Creating pseudo Kondo-resonances by field-induced diffusion of atomic hydrogen

In low temperature scanning tunneling microscopy (STM) experiments a cerium adatom on Ag(100) possesses two discrete states with significantly different apparent heights. These atomic switches also exhibit a Kondo-like feature in spectroscopy experiments. By extensive theoretical simulations we find that this behavior is due to diffusion of hydrogen from the surface onto the Ce adatom in the presence of the STM tip field. The cerium adatom possesses vibrational modes of very low energy (3-4meV) and very high efficiency (> 20%), which are due to the large changes of Ce-states in the presence of hydrogen. The atomic vibrations lead to a Kondo-like feature at very low bias voltages. We predict that the same low-frequency/high-efficiency modes can also be observed at lanthanum adatoms.Comment: five pages and four figure

Higher-order contributions to the Rashba-Bychkov effect with application to Bi/Ag(111) surface alloy

In order to explain the anisotropic Rashba-Bychkov effect observed in several metallic surface-state systems, we use k.p perturbation theory with a simple group-theoretical analysis and construct effective Rashba Hamiltonians for different point groups up to third order in the wavenumber. We perform relativistic ab initio calculations for the Bi/Ag(111) ordered surface alloy and from the calculated splitting of the band dispersion we find evidence of the predicted third-order terms. Furthermore, we derive expressions for the corresponding third-order Rashba parameters to provide a simple explanation to the qualitative difference concerning the Rashba-Bychkov splitting of the surface states at Au(111) and Bi/Ag(111).Comment: 7 pages, 3 figure

Electron scattering in atomic force microscopy experiments

It has been shown that electron transitions, as measured in a scanning tunnelling microscope (STM), are related to chemical interactions in a tunnelling barrier. Here, we show that the shape and apparent height of subatomic features in an atomic force microscopy (AFM) experiment on Si(111) depend directly on the available electron states of the silicon surface and the silicon AFM tip. Simulations and experiments confirm that forces and currents show similar subatomic variations for tip-sample distances approaching the bulk bonding length.Comment: 5 pages and 4 figure

Gene expression biomarkers of response to citalopram treatment in major depressive disorder

There is significant variability in antidepressant treatment outcome, with ∼30–40% of patients with major depressive disorder (MDD) not presenting with adequate response even following several trials. To identify potential biomarkers of response, we investigated peripheral gene expression patterns of response to antidepressant treatment in MDD. We did this using Affymetrix HG-U133 Plus2 microarrays in blood samples, from untreated individuals with MDD (N=63) ascertained at a community outpatient clinic, pre and post 8-week treatment with citalopram, and used a regression model to assess the impact of gene expression differences on antidepressant response. We carried out technical validation of significant probesets by quantitative reverse transcriptase PCR and conducted central nervous system follow-up of the most significant result in post-mortem brain samples from 15 subjects who died during a current MDD episode and 11 sudden-death controls. A total of 32 probesets were differentially expressed according to response to citalopram treatment following false discovery rate correction. Interferon regulatory factor 7 (IRF7) was the most significant differentially expressed gene and its expression was upregulated by citalopram treatment in individuals who responded to treatment. We found these results to be concordant with our observation of decreased expression of IRF7 in the prefrontal cortex of MDDs with negative toxicological evidence for antidepressant treatment at the time of death. These findings point to IRF7 as a gene of interest in studies investigating genomic factors associated with antidepressant response

Crucial role of calbindin-D28k in the pathogenesis of Alzheimer's disease mouse model

Calbindin-D28k (CB), one of the major calcium-binding and buffering proteins, has a critical role in preventing a neuronal death as well as maintaining calcium homeostasis. Although marked reductions of CB expression have been observed in the brains of mice and humans with Alzheimer disease (AD), it is unknown whether these changes contribute to AD-related dysfunction. To determine the pathogenic importance of CB depletions in AD models, we crossed 5 familial AD mutations (5XFAD; Tg) mice with CB knock-out (CBKO) mice and generated a novel line CBKO·5XFAD (CBKOTg) mice. We first identified the change of signaling pathways and differentially expressed proteins globally by removing CB in Tg mice using mass spectrometry and antibody microarray. Immunohistochemistry showed that CBKOTg mice had significant neuronal loss in the subiculum area without changing the magnitude (number) of amyloid β-peptide (Aβ) plaques deposition and elicited significant apoptotic features and mitochondrial dysfunction compared with Tg mice. Moreover, CBKOTg mice reduced levels of phosphorylated mitogen-activated protein kinase (extracellular signal-regulated kinase) 1/2 and cAMP response element-binding protein at Ser-133 and synaptic molecules such as N-methyl-D-aspartate receptor 1 (NMDA receptor 1), NMDA receptor 2A, PSD-95 and synaptophysin in the subiculum compared with Tg mice. Importantly, this is the first experimental evidence that removal of CB from amyloid precursor protein/presenilin transgenic mice aggravates AD pathogenesis, suggesting that CB has a critical role in AD pathogenesis