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The production of atomically dispersed metal catalysts remains a significant challenge in the field of heterogeneous catalysis due to coexistence with continuously packed sites such as nanoclusters and nanoparticles. This work presents a comprehensive guidance on how to increase the degree of atomization through a selection of appropriate experimental conditions and supports. It is based on a rigorous macro-kinetic theory that captures relevant competing processes of nucleation and formation of single atoms stabilized by point defects. The effects of metal–support interactions and deposition parameters on the resulting single atom to nanocluster ratio as well as the role of metal centers formed on point defects in the kinetics of nucleation have been established, thus paving the way to guided synthesis of single atom catalysts. The predictions are supported by experimental results on sputter deposition of Pt on exfoliated hexagonal boron nitride, as imaged by aberration-corrected scanning transmission electron microscopy.

In this work, we demonstrate that the synergistic effect of PdAu nanoparticles (NPs) in hydrogenation reactions is not only related to high activity but also to their stability when compared to Pd mono-metallic NPs. To demonstrate this, a series of mono- and bi-metallic NPs: Pd, Pd0.75Au0.25, Pd0.5Au0.5, Pd0.25Au0.75and Au in ionic liquid [C4C1Im][NTf2] have been fabricated viaa magnetron sputtering process. Bi-metallic NPs possess external shells enriched with Pd atoms that interact with [NTf2]−of the ionic liquid resulting in enhanced catalytic performance in hydrogenation of cinnamaldehyde compared to their mono-metallic counterparts. This is ascribed to their higher stability over 24 h of reaction, whilst the catalytic activity and selectivity are comparable for both catalysts. Using a bespoke kinetic model for in situcatalyst deactivation investigations and electron microscopy imaging at the nanoscale, we have shown that PdAu has a deactivation rate constant of 0.13 h−1, compared to 0.33 h−1for Pd NPs, leaving 60% and 40% of available sites after the reaction, respectively. Beyond that, the kinetic model demonstrates that the reaction product has a strong stabilizing factor for bimetallic NPs against coarsening and deactivation, which is not the case for Pd NPs. In summary, our kinetic model enables the evaluation of the catalyst performance over the entire chemical reaction space, probing the contribution of each individual component of the reaction mixture and allowing the design of high-performance catalysts.

We sought to identify resting-state characteristics related to attention deficit/hyperactivity disorder, both as a categorical diagnosis and as a trait feature, using large-scale samples which were processed according to a standardized pipeline. In categorical analyses, we considered 1301 subjects with diagnosed ADHD, contrasted against 1301 unaffected controls (total N= 2602; 1710 males (65.72%); mean age = 10.86 years, sd = 2.05). Cases and controls were 1:1 nearest neighbor matched on in-scanner motion and key demographic variables and drawn from multiple large cohorts. Associations between ADHD-traits and resting-state connectivity were also assessed in a large multi-cohort sample (N= 10,113). ADHD diagnosis was associated with less anticorrelation between the default mode and salience/ventral attention (B = 0.009, t = 3.45, p-FDR = 0.004, d = 0.14, 95% CI = 0.004, 0.014), somatomotor (B = 0.008, t = 3.49, p-FDR = 0.004, d = 0.14, 95% CI = 0.004, 0.013), and dorsal attention networks (B = 0.01, t = 4.28, p-FDR < 0.001, d = 0.17, 95% CI = 0.006, 0.015). These results were robust to sensitivity analyses considering comorbid internalizing problems, externalizing problems and psychostimulant medication. Similar findings were observed when examining ADHD traits, with the largest effect size observed for connectivity between the default mode network and the dorsal attention network (B = 0.0006, t = 5.57, p-FDR < 0.001, partial-r = 0.06, 95% CI = 0.0004, 0.0008). We report significant ADHD-related differences in interactions between the default mode network and task-positive networks, in line with default mode interference models of ADHD. Effect sizes (Cohen’s d and partial-r, estimated from the mega-analytic models) were small, indicating subtle group differences. The overlap between the affected brain networks in the clinical and general population samples supports the notion of brain phenotypes operating along an ADHD continuum.

While much research has highlighted phenotypic heterogeneity in obsessive compulsive disorder (OCD), less work has focused on heterogeneity in neural activity. Conventional neuroimaging approaches rely on group averages that assume homogenous patient populations. If subgroups are present, these approaches can increase variability and can lead to discrepancies in the literature. They can also obscure differences between various subgroups. To address this issue, we used unsupervised machine learning to identify subgroup clusters of patients with OCD who were assessed by task-based fMRI. We predominantly focused on activation of cognitive control and performance monitoring neurocircuits, including three large-scale brain networks that have been implicated in OCD (the frontoparietal network, cingulo-opercular network, and default mode network). Participants were patients with OCD (n= 128) that included both adults (ages 24–45) and adolescents (ages 12–17), as well as unaffected controls (n= 64). Neural assessments included tests of cognitive interference and error processing. We found three patient clusters, reflecting a “normative” cluster that shared a brain activation pattern with unaffected controls (65.9% of clinical participants), as well as an “interference hyperactivity” cluster (15.2% of clinical participants) and an “error hyperactivity” cluster (18.9% of clinical participants). We also related these clusters to demographic and clinical correlates. After post-hoc correction for false discovery rates, the interference hyperactivity cluster showed significantly longer reaction times than the other patient clusters, but no other between-cluster differences in covariates were detected. These findings increase precision in patient characterization, reframe prior neurobehavioral research in OCD, and provide a starting point for neuroimaging-guided treatment selection.

