Charge polarization at catalytic metal-support junctions : Part A : Kelvin probe force microscopy results of noble metal nanoparticles

Metal oxide-supported nanoparticles of the platinum group metals Pt, Rh and Pd were studied at ambient temperature and atmosphere using Kelvin probe force microscopy. In all cases, the results reveal electron transfer from the metal to the oxide support which decreases in the order TiO2 > CeO2 >> Al2O3, leading to charge polarization at the Schottky type interfaces analogous to that of a parallel plane capacitor. This polarization cancels out to a large extent for the Kelvin signal. On top of this there is a much smaller number of positive charges at the outer catalyst particle surface, compensated by negative charges near the oxide surface. They show the same trend over the different oxides. These charges determine the constant electrical potential of the metal and are suggested to be the important component of the electronic catalytic metal-support interaction which are known to be much stronger for reducible than for non-reducible oxides.http://pubs.acs.org/journal/jpcafh2017-06-30hb2016Chemistr

Tuning the mobility of a driven Bose-Einstein condensate via diabatic Floquet bands

We study the response of ultracold atoms to a weak force in the presence of a temporally strongly modulated optical lattice potential. It is experimentally demonstrated that the strong ac-driving allows for a tailoring of the mobility of a dilute atomic Bose-Einstein condensate with the atoms moving ballistically either along or against the direction of the applied force. Our results are in agreement with a theoretical analysis of the Floquet spectrum of a model system, thus revealing the existence of diabatic Floquet bands in the atom's band spectra and highlighting their role in the non-equilibrium transport of the atoms

Charge polarization at catalytic metal-support junctions : Part B : Theoretical modeling of Kelvin probe force microscopy

Existing models for the analysis of Kelvin probe microscopy experiments are extended and used to analyze the experimental electrical potential profiles for a Pt/TiO2 model nanoparticle. The derived model reproduces in detail the Kelvin probe image that reveals a characteristic ring-shaped negative charge zone at the surface around the particle: A planar negative charge zone at the surface of the support extends beyond the diameter of the Pt particle. It is compensated mostly by a planar layer of positive charges in the metal across the interface, and by a smaller number of positive charges at the metal-air interface. These latter charges determine the positive electrical potential of the metal particle, and they are likely responsible for the extent of the metal-support interaction in catalytic reactions.http://pubs.acs.org/journal/jpcafh2017-06-30hb2016Chemistr

The Ig cell adhesion molecule Basigin controls compartmentalization and vesicle release at Drosophila melanogaster synapses

Synapses can undergo rapid changes in size as well as in their vesicle release function during both plasticity processes and development. This fundamental property of neuronal cells requires the coordinated rearrangement of synaptic membranes and their associated cytoskeleton, yet remarkably little is known of how this coupling is achieved. In a GFP exon-trap screen, we identified Drosophila melanogaster Basigin (Bsg) as an immunoglobulin domain-containing transmembrane protein accumulating at periactive zones of neuromuscular junctions. Bsg is required pre- and postsynaptically to restrict synaptic bouton size, its juxtamembrane cytoplasmic residues being important for that function. Bsg controls different aspects of synaptic structure, including distribution of synaptic vesicles and organization of the presynaptic cortical actin cytoskeleton. Strikingly, bsg function is also required specifically within the presynaptic terminal to inhibit nonsynchronized evoked vesicle release. We thus propose that Bsg is part of a transsynaptic complex regulating synaptic compartmentalization and strength, and coordinating plasma membrane and cortical organization

Non-mental diseases associated with ADHD across the lifespan:Fidgety Philipp and Pippi Longstocking at risk of multimorbidity?

Several non-mental diseases seem to be associated with an increased risk of ADHD and ADHD seems to be associated with increased risk for non-mental diseases. The underlying trajectories leading to such brain-body co-occurrences are often unclear - are there direct causal relationships from one disorder to the other, or does the sharing of genetic and/or environmental risk factors lead to their occurring together more frequently or both? Our goal with this narrative review was to provide a conceptual synthesis of the associations between ADHD and non-mental disease across the lifespan. We discuss potential shared pathologic mechanisms, genetic background and treatments in co-occurring diseases. For those co-occurrences for which published studies with sufficient sample sizes exist, meta-analyses have been published by others and we discuss those in detail. We conclude that non-mental diseases are common in ADHD and vice versa and add to the disease burden of the patient across the lifespan. Insufficient attention to such co-occurring conditions may result in missed diagnoses and suboptimal treatment in the affected individuals

Genomic Relationships, Novel Loci, and Pleiotropic Mechanisms across Eight Psychiatric Disorders

Genetic influences on psychiatric disorders transcend diagnostic boundaries, suggesting substantial pleiotropy of contributing loci. However, the nature and mechanisms of these pleiotropic effects remain unclear. We performed analyses of 232,964 cases and 494,162 controls from genome-wide studies of anorexia nervosa, attention-deficit/hyper-activity disorder, autism spectrum disorder, bipolar disorder, major depression, obsessive-compulsive disorder, schizophrenia, and Tourette syndrome. Genetic correlation analyses revealed a meaningful structure within the eight disorders, identifying three groups of inter-related disorders. Meta-analysis across these eight disorders detected 109 loci associated with at least two psychiatric disorders, including 23 loci with pleiotropic effects on four or more disorders and 11 loci with antagonistic effects on multiple disorders. The pleiotropic loci are located within genes that show heightened expression in the brain throughout the lifespan, beginning prenatally in the second trimester, and play prominent roles in neurodevelopmental processes. These findings have important implications for psychiatric nosology, drug development, and risk prediction.Peer reviewe

A genetic investigation of sex bias in the prevalence of attention-deficit/hyperactivity disorder

Background Attention-deficit/hyperactivity disorder (ADHD) shows substantial heritability and is 2-7 times more common in males than females. We examined two putative genetic mechanisms underlying this sex bias: sex-specific heterogeneity and higher burden of risk in female cases. Methods We analyzed genome-wide autosomal common variants from the Psychiatric Genomics Consortium and iPSYCH Project (20,183 cases, 35,191 controls) and Swedish populationregister data (N=77,905 cases, N=1,874,637 population controls). Results Genetic correlation analyses using two methods suggested near complete sharing of common variant effects across sexes, with rg estimates close to 1. Analyses of population data, however, indicated that females with ADHD may be at especially high risk of certain comorbid developmental conditions (i.e. autism spectrum disorder and congenital malformations), potentially indicating some clinical and etiological heterogeneity. Polygenic risk score (PRS) analysis did not support a higher burden of ADHD common risk variants in female cases (OR=1.02 [0.98-1.06], p=0.28). In contrast, epidemiological sibling analyses revealed that the siblings of females with ADHD are at higher familial risk of ADHD than siblings of affected males (OR=1.14, [95% CI: 1.11-1.18], p=1.5E-15). Conclusions Overall, this study supports a greater familial burden of risk in females with ADHD and some clinical and etiological heterogeneity, based on epidemiological analyses. However, molecular genetic analyses suggest that autosomal common variants largely do not explain the sex bias in ADHD prevalence