Results Childhood BI prospectively predicted social-specific ERN increases and social anxiety symptoms in adolescence; these symptoms directly related to clinical diagnoses. Serial mediation analysis revealed social ERN changes explained relations between BI and both social anxiety symptoms (n = 107) and diagnosis (n = 92), but only insofar as social context also led to increased post-error RT slowing (a measure of error preoccupation); this model was not significantly related to generalized anxiety. Conclusion Results extend prior work on socially-induced changes in error monitoring and error preoccupation. These measures may index a neurobehavioral mechanism linking behavioral inhibition to adolescent social anxiety symptoms and diagnosis. This mechanism may relate more strongly to social than generalized anxiety in the peri-adolescent period.

Baseline electroencephalogram (EEG) data were collected from twenty-nine 4-year-old children who also completed batteries of representational theory-of-mind (RTM) tasks and executive functioning (EF) tasks. Neural sources of children's EEG alpha (6-9 Hz) were estimated and analyzed to determine whether individual differences in regional EEG alpha activity predicted children's RTM performance, while statistically controlling for children's age and EF skills. Results showed that individual differences in EEG alpha activity localized to the dorsal medial prefrontal cortex (dMPFC) and the right temporal-parietal juncture (rTPJ) were positively associated with children's RTM performance. These findings suggest that the maturation of dMPFC and rTPJ is a critical constituent of preschoolers' explicit theory-of-mind development.

Using a standardized assessment instrument, the authors compared 182 adults with congenital deaf-blindness and those with acquired deaf-blindness. They found that those with congenital deaf-blindness were more likely to have impairments in cognition, activities of daily living, and social interactions and were less likely to use speech for communication.

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Nitric oxide (NO) activates soluble guanylate cyclase (sGC) by binding its prosthetic heme group, thereby catalyzing cyclic guanosine monophosphate (cGMP) synthesis. cGMP causes vasodilation and may inhibit smooth muscle cell proliferation and platelet aggregation. The NO-sGC-cGMP pathway is disordered in pulmonary arterial hypertension (PAH), a syndrome in which pulmonary vascular obstruction, inflammation, thrombosis, and constriction ultimately lead to death from right heart failure. Expression of sGC is increased in PAH but its function is reduced by decreased NO bioavailability, sGC oxidation and the related loss of sGC’s heme group. Two classes of sGC modulators offer promise in PAH. sGC stimulators (e.g. riociguat) require heme-containing sGC to catalyze cGMP production, whereas sGC activators (e.g. cinaciguat) activate heme-free sGC. Riociguat is approved for PAH and yields functional and hemodynamic benefits similar to other therapies. Its main serious adverse effect is dose-dependent hypotension Riociguat is also approved for inoperable chronic thromboembolic pulmonary hypertension.