While childhood attention-deficit/hyperactivity disorder (ADHD) is more prevalent in males than females, genetic contributors to this effect have not been established. Here, we explore sex differences in the contribution of common and/or rare genetic variants to ADHD. Participants were from the Adolescent Brain and Cognitive Development study (N= 1253 youth meeting DSM-5 criteria for ADHD [mean age = 11.46 years [SD = 0.87]; 31% female] and 5577 unaffected individuals [mean age = 11.42 years [SD = 0.89]; 50% female], overall 66% White, non-Hispanic (WNH), 19% Black/African American, and 15% other races. Logistic regression tested for interactions between sex (defined genotypically) and both rare copy number variants (CNV) and polygenic (common variant) risk in association with ADHD. There was a significant interaction between sex and the presence of a CNV deletion larger than 200 kb, both in the entire cohort (β = −0.74, CI = [−1.27 to −0.20], FDR-corrected p= 0.048) and, at nominal significance levels in the WNH ancestry subcohort (β = −0.86, CI = [−1.51 to −0.20], p= 0.010). Additionally, the number of deleted genes interacted with sex in association with ADHD (whole cohort. β = −0.13, CI = [−0.23 to −0.029], FDR-corrected p = 0.048; WNH. β = −0.17, CI = [−0.29 to −0.050], FDR-corrected p = 0.044) as did the total length of CNV deletions (whole cohort. β = −0.12, CI = [−0.19 to −0.044], FDR-corrected p= 0.028; WNH. β = −0.17, CI = [−0.28 to −0.061], FDR-corrected p= 0.034). This sex effect was driven by increased odds of childhood ADHD for females but not males in the presence of CNV deletions. No similar sex effect was found for CNV duplications or polygenic risk scores. The association between CNV deletions and ADHD was partially mediated by measures of cognitive flexibility. In summary, CNV deletions were associated with increased odds for childhood ADHD in females, but not males.

Childhood attention deficit hyperactivity disorder (ADHD) shows a highly variable course with age: some individuals show improving, others stable or worsening symptoms. The ability to predict symptom course could help individualize treatment and guide interventions. By studying a cohort of 362 youth, we ask if polygenic risk for ADHD, combined with baseline neural and cognitive features could aid in the prediction of the course of symptoms over an average period of 4.8 years. Compared to a never-affected comparison group, we find that participants with worsening symptoms carried the highest polygenic risk for ADHD, followed by those with stable symptoms, then those whose symptoms improved. Participants with worsening symptoms also showed atypical baseline cognition. Atypical microstructure of the cingulum bundle and anterior thalamic radiation was associated with improving symptoms while reduction of thalamic volume was found in those with stable symptoms. Machine-learning algorithms, trained and tested on independent groups, performed well in classifying those never affected against groups with worsening, stable, and improving symptoms (area under the curve >0.79). We conclude that some measures of polygenic risk, cognition, and neuroimaging show significant associations with the future course of ADHD symptoms and may have modest predictive power. These features warrant further exploration as prognostic tools.

Previous cross-sectional work has demonstrated resting-state connectivity abnormalities in children and adolescents with attention/deficit hyperactivity disorder (ADHD) relative to typically developing controls. However, it is unclear to what extent these neural abnormalities confer risk for later symptoms of the disorder, or represent the downstream effects of symptoms on functional connectivity. Here, we studied 167 children and adolescents (mean age at baseline = 10.74 years (SD = 2.54); mean age at follow-up = 13.3 years (SD = 2.48); 56 females) with varying levels of ADHD symptoms, all of whom underwent resting-state functional magnetic resonance imaging and ADHD symptom assessments on two occasions during development. Resting-state functional connectivity was quantified using eigenvector centrality mapping. Using voxelwise cross-lag modeling, we found that less connectivity at baseline within right inferior frontal gyrus was associated with more follow-up symptoms of inattention (significant at an uncorrected cluster-forming threshold of p≤ 0.001 and a cluster-level familywise error corrected threshold of p< 0.05). Findings suggest that previously reported cross-sectional abnormalities in functional connectivity within inferior frontal gyrus in patients with ADHD may represent a longitudinal risk factor for the disorder, in line with efforts to target this region with novel therapeutic methods.

The aim of the current paper is to provide the first comparison of computational mechanisms and neurofunctional substrates in adolescents with attention-deficit/hyperactivity disorder (ADHD) and adolescents with obsessive-compulsive disorder (OCD) during decision making under ambiguity.

Autism spectrum disorder (ASD) and obsessive-compulsive disorder (OCD) are often comorbid and share similarities across some cognitive phenotypes, including certain aspects of attention. However, no functional magnetic resonance imaging studies have compared the underlying neural mechanisms contributing to these shared phenotypes.

Education has been hailed as the solution to most of Africa's problems; however the low employment rates in countries like Uganda mainly due to global recession, is are of no help in improving the plight of the people. Students study but are later unable to find gainful employment and improve their standard of living.

The article reports that according to IRB president Bernard Lapasset, facilities in Rio de Janeiro, Argentina may not be fit to host rugby football games alongside Olympics in 2016